an expository essay on ebola virus

Open Access is an initiative that aims to make scientific research freely available to all. To date our community has made over 100 million downloads. It’s based on principles of collaboration, unobstructed discovery, and, most importantly, scientific progression. As PhD students, we found it difficult to access the research we needed, so we decided to create a new Open Access publisher that levels the playing field for scientists across the world. How? By making research easy to access, and puts the academic needs of the researchers before the business interests of publishers.

We are a community of more than 103,000 authors and editors from 3,291 institutions spanning 160 countries, including Nobel Prize winners and some of the world’s most-cited researchers. Publishing on IntechOpen allows authors to earn citations and find new collaborators, meaning more people see your work not only from your own field of study, but from other related fields too.

Brief introduction to this section that descibes Open Access especially from an IntechOpen perspective

Want to get in touch? Contact our London head office or media team here

Our team is growing all the time, so we’re always on the lookout for smart people who want to help us reshape the world of scientific publishing.

Home > Books > Emerging Challenges in Filovirus Infections

Essay on the Elusive Natural History of Ebola Viruses

Submitted: 15 April 2019 Reviewed: 29 July 2019 Published: 01 October 2019

DOI: 10.5772/intechopen.88879

Cite this chapter

There are two ways to cite this chapter:

From the Edited Volume

Emerging Challenges in Filovirus Infections

Edited by Samuel Ikwaras Okware

To purchase hard copies of this book, please contact the representative in India: CBS Publishers & Distributors Pvt. Ltd. www.cbspd.com | [email protected]

Chapter metrics overview

1,286 Chapter Downloads

Impact of this chapter

Total Chapter Downloads on intechopen.com

Total Chapter Views on intechopen.com

This chapter presents a review of what is known about the natural history of the Ebolaviruses in Central and West Africa as well as in the Philippines. All the previous hypotheses on the natural cycle of Ebolavirus are revisited. Also, the main factors driving the virus natural cycle are summarized for the different ecosystems where the Ebolavirus is known to have emerged, including the virus species, the date of emergence, the seasonality, the environmental features, as well as the potential risk and associated factors of emergence. The proposed hypothesis of the Ebolavirus natural cycle prevails an inter-species spillover involving several vertebrate hosts, as well as biotic and abiotic changing environmental factors among other original features of a complex natural cycle. It is also compared with other virus having such type of cycle involving chiropteran as potential reservoir and vector and presenting such original inter-outbreak epidemiological silences. Ultimately, these observations and hypotheses on Ebolavirus natural cycles give some insight into the potential drivers of virus emergence, host co-evolution, and a spatiotemporal dimension of risk leading to identify high risk areas for preventing emerging events and be prepared for an early response.

• natural cycle

Author Information

Jean-paul gonzalez *.

• Division of Biomedical Graduate Research Organization, Department of Microbiology and Immunology, School of Medicine, Georgetown University, USA
• Centaurus Biotech LLC, USA

Marc Souris

• Institute of Research for Development (IRD), France

Massamba Sylla

• Ministry of Health, Senegal

Francisco Veas

• Faculty of Pharmacy, Montpellier University, France

Tom Vincent

• CRDF Global, USA

*Address all correspondence to: [email protected]

1. Introduction

It has been several decades since an unknown fever dramatically emerged, close to the Ebola river, a small tributary of the great Ubangi river in the heart of the Congolese tropical forest of Africa. Since that time, even though the virus responsible for this new hemorrhagic fever has been identified and characterized, the natural history of the eponymic Ebolavirus remains largely unknown. The cradle of the virus remains enigmatic and the emergence of the Ebola fever unsolved. Indeed, the arcane of Ebolavirus natural history is still hypothesized, thanks to an elusive virus that always risen where it was not expected, violent and devastating, and surprising local populations and health systems, as well as the international scientific community. This Ebolavirus eco-epidemiology remains complex while the Ebola fever (alias Ebolavirus Disease) can be considered as an exemplary disease that can be eventually comprehended only with a transdisciplinary approach that has recently been promoted as a One Health concept. Indeed, it is only when we take into account all disease and virus drivers, including biotic and abiotic factors of the natural and human environments, that some mechanisms of the Ebolavirus disease emergence, such as spread and circulation, can be ultimately unveiled. For that, we have collected all information available, often estimated, from the time and place of the virus emergence long before the emerging event was identified as it and the epidemic phase was brought to public attention. Moreover, when available we also collect all data on potential natural and accidental hosts, weather and environment chorology, among other multiple factors potentially involved.

Historically, Ebolavirus emerged in Central Africa in the late 1970s, and has re-emerged most recently with the active epidemic (April 2019) in the eastern Democratic Republic of Congo (DRC), by encompassing more than 24 epidemic events from Central to West Africa, to imported infected monkey from Asia to Virginia, and the emerging new Ebola species of the Philippines archipelago [ 1 ].

Among the negative sense RNA viruses of the Filoviridae family five genera are known, including Cuevavirus, Ebolavirus, Marburgvirus , Thamnovirus . Among the Ebolavirus genus, five Ebolavirus (EBOV) species have been identified [ 2 ].

Ebolavirus’ (EBOV) first emergence occurred in 1976, as two different EBOV species in two different places in sub Saharan Africa. The Zaire Ebolavirus (ZEBOV) species and the Sudan Ebolavirus (SUDV) were detected concomitantly, a few weeks apart, respectively in the Northeastern Equator province of the Democratic Republic of Congo, DRC (alias Zaire), and in the Bahr el Ghazal province of South Sudan. On the 26th of August 1976 ZEBOV was isolated from missionaries and local villagers of the Yambuku, in the rain forest close to the Ebola river. However, earlier in June 1976, the SUDV had broken out among cotton factory workers in Nzara, Sudan (now in South Sudan) [ 3 ].

Then, in 1989, the Reston Ebolavirus species surprisingly (RESTV) emerged in the US (!) and was identified during an outbreak of simian hemorrhagic fever virus in crab-eating macaques from Hazleton Laboratories (now Covance) of Reston county, Virginia. Such primate specimens were found to be recently imported from the Philippines. Then, in 1994 a fourth new species of Ebolavirus was isolated from chimpanzee leaving in the Tai Forest of Côte d’Ivoire and named Côte d’Ivoire ebolavirus (CIEBOV). Finally, in November 2007, a fifth Ebolavirus species, was detected from infected patients in Uganda in the Bundibugyo District and was subsequently identified by the eponymic name of Bundibugyo Ebolavirus [ 4 ].

Briefly and extraordinarily among the world of the viruses, the filovirus virion presents a bacilliform (filamentous) shape, like a Rhabdovirus, but presents unique pleomorphic figures with branches and other tortuous shapes. Ebolaviruses have also an unusual and variable long length - up to 805 nanometers (only some plant virus can compete to this filamentous extensive length). However, the internal structure is more classical with a ribonucleoprotein nucleocapsid, a lipid envelope and seven nanometers size spikes. The genome is non-segmented, single stranded RNA of negative polarity with lengths of about 18.9 kb that code for seven proteins, each one having a specific function [ 5 ].

Ebolaviruses are known for their high case-fatality rate (CFR) with always less than 2/3 of survivors among the identified cases. ZEBOV, the most frequently isolated Ebolavirus species during the outbreaks, has the highest CFR, up to 90% in some instances, with an average of 83% for the past 37 years. The Uganda BDBV outbreak had a mortality rate of 34%. RESTV imported to the US did not cause disease in exposed human laboratory workers. The scientist performing the necropsies on CIEBOV infected chimpanzees got infected and developed a Dengue-like fever, fully recovered 6 weeks after the infection while treated in Switzerland.

2. When Ebolavirus raised his head in the heart of darkness

Dates and time make History. Indeed, the various reports on the emergence of Ebolavirus in Africa show discrepancies and lack accuracy, for multiple reasons (remote event, reports by different person or team, at different time…) but the only way to forge the history is to label the events with date, time and the environmental factors observed. On July 27, 1976, the first (known) victim to contract Ebolavirus was a cotton factory worker from Nzara, Sudan. Then, in Zaire (DRC) on September 1, 1976, the first Ebolavirus (Zaire ebolavirus, ZEBOV) victim was a teacher who had just returned from a family visit to northern Zaire (6 Jennifer Rosenberg Internet). These two events were the very beginning of the boundless journey of a deadly Ebolavirus outbreaks.

2.1 The Ebolavirus species emerging events

When the virus becomes epidemic in a human population, it does so weeks or months after the emergent event of the virus switching from its silent transmission in a natural cycle to a zoonotic/epidemic manifestation, revealed to the local health system. Let us see in more detail such emerging events of Ebolavirus species (ICTV, 2018) as there were reported or sometime interpreted, in time and place.

Sudan ebolavirus (SEBOV) occurred when the first recorded SUDV broke out among cotton factory workers in Nzara, South Sudan in June 271,976. This was indeed, the first case of Ebolavirus infection recorded and confirmed and also reported as potentially exposed to chiropteran. Indeed, at the Nzara Cotton Manufacturing Factory this first patient was a cloth room worker where bats (mostly Tadarida - mops - trevori ) have a large population in the roof space of their premises. He died in the Nzara hospital on July 6, 1976. Local animals and insects were tested for Ebolavirus without success [ 6 , 7 ].

Zaire ebolavirus (ZEBOV) was reported in the Mongala district of the Democratic Republic of Congo (DRC; alias Zaire) in August 1976, when a 44-year-old schoolteacher of the Yambuku village, became the first recorded case of Ebolavirus infection in DRC. Also, the schoolteacher travel earlier in August 1976 near the Central African Republic border and along the Ebola River, estimated 90 km NW from the village [ 6 ].

Reston ebolavirus (REBOV) had its first emerging event as an imported infected cynomolgus monkey ( Macaca fascicularis ) in October 1989 imported from a facility in the Philippines (Mindanao Island) to Reston, Virginia, USA, where the primate got sick and the virus isolated [ 8 ]. In the Philippines, in several instances, the virus was found to infect pigs, in June and September 2008 ill pigs were confirmed to be infested by REBOV (Ecija and Bulacan, Manila island), as well during 2008–2009 epizootics in the island of Luzon (Philippines) [ 9 ].

Cote d’Ivoire ebolavirus (CIEBOV) was isolated for the first time, and as an only known appearance, in November 1994, from wild chimpanzees presenting severe internal bleeding of the Taï Forest in Côte d’Ivoire, Africa. A researcher became infected when practicing a necropsy on one of these primates, he developed a dengue syndrome and survived. At that time, many dead chimpanzees were discovered and tested positive for Ebolavirus. However, the source of the virus was believed to be of infected western red colobus monkeys ( Piliocolobus badius ) upon which the chimpanzees preyed [ 10 ].

Bundibugyo ebolavirus (BDBV) was then discovered during an outbreak of Ebolavirus in the Bundibugyo District (Bundibugyo and Kikyo townships), on August 1st, 2007, in Western Uganda (Towner et al. [ 11 ]). BDBV second emerging event was observed in the DRC in August 17, 2012 in Isiro, Pawa and Dungu, districts of the Province Orientale [ 11 ].

With the exception of REBOV in Philippines and CIEBOV in West Africa, all other EBOVs species emerged in the Central African region. Also, all EBOVs are known to emerged in the tropical rain forest during the inter-season between dry and rainy seasons. Also, REBOV appears to actively circulate in the tropical rain or moist deciduous forest of the Philippines [ 12 ].

2.2 From Central Africa to West Africa

2.2.1 concurrent emergences of ebolaviruses.

On several occasions, concurrent emerging events of Ebolavirus have been observed. Indeed, such events occurred in places geographically distant, independent, and unconnected. The Ebolavirus was isolated and the strains different, even they belonged to the same species of Ebolavirus, altogether in favor of a different origin from an elusive natural reservoir, thus eliminating the notion of leaping from one site to the other. In that matter, the following observations are a paradigm: From its inceptive emergence the Ebolavirus was identified in Sudan at the cotton factory and a few days later at Yambuku, Zaire. The Ebola Sudan and Ebola Zaire viruses emerged concurrently in 1976 in the Congo basin of Central Africa; More than 20 years later the virus emerged and reemergence from 1994 to 1996 in a different places in Gabon, in a successive and timely overlapping events but in unconnected areas from where different strains of the same EBOVZ were isolated [ 13 ]; More recently, during the 2014–2016 dramatic Ebolavirus disease (EVD) emergence of in West Africa where the virus emerged in late December 2013 of a 18-month-old boy from the small village of Meliandou (Guéckédou district, South-Eastern Guinea) believed to have been infected by bats [ 14 ], concurrently, in August 2013, the Ebolavirus reemerged in the Equator province of DRC - different places and different strain of ZEBOV [ 15 ].

It is remarkable that most of these emerging events occurred during or close to the end of the rainy season which generally stretches from August to October in the domain of the Congo basin tropical rain forest.

Altogether, these observations are in favor of environmental factors of emergence favoring, when they occur synchronously in the same place, the spillover of the virus from its hidden natural cycle to an accidental and susceptible host. Therefore, these plural and concomitant emerging events play against the theory of Ebola virus diffusing in oil spot in Central Africa [ 16 ]. This original pattern of concurrent emergences could explain also the relative stability of the virus strains which remain for years in the same environment, and the interepidemic silences which require several fundamentals (i.e. concurrent risk factors) to be broken.

2.2.2 An unexpected broader domain of Ebolavirus circulation

The first evidence that showed that Ebola virus had previously circulated in areas without any known cases of disease came in 1977, near the Ebola outbreak in Tandala, DRC, just 200 miles west of the first known cases in 1976 [ 17 ]. Blood samples obtained from individuals in areas with no previous symptoms of Ebola were found to contain antibodies for Ebolavirus, indicating a previous or ongoing infection with that virus. Because subclinical illness is always a possibility with viral infections, the presence of these Ebolavirus-specific antibodies could only be explained by exposure to the virus, which is somewhat reasonable in an area that is endemic to the disease. But how do we know the true endemic zone of a virus such as Ebolavirus?

Endemic zones are primarily based on where disease can most likely be expected, and are determined by historical accounts of disease, as well as supplemental information such as where animals or insects that might transmit the disease are located. With respect to the Ebola virus, outbreaks that occur in Central Africa, in or near the Congo River Basin, are expected; outbreaks that take place elsewhere are unexpected and can be problematic, as was the case for the 2014–2016 West African outbreak. And yet, scientists have highlighted the presence of Ebola antibodies well outside the endemic zone for disease for decades.

In the early 1980’s, research based at the Pasteur Institute in Bangui, Central African Republic, demonstrated for the first time that the population of central Africa presented natural antibodies against the Ebolavirus strains of Zaire and Sudan [ 3 , 4 ]. Research also showed for the first time that several mammal species had Ebolavirus-reacting antibodies, including rodents, dogs, and others. Initially, the scientific community was skeptical of the findings, due to the type of antibody tests used, and because the prevalence of these antibodies was unbelievably dispersed and at a high level of prevalence. However, a 1989 follow-up study confirmed methodology and preliminary observations, and expanded the results to include similar observations in Cameroon, Chad, Gabon, and Republic of Congo (the latter two of these countries would have their first Ebola outbreaks in 1994 and 2001, respectively) [ 5 ]. Moreover, such Ebolavirus antibody prevalence was found in West Africa (e.g. Senegal, Chad, Sierra Leone), preceding the catastrophic 2014–2016 Ebolavirus outbreak [ 18 ]. Subsequent studies have determined that 20–25% of persons living in or near the Congolese rain forest are seropositive for Ebola, despite never exhibiting symptoms [ 19 ].

Today, Ebola antibody prevalence is widely distributed across the African continent in the absence of severe clinical presentation and/or outbreak manifestation. A 1989 study even found Ebola Zaire antibodies among people living in Madagascar, an island country that has never had a single known case of Ebola, and which has been geographically separated from continental Africa for 100 million years [ 20 ].

Risk mapping, including ecological and geographical distribution <10-13 cm/s first hour, and extended, highly sensitive and specific environmental and biogeographical models based on EBOVs susceptible mammalian biogeography in Africa, show a robust and precise potential distribution of EBOVs in Africa that clearly overlap the African tropical rain forest biome of the Guinea-Congo forests (including the Congo basin rain forest, and the Occidental relic of the Congolese rain forest spreading from Guinea to Ghana) and the southern band of the Sudan-Guinea Savanna [ 21 ].

Also, as a result of potential Ebolavirus (or Ebolavirus antigen) exposure, serological markers have been found in vertebrates outside of Africa. With the exception of Philippines, where REBOV is known to circulate in monkeys and pigs, thus showing its ability to infect multiple animal species, in several instances serological evidence of Ebolavirus exposure has been detected in many vertebrates, particularly chiropterans [ 9 ]. Definitely, bat populations in Bangladesh and China present antibodies against ZEBOV and REBOV proteins [ 22 , 23 ]. Ultimately, it appears that EBOVs are widely distributed throughout Africa, West and Central, and Asia. Moreover, risk mapping of filovirus ecologic niches suggests potential areas of EBOVs distribution in Southeast Asia [ 24 ].

The unexpected detection of REBOV first in Virginia, for the reason we know, and then the astonishing discovery of its circulation and natural cycle in the Philippines gave a rethinking of the entire family of Ebola viruses previously known mainly on the African continent [ 25 ].

From these observation and facts, the potential circulation of EBOVs in its natural cycle appears much wider than expected, while the emerging events we can witness appears to be only a tip of the iceberg in the wide Congolese tropical rain forest.

2.3 From the index case to the epidemic chain, outbreak, and pandemic

The fundamentals of emergence are changing in the heart of the rainforest and elsewhere: changing times, when the means of transmission switch from foot to motorbike, when knowledge conveyance has switched from paper reporting to the internet.

Let us examine the risk of expansion for Ebolavirus. Indeed, the factors of transmission of the virus to man and man to man are essential to take into account in this context. Moreover, it is extremely important to note that these factors are subject to permanent changes in societies whose trade and means of communication are drastically changing as a result of health systems, responses and preparedness for epidemics at national and international levels, policies, and the economy.

So, with the experience gained for more than 40 years, the strategies of struggle are clearly defined, but the societal changes that are taking place make their application difficult and sometimes impossible (e.g., the 2019 outbreak in the DRC, where political institutions have prevented an adapted response). Situation and the epidemic are perpetuated.

There is also a growing means of communication, both smartphones and motorized transport, to travel more quickly as ever, between the epidemic zone of EVD and the family [ 26 ].

Thus, during the emergence of the Ebola virus in West Africa, all of this means of communication played a fundamental role in the regional spread of the epidemic, until it became a pandemic risk when the virus was exported to other countries of the African continent and, outside Africa in Europe and North America [ 27 ].

3. A strange iteration of epidemic events with unexplained virus disappearance

It is known for several other transmitted viruses that during the inter-epidemic silences several factors can be responsible. In general mass herd immunity (natural of due to acquired immunization i.e. vaccine) of the permissive hosts force the virus in its natural cycle without apparent clinical manifestation in the hosts (e.g. Most by the arbovirus classically yellow fever, Dengue, Japanese encephalitis, West Nile, Zika etc.).

The Paramyxoviridae and Rhabdoviridae are the two other viral families in the order Mononegavirales, genetically closely related to the Filoviridae and having chiropteran as reservoir and/or vector [ 28 ]. Indeed, it is interesting to note that megachiropteran fruit bats are reservoirs of Hendra and Nipah viruses of the Paramyxoviridae family [ 29 ]. When, Microchiroptera bats are the probable ancestors of all rabies virus variants of the Lyssavirus genus in the family Rhabdoviridae and infecting presently terrestrial mammals [ 30 ]. Both also present this cryptic interepidemic silences that has not been yet clearly understood. The Nipah emerged one time in Malaysia (1999), thought to have its original cycle in PNG, and ultimately reemerged more than 3500 km away in Bangladesh in 2001. From its inception, again the Marburgvirus (the closest to EBOVs in the family of Filovirus), emerging events from an expected natural foci occurred within the path of time including 4 to 11 years of inter-epidemic silences occurring mostly in distant sites of Eastern and South Africa (Uganda, Zimbabwe, Angola, Kenya).

If one were to describe the history of Ebola outbreaks, one could simply construct a timeline, with a point on the line for each outbreak. You could create this timeline with a varying number of points, depending on your methodology, but regardless of how you built your timeline, there would be spaces between these points. This is due to the nature of Ebola; it appears, it disappears, and it appears again. To the Ebola virus, these gaps are periods of convalescence. To us, they are periods of absence and mystery, and one of these gaps stands out as the most mysterious ( Figure 1 ).

Timeline of Ebolavirus emergence. Emerging events (bars) red = EBOV; blue = SEBOV; green = BDBV; horizontal axis = years 1972–2018; vertical axis = no value. Numbers above brackets = years of silent inter-emerging event.

The CDC lists five Ebola outbreaks in the late 1970’s. The “first” Ebola outbreak took place in 1976, though we now recognize the event as two simultaneous and separate outbreaks. Between June and November 1976, 284 cases (151 deaths) of Ebola Sudan occurred near what is now Nzara, South Sudan; between September and October 1976, 318 cases (280 deaths) of Ebola Zaire occurred near what is now Yambuku, Democratic Republic of Congo (DRC). In November 1976, a researcher in England that was working with samples from the Nzara outbreak accidentally infected himself; CDC lists this accident as the third Ebola outbreak (the individual recovered). In June 1977, a child became sick and died from Ebola Zaire in Tandala, DRC though there was only one confirmed case, subsequent epidemiological investigations of the area uncovered several other historical, probable cases. Finally, between July and October 1979, 34 cases (22 deaths) of Ebola Sudan occurred, unbelievably, in Nzara, Sudan – the same community where the first cases of Ebola emerged just 3 years prior. In the span of just 39 months, the terror of Ebola had introduced itself to the world five times (638 cases, 454 deaths) and then… silence.

Ebola would not reappear for 10 whole years, and even then, the subtype was Ebola Reston, which we now know does not affect humans. Though CDC lists four Ebola Reston outbreaks between 1989 and 1992, the world would not see another case of Ebola virus disease in humans until late-1994, in Gabon. Even then, the outbreak (52 cases, 31 deaths) was mischaracterized as yellow fever for several months. Perhaps the virus’s long absence from the spotlight had removed it from the collective consciousness in 1994, certainly in the presence of those pathogens that had been circulating and consuming our attention in the meantime.

This fifteen-year disappearance of Ebola, particularly in light of its frequent and severe outbreaks in the late 1970’s, has perplexed researchers for decades. The mystery lay, to some extent, within the lack of complete knowledge of the virus reservoir, though scientists are now having their long-held suspicions in bats confirmed. It’s hard to detect disease when you cannot pinpoint the source. Surveillance and reporting have been another confounding element. How many times in that fifteen-year period was an illness misdiagnosed as yellow fever, dengue hemorrhagic fever, or some other similar illness, because of lack of knowledge or diagnostic capabilities, or simply because there was no health care around? We will probably never be able to answer this question. Finally, our perceived zone of endemicity at the time was limited to northern DRC and southern Sudan. Was the virus appearing elsewhere, unbeknownst to us? We certainly were not expecting it to emerge in Gabon in 1994, and Uganda in 2000, and West Africa in 2014 [ 31 ].

Scientists today continue to be perplexed by the emergence of the virus. What brings Ebola out from its hiding place? Is its emergence/re-emergence tied to climate change? globalization? the changing interface between humans and wildlife? If it has to do with any of these increasingly significant factors, how do they explain the fifteen-year disappearance?

These days, the virus comes and goes with some predictability—since 2000, outbreaks have approached a near-annual incidence, sometimes skipping a year, sometimes lasting more than a year. The periods between outbreaks are growing shorter. Is this because our capability to detect Ebola outbreaks is improving, or is the virus able to infect humans more frequently? One thing is for sure: the world knows that when one outbreak ends, another will eventually follow, and we need not wait 15 years.

4. Toward the discovery of the natural cycle of the Ebolaviruses

4.1 the discovery of a putative natural reservoir of ebolavirus.

Since the ZEBOV and SEBOV emergence, extended field studies have been conducted to discover the reservoir of EBOVs [ 32 ] including the 1976 first recorded DRC outbreaks and Sudan, the 1979 outbreak in DRC in 1979 and 1995 following the Kikwit outbreak, the same year in the Tai Forest and in 1999 in the Central African Republic [ 33 , 34 , 35 , 36 , 37 , 38 ] . A total of more than 7000 vertebrates and 30,000 invertebrates were sampled and tested for the presence of EBOVs. Limited finding was inconclusive for an potential EBOVs reservoir status among all these animals. Moreover, while several animal species (Bats, birds, reptiles, mollusks, arthropods, and plants) were experimentally infected with ZEBOV, only two fruit bat species ( Epomophorus spp. and Tadarida spp.) developed a subclinical transient viremia [ 39 ]. If these results were not confirmed in the natural settings, they indicated the potential for chiropteran to be natural for EBOVs [ 40 ].

Also, historically, the first documented case of EVD in Sudan in 1976, the index case was located (by the World Health Organization) in a cotton factory far from the forest block, where the only wild significantly abundant species was an insectivorous bat species [ 21 ].

Since the discovery of EBOV in 1976, more than half of the epidemic outbreaks caused by EBOVs have broken down between Gabon and the DRC. Following the successive EBOV outbreaks in Gabon from 1995 to 2001 affecting several animal species non-human primates, and wild ungulates and responsible of the dramatic decline of great apes (gorilla and chimpanzee) populations in the region (Leroy et al. [ 16 ]), researchers engaged several missions of captures of wild animals in the forest areas affected by the recent past epidemics. Also, 1030 animals were captured and analyzed, only three species of fruit bats were found infected with the ZEBOV by PCR including: Hypsignathus monstrosus ; Epomops franqueti; and Myonycteris torquata . Moreover, antibody reacting anti-Ebola were detected in these species as well as for the genus Myonycteris spp. leading ultimately to design Chiropteran as a potential reservoir of EBOVs [ 41 ].

Since then, many studies have converged in favor of the role of chiropters in maintaining EBOV in the wild (Caron et al. [ 42 ], Leendertz). In addition, a recent study of bats in Sierra Leone showed the association of an EBOV like with several species of bats ( Mops condylurus and Chaerephon pumilus ) from the Molossus family [ 43 ]. Moreover, a potential direct exposure to Ebola infected fruit bats was also reported as a putative index case of large epidemics [ 44 , 45 ]. Moreover, further studies reported on direct infection of natural hosts (primates) by EBOV infected bats as highly plausible, given that bats, especially fruit bats, are frequently hunted and consumed as bushmeat by human when Cercopithecus species hunt roosting bats for consumption [ 46 ] also preying on bats has been reported in Cercopithecus ascanius and C. mitis (East Africa) as well as bonobos (DRC) [ 47 ]. It is also possible that different modes of exposure to Ebola virus could lead to different antibody profiles, that is, contaminated fruit vs. contact with infected bats during hunting [ 44 , 47 , 48 ].

Altogether, several fruit bats ( Epomophorus wahlbergi ) and insectivorous bats ( Chaerephon pumilus, Mops condylurus ) experimentally survive to EBOV infections [ 39 ], EBOV RNA and/or anti EBOV reacting antibodies were detected also in several other fruit bat species ( Epomops franqueti, Hypsignathus monstrosus, Myonycteris torquata , Eidolon helvum, Epomophorus gambianus, Micropteropus pusillus, Mops condylurus, Rousettus aegyptiacus, Rousettus leschenaultia ) giving more insight of the potential for chiropteran to be a potential host or reservoir host of EBOVs [ 22 , 49 , 50 ].

Interestingly, REBOV was also found associated with the bats in its natural habitat of the Philippines [ 51 ]. Also, again in this same Filoviridae family, Marburg viruses in Africa are clearly associated with bats [ 32 , 52 ] as well as the Cueva virus in Europe [ 53 ]. While REBOV has been find associated with fruit bats, Roussetus spp. (Pteropodid family), each filovirus genus is associated with a specific chiropteran group including: Marburgvirus with a specific fruit bat, Roussetus aegyptiacus (Pteropodid family); and Cuevavirus with insectivorous bat, Miniopterus schreibersii (Miniopterid family); except for Thamnovirus isolated form fresh water fish.

Moreover, several virus groups are known to hold bat-borne viruses including the coronaviruses, hantaviruses, lyssaviruses, lassa virus, Henipavirus, filovirus which are among the most severe of the emerging viruses [ 54 , 55 ].

Conclusively, this was the first evidence of chiropteran as a potential reservoir and/or vector of EBOV, while several wild animals, in particular great apes were find highly sensitive to EBOV infection. Also, if several species of chiropteran have been identified as a potential virus reservoir,

4.2 The most complete figure of a putative Ebolavirus natural cycle in the central African raining forest

From all above observations, records and historical events of EBOVs emerging events, several fundamentals of emergence have been identified as well putative time and space of such events where, that is when the virus jump from the cryptic natural cycle of the reservoir-vector to manifest itself clearly as an open index case of infection in a susceptible host and the potential opening epizootic or epidemic chain.

4.2.1 The actors

Again, from the literature numerous vertebrates appears to be permissive to infection by EBOVs, however, due to their ethology, including environmental habits, societal structure, density and their ability of intra and interspecies to mingle. Altogether primates appear highly susceptible to EBOVs infection including non-human primate apes, gorilla and chimpanzee, but also cercopithecids (e.g. colobus) but also small wild ungulates (e.g. forest duikers) and eventually domestic animals (e.g. dogs) [ 32 , 56 , 57 , 58 ].

One can summarize that EBOVs natural hosts belongs to chiropteran as a potential host reservoir represented mostly by Pteropodidae in Africa (REBOV and Roussetus; Bombali virus and Molossidae), and as secondary natural or accidental wild and domestic hosts including several other mammals: primates (Colobus, Cercopithecus), non-human primates (Gorilla, chimpanzee), wild ungulates (duikers) and, human primates. Also this needs to be taken into account with respect to other permissive species to EBOVs, indeed, as an example, if Roussetus spp. was shown to carry EBOVs reacting antibodies more recently R. aegyptiacus bats were demonstrated to unlikely able to maintain and perpetuate EBOV in nature while the natural transmission of filovirus in R. aegyptiacus , resulting viral replication and shedding are unknown [ 59 ].

4.2.2 The stages

The African Rain forest of the Congolese basin appears to be the epicenter of EBOVs emerging events. More than 80% of the emerging events of EBOVs occurred in the Tropical zone under the influence of the (Intertropical converging zone, ITCZ) from five degree North to 5 degrees south and oscillating as much as 40 to 45° of latitude north or south of the equator based on the pattern of land and ocean beneath it [ 28 ] ( Figure 2 ).

Emerging events of Ebolavirus and climate since the Ebola fever inception in Africa. Left = annual rainfall; right = annual temperature. To illustrate the association temperature/rainfall and emergence, the month of May was chosen because it is at this time of the year that we observe the most emergent events of the Ebola virus. Temperature and rainfall are expressed as an annual average for the period under consideration. The precise location of 32 Ebola emergent events are here integrated into the global climatic map of Africa. Only 30-year average values per month of rainfall are available for the study period (ref.: WorldClim world databases) as well for the average monthly temperature.

Temperature and precipitation data for Africa (average data computed from 1960 to 1990, 300 m resolution [HIJ 05]) were integrated with the distribution map of the emergent events of the Ebola virus and the values ​​calculated for each of the emergence points [ 60 ].

On all emergence points, the temperature at the time of emergence is not significantly different from the average annual temperature over 30 years. The difference in temperature between the moment of emergence and the average temperature (of 30 years monthly average) of the hottest month does not show any difference either. Emergence would not be directly related to temperature.

When we compare Ebolavirus emerging events time and the rainfall, there is strict quantitative correlation between rainfall and emergence: Most of the emergent events (93.8%) occurred during the rainy season ( Figure 2 ). For precipitation values, there is a slightly statistically significant (p = 0.02) positive difference between the average precipitation of the month of emergence and the average of the monthly average precipitation (over 30 years), indicating that precipitations are higher when emergences occur. There is an even more statistically significant (p = 0.003) positive difference when considering precipitation of the month preceding the emergence. Emergence is therefore likely to be associated with rainfall intensity and the rainy season. 10/32 emergences occur at the beginning of the rainy season, 9/32 in the middle, and 11/32 at the end. Only 2/32 emergences occurred in the dry season.

When referring to land use ( Figure 3 ) the temperature at the 6 emergence points in “Cropland” is highly significantly less (p = 0.005) than 15% (21.6°C) at temperature (24.4°C) to the 9 points in “Tree cover, broadleaved, evergreen, closed to open”, however the average temperature of the Cropland (21.6°) is to a degree less, significantly lower (p = 0.01) than that of the “Tree cover” (24.5°C).

Environmental factors surrounding Ebolavirus emerging event: Land use and places of Ebola virus emergence in Africa from 1976 to 2014. Land use from ESA 2015, 300 m resolution; red circle = putative place of the Ebola virus emergence (index case). Estimated Ebola emergence places are superimposed on the land use layer. The identification of the land use types were 32 points (red circle) representing the putative places of Ebolavirus emergence are superimposed and are distributed as follows: (1) cropland: 6, (2) herbaceous cover: 5, (3) cropland mosaic: 5 (> 50% natural vegetation vs. <50% tree, shrub, herbaceous cover), (4) tree cover with: (a) 15% of broadleaved, evergreen, closed to open: 9, (b) 15–40% of broadleaved, deciduous, open: 2, (5) flooded, fresh or brackish water: 1, (6) urban areas: 3, and (7) water bodies: 1. The limitations of this interpretation are linked to the accuracy of the location of Ebolavirus emergence sites (from literature and reports) and, to the evolution of vegetation cover over the past decades since the first emergence of the Ebolavirus occurred in Africa.

Ultimately, taking into account these environmental factors, when we look for an association between the emergent events of the Ebola virus and the characteristics of the places of these emergences (i.e. land use, temperature, rainfall) it turns out that the emergences are always in the zone of heavy rainfall, but nevertheless do not follow the moving of the rainy season. Moreover, these emergences remain always and remarkably close enough to the Equator, therefore in the equatorial forest area with a high hygrometry, and a moderate annual temperature. However, the temperature at the time of emergence is not significantly different from the average annual temperature (at the points of emergence) which does not allow to distinguish seasonal effect in the emergence-temperature relationship. Conclusively, we did not identify a seasonality associated with the time of emergence, however the emerging events occur in specific geographic zone characterized by several environmental factors. Finally, the emergence zones are in areas of Land Use with specific temperatures not related to seasonality. Ultimately, it is also remarkable that all these emerging events occurred in an area with a highly potential presence of apes, virus-sensitive hosts.

4.2.3 Fundamentals and domains of emergence: a theory for a natural cycle of EBOVs in Africa

Also, the EBOVs species are closely genetically related, their seems to occur by foci in nature. The host appears to be the same, natural or accidental, and the transmission done by direct contact with infected hosts or its biological products [ 50 , 61 ]. Altogether, in the early 2000s, before the identification of chiropteran as a potential host-reservoir of the EBOVs, a hypothetic natural cycle was described empirically based on seasonal environmental climatic factors [ 55 ]. Then, taking into account bats as a potential reservoir-host, the question of virus transmission was central to consider while environmental factors appears to play a major role to the host and their natural cycle (Chiropteran physiology) (climate/fructification, chorology, bats physiology). Several factors of emergence were then listed including: Chronic infection, infected organs, virus shedding, close encounters between reservoir and susceptible hosts, food and water resource, seasonality, chorology (i.e. causal effect between geographical phenomena – season) in the tropical rain forest and the spatial distribution of chiropteran (i.e. index site of Ebola emerging events).

Epidemiological field surveys indicate that mass mortalities of apes and monkey species due to Ebola virus often appear at the end of the dry season, a period when food resources are scarce. Restricted access to a limited number of fruit-bearing trees can lead to spatiotemporal clustering of diverse species of frugivorous animals, such as bats, nonhuman primates, and other terrestrial species foraging on fallen partially eaten (by bats) fruits. These aggregates of wild animal species favor the contact between infected and susceptible individuals and promote virus transmission. The dry season aggregation of reservoir host species involved in natural maintenance cycles, augmented by incidentally infected secondary hosts serving as sources for intra- and interspecific transmission chains independent of repeated spillover from the reservoir host, provides an ecological setting for amplifying enzootic transmission of Ebola virus when a vertebrate hosts are concentrated around a scarce number of water sources [ 62 ].

In addition to this dietary impoverishment, there are behavioral and physiological events occurring among bats during the tropical dry favor the contact frequency and intimacy between bats, which can promote transmission of Ebola virus to others and increase R0. As an example, megachiropteran fruit bats breeding activities and intraspecific competitions between males and grouped kidding of females favor the contact between individuals. Moreover, pregnancy can involve physiological changes among female bats that alter immune functions and eventually favor virus shedding. Parturition among the African megachiropteran bats occurs throughout the year, although seasonal peaks provide birthing fluids, blood, and placental tissues, potentially Ebolavirus infected, falling on the ground as a medium highly attractive and readily available to scavenging terrestrial mammals [ 50 , 56 , 63 ] ( Figure 4A and B ).

(A) Understanding Ebolavirus enzootic and epidemics. Red arrows = cycles of transmission; dashed square = a putative natural cycle of Ebolavirus in Central Africa (see B). Fruit bats are considered to be a putative reservoir of Ebola virus in Central Africa after 2004; In 2009, several non-human primate epizootic are reported; 1976 was the first emerging events and subsequent epidemic chains in remote area of the rain forest and close by; 2012 showed a dramatic spread of the virus associated with motorized transportation and ground network; In 2014 urban epidemics are reported as well as a pandemic risk and become an international public health emergency. (B) Putative natural cycle of Ebolavirus in Central Africa. Red arrow indicates Ebolavirus transmission. Numbered red circle of transmission: (1) sylvatic inter- and intra-species transmission; (2) chiropteran migration; (3) chiropter to primate (close contact of dejection); (4) primate inter species (Cercopithecus/chimpanzee); (5) primate to primate (non-human primates); (6) non-human primate epizootic (gorillas); (7) chiropter to duikers; and (8) consumption of chiropteran infected food by shrew or wild pig.

5. If we had to conclude

Based on historical data and observations, the presented hypothesis of the natural cycle of Ebolavirus emergence prevail an inter-species spillover as the complex natural cycle involving several hosts (reservoir, vector, amplifier), as well as biotic and abiotic factors in a changing environment among other original features.

Although the natural cycle of EBOVs remains in the darkness of the rain forest, strong findings and comparative analysis of close parents of the filovirus throw some light to a potential natural cycle of EBOVs in Africa. EBOVs clearly appear linked to chiropteran and dependent for merging events in the environmental factors. Indeed, it appears that filoviridae are often associated with chiropteran while the emergence of the virus strains occurs as a sparse focus with a silent period of cryptic virus circulation. When virus transmission, i.e. spillover, from a hidden natural cycle, to accidental hosts occurs, it happened in a specific time-frame often linked to the season.

One can retain is that the EBOVs complex natural cycle is yet not on entirely elucidated and certainly dependent on environmental factors – associated with a specific environment of the chiropteran species incriminated (i.e. Different territories, different cycle) - leading to multiple, sometime concurrent, temporally and timely emergence in focus.

Although, other hypothesis has been suggested elsewhere including the Ebola virus Disease as an arthropod borne disease among others [ 42 ], there is important fundamental matters to consider as well before providing more.

However, beyond these hypotheses, fundamental questions subsist in order to go further learn. We can cite in particular the mystery of kin between the Reston virus of Asia and the Ebola viruses of Africa, would there not be a missing link in a geographic area yet to discover. Do the filovirus exist in the Americas hidden in the darkness of the tropical forest? Also, the Ebolavirus seems genetically stable, related to particular species of chiropter, was it to think about a co-evolution of the host and the virus in this closed environment of the forest of the tropical? Today, with the endless epidemic unfolding in the DRC, should we revisit our tools and strategy of struggle in an ever-changing world? [ 64 ].

Acknowledgments

We sincerely thank for their supports, brings to all the authors of this deep and never-ending research and scientific thought around an outstanding and fascinating subject: Georgetown University, Centaurus Biotech LLC., The DHS Emeritus Center for Emerging Zoonotic and Animal Diseases at Kansas State University.

Conflict of interest

All authors do not have any conflict of interest whatsoever with this published manuscript.

• 1. CDC. Page last reviewed. Content source: Centers for Disease Control and Prevention, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID), Division of High-Consequence Pathogens and Pathology (DHCPP), Viral Special Pathogens Branch (VSPB). 2019. Available from: https://www.cdc.gov/vhf/ebola/history/2014-2016-outbreak/index.html
• 2. ICTV. Filoviridae. 2019. Available from: https://talk.ictvonline.org/ictv-reports/ictv_online_report/negative-sense-rna-viruses/mononegavirales/w/filoviridae
• 3. Kuhn JH, Andersen KG, Baize S, Bào Y, Bavari S, Berthet N, et al. Nomenclature- and database-compatible names for the two Ebola virus variants that emerged in Guinea and the Democratic Republic of the Congo in 2014. Viruses. 2014; 6 (11):4760-4799. DOI: 10.3390/v6114760
• 4. MacNeil A, Farnon EC, Morgan OW, et al. Filovirus outbreak detection and surveillance: Lessons from Bundibugyo. The Journal of Infectious Diseases. 2011; 204 :S761-S767
• 5. Kiley MP, Bowen ET, Eddy GA, Isaäcson M, Johnson KM, McCormick JB, et al. Filoviridae: A taxonomic home for Marburg and Ebola viruses? Intervirology. 1982; 18 (1-2):24-32
• 6. Anonymous. WHO/INTERNATIONAL STUDY TEAM. Ebola haemorrhagic fever in Zaire, 1976. Bulletin of the World Health Organization. 1978; 56 (2):271-293
• 7. Anonymous. WHO/INTERNATIONAL STUDY TEAM. Ebola haemorrhagic fever in Sudan, 1976. Bulletin of the World Health Organization. 1978; 56 (2):247-270
• 8. Centers for Disease Control. Ebola-Reston virus infection among quarantined nonhuman primates–Texas, 1996. Morbidity and Mortality Weekly Report. 1996; 45 :314-316
• 9. Miranda MEG, Lee N, Miranda J. Reston ebolavirus in humans and animals in the Philippines: A review. The Journal of Infectious Diseases. 2011; 204 (suppl_3):S757-S760. DOI: 10.1093/infdis/jir296
• 10. Le Guenno B, Formenty P, Wyers M, Gounon P, Walker F, Boesch C. Isolation and partial characterisation of a new strain of Ebola virus. The Lancet. 1995; 345 (8960):1271-1274
• 11. Towner JS, Sealy TK, Khristova ML, Albariño CG, Conlan S, Reeder SA, et al. Newly discovered ebola virus associated with hemorrhagic fever outbreak in Uganda. PLoS Pathogens. 2008; 4 (11):e1000212. DOI: 10.1371/journal.ppat.1000212
• 12. Miranda ME, Ksiazek TG, Retuya TJ, Khan AS, Sanchez A, Fulhorst CF, et al. Epidemiology of Ebola (subtype Reston) virus in the Philippines, 1996. The Journal of Infectious Diseases. 1999; 179 (Suppl 1):S115-S119
• 13. Georges AJ, Leroy EM, Renaud AA, et al. Ebola hemorrhagic fever outbreaks in Gabon, 1994-1997: Epidemiologic and health control issues. The Journal of Infectious Diseases. 1999; 179 :S65-S75
• 14. Baize S, Pannetier D, Oestereich L, Rieger T, Koivogui L, Magassouba N, et al. Emergence of Zaire Ebola virus disease in Guinea. The New England Journal of Medicine. 2014; 371 (15):1418-1425. DOI: 10.1056/NEJMoa1404505
• 15. WHO. Disease Outbreak News. 2018a. Available from: https://www.who.int/ebola/situation-reports/drc-2018/en/ [Accessed: 13-01-19]
• 16. Leroy EM, Rouquet P, Formenty P, Souquiere S, Kilbourne A, Froment JM, et al. Multiple Ebola virus transmission events and rapid decline of central African wildlife. Science. 2004a; 303 :387-390
• 17. Heymann DL, Weisfeld JS, Webb PA, Johnson KM, Cairns T, Berquist H. Ebola hemorrhagic fever: Tandala, Zaire, 1977-1978. The Journal of Infectious Diseases. 1980; 142 :372-376
• 18. O’Hearn AE, Voorhees MA, Fetterer DP, Wauquier N, Coomber MR, Bangura J, et al. Serosurveillance of viral pathogens circulating in West Africa. Virology Journal. 2016; 13 (1):163
• 19. Becquart P, Wauquier N, Mahlakõiv T, Nkoghe D, Padilla C, Souris M, et al. High prevalence of both humoral and cellular immunity to Zaire ebolavirus among rural populations in Gabon. PLoS One. 2010; 5 (2):e9126
• 20. Vincent T. Ebola Footprint—Broader Than You Think. Available from: http://oneill.law.georgetown.edu/the-ebola-footprint-broader-than-you-think/
• 21. Olivero J, Fa JE, Real R, Farfan MA, Marquez AN, Vargas JM, et al. Mammalian biogeography and the Ebola virus in Africa. Mammal Review. 2016; 47 :24-37
• 22. Olival KJ, Islam A, Yu M, Anthony SJ, Epstein JH, Khan SA, et al. Ebola virus antibodies in fruit bats, Bangladesh. Emerging Infectious Diseases. 2013; 19 :270-273. DOI: 10.3201/eid1902.120524
• 23. Yuan JF, Zhang YJ, Li JL, Zhang YZ, Wang LF, Shi ZL. Serological evidence of ebolavirus infection in bats, China. Virology Journal. 2012; 9 :236. DOI: 10.1186/1743-422X-9-236
• 24. Peterson AT, Bauer JT, Mills JN. Ecologic and geographic distribution of filovirus disease. Emerging Infectious Diseases. 2004; 10 :40-47. DOI: 10.3201/eid1001.030125
• 25. Rollin PE, Williams RJ, Bressler DS, Pearson S, Cottingham M, Pucak G, et al. Ebola (subtype Reston) virus among quarantined nonhuman primates recently imported from the Philippines to the United States. The Journal of Infectious Diseases. 1999; 179 (Suppl 1):S108-S114
• 26. Wauquier N, Bangura J, Moses L, Humarr Khan S, Coomber M, Lungay V, et al. Understanding the emergence of ebola virus disease in Sierra Leone: Stalking the virus in the threatening wake of emergence. PLOS Currents. 2015; 7
• 27. Ebola virus cases in the United States. Available from: https://en.wikipedia.org/wiki/Ebola_virus_cases_in_the_United_States
• 28. Monath TP. Ecology of Marburg and Ebola viruses: Speculations and directions for the future research. The Journal of Infectious Diseases. 1999; 179 :S127-S138
• 29. Yob JM, Field H, Rashdi AM, Morrissy C, van der Heide B, Rota P, et al. Nipah virus infection in bats (order Chiroptera) in peninsular Malaysia. Emerging Infectious Diseases. 2001; 7 (3):439-441
• 30. Badrane H, Tordo N. Host switching in Lyssavirus history from the Chiroptera to the Carnivora orders. Journal of Virology. 2001; 75 :8096-8104
• 31. Tom Vincent. EBOLA: FIFTEEN YEARS OF SILENCE. 2019. Available from: http://oneill.law.georgetown.edu/ebola-fifteen-years-of-silence/
• 32. Pourrut X, Souris M, Towner JS, Rollin PE, Nichol ST, Gonzalez JP, et al. Large serological survey showing cocirculation of Ebola and Marburg viruses in Gabonese bat populations, and a high seroprevalence of both viruses in Rousettus aegyptiacus. BMC Infectious Diseases. 2009; 9 :159
• 33. Breman JG, Johnson KM, van der Groen G, Robbins CB, Szczeniowski MV, Ruti K, et al. A search for Ebola virus in animals in the Democratic Republic of the Congo and Cameroon: Ecologic, virologic, and sero- logic surveys, 1979-1980. The Journal of Infectious Diseases. 1999; 179 :S139-S147
• 34. Arata AA, Johnson B. Approaches towards studies on potential reservoirs of viral haemorrhagic fever in southern Sudan. In: Pattyn SR, editor. Ebola Virus Haemor- Rhagic Fever. Amsterdam: Elsevier/Netherland biomedical; 1977. pp. 191-202
• 35. Leirs H, Mills JN, Krebs JW, Childs JE, Akaibe D, Woollen N, et al. Search for the Ebola virus reservoir in Kikwit Democratic Republic of the Congo: Reflections on a vertebrate collection. The Journal of Infectious Diseases. 1999; 179 :S155-S163
• 36. Morvan JM, Deubel V, Gounon P, Nakoune E, Barriere P, Murri S, et al. Identification of Ebola virus sequences present as RNA or DNA in organs of terrestrial small mammals of the Central African Republic. Microbes and Infection. 1999; 1 :1193-1201
• 37. Reiter P, Turell M, Coleman R, Miller B, Maupin G, Liz J, et al. Field investigations of an outbreak of Ebola hemorrhagic fever Kikwit Democratic Republic of the Congo, 1995: Arthropod studies. The Journal of Infectious Diseases. 1999; 179 :S148-S154
• 38. Formenty P, Boesch C, Wyers M, Steiner C, Donati F, Dind F, Walker F, Le Guenno B. Ebola virus outbreak among wild chimpanzees living in a rain forest of cote d’Ivoire. The Journal of Infectious Diseases. 1999; 179 (Suppl 1):S120-S126
• 39. Swanepoel R, Leman PA, Burt FJ. Experimental inoculation of plants and animals with Ebola virus. Emerging Infectious Diseases. 1996; 2 :321-325
• 40. Xavier P, Gonzalez JP, Leroy E. Spatial and temporal patterns of Ebola virus antibody prevalence in the putative bat species reservoir. The Journal of Infectious Diseases. 2007; 196 (Suppl 2):S176-S183
• 41. Eric L, Kumulungui B, Pourrut X, Rouquet P, Yaba P, Délicat A, et al. Fruit bats as reservoirs of Ebola virus. Nature. 2005; 438 (7068):575-576
• 42. Caron A, Bourgarel M, Cappelle J, Liégeois F, De Nys HM, Roger F. Ebola virus maintenance: If not (only) bats, what Else? Viruses. 2018; 10 (10):549. DOI: 10.3390/v10100549
• 43. Goldstein T, Anthony SJ, Gbakima A, Bird BH, Bangura J, Tremeau-Bravard A, et al. The discovery of Bombali virus adds further support for bats as hosts of ebolaviruses. Nature Microbiology. 2018; 3 :1084-1089
• 44. Leroy EM, Epelboin A, Mondonge V, Pourrut X, Gonzalez JP, Muyembe-Tamfum JJ, et al. Ebola outbreak associated with direct exposure to fruit bats in Luebo, Democratic Republic of the Congo, 2007. Vector Borne and Zoonotic Diseases. 2009; 9 (6):723-728
• 45. Marí Saéz A, Weiss S, Nowak K, Lapeyre V, Zimmermann F, Düx A, et al. Investigating the zoonotic origin of the west African Ebola epidemic. EMBO Molecular Medicine. 2015; 7 (1):17-23. DOI: 10.15252/emmm.201404792
• 46. Tapanes E, Detwiler KM, Cords M. Bat predation by Cercopithecus monkeys: Implications for zoonotic disease transmission. EcoHealth. 2016; 13 :405-409
• 47. Bermejo M, Illera G, Sabater P. Animals and mushrooms consumed by bonobos (pan paniscus): New records from Lilungu (Ikele), Zaire. International Journal of Primatology. 1994; 15 :879-898
• 48. Leendertz SAJ, Gogarten JF, Düx A, Calvignac-Spencer S, Leendertz FH. Assessing the evidence supporting fruit bats as the primary reservoirs for Ebola viruses. EcoHealth. 2016; 13 (1):18-25
• 49. Olival KJ, Hayman DT. Filoviruses in bats: Current knowledge and future directions. Viruses. 2014; 6 (4):1759-1788. DOI: 10.3390/v6041759
• 50. Gonzalez JP, Pourrut X, Leroy E. Ebolavirus and other filoviruses. Current Topics in Microbiology and Immunology. 2007; 315 :363-387
• 51. Jayme SI, Field HE, de Jong C, Olival KJ, Marsh G, Tagtag AM, et al. Molecular evidence of Ebola Reston virus infection in Philippine bats. Virology Journal. 2015; 12 :107. DOI: 10.1186/s12985-015-0331-3
• 52. Pawęska JT, Jansen van Vuren P, Kemp A, Storm N, Grobbelaar AA, Wiley MR, et al. Marburg virus infection in Egyptian Rousette bats, South Africa, 2013-20141. Emerging Infectious Diseases. 2018 Jun; 24 (6):1134-1137. DOI: 10.3201/eid2406.172165
• 53. de Arellano ER, Sanchez-Lockhart M, Perteguer MJ, Bartlett M, Ortiz M, Campioli P, et al. First evidence of antibodies against Lloviu virus in Schreiber’s bent-winged insectivorous bats demonstrate a wide circulation of the virus in Spain. Viruses. 2019; 11 :360. DOI: 10.3390/v11040360
• 54. Calisher CH, Childs JE, Field HE, Holmes KV, Schountz T. Bats: Important reservoir hosts of emerging viruses. Clinical Microbiology Reviews. 2006; 19 :531-545
• 55. Gonzalez JP, Pourrut X, Leroy E. Ebolavirus and other filoviruses. In: Childs JE, Mackenzie JS, Richt JA, editors. Wildlife and Emerging Zoonotic Diseases: The Biology, Circumstances and Consequences of Cross-Species Transmission. New York, NY, USA: Springer; Heidelberg, Germany; 2007. pp. 363-388
• 56. Allela L, Bourry O, Pouillot R, Délicat A, Yaba P, Kumulungui B, et al. Ebola virus antibody in dogs and human risk. Emerging Infectious Diseases. 2005; 11 (3):385-390
• 57. Ayouba A, Ahuka-Mundeke S, Butel C, Mbala Kingebeni P, Loul S, Tagg N, et al. Extensive serological survey of multiple African non-human primate species reveals low prevalence of IgG antibodies to four Ebola virus species. The Journal of Infectious Diseases. 2019. DOI: 10.1093/infdis/jiz006
• 58. Pigott DM, Golding N, Mylne A, et al. Mapping the zoonotic niche of Ebola virus disease in Africa. eLife. 2014; 3 :e04395
• 59. Paweska JT, Storm N, Grobbelaar AA, Markotter W, Kemp A, Jansen van Vuren P. Experimental inoculation of Egyptian fruit bats ( Rousettus aegyptiacus ) with Ebola virus. Viruses. 2016; 8 (2). pii: E29. DOI: 10.3390/v8020029
• 60. Hijmans RJ, Cameron SE, Parra JL, Jones PG, Jarvis A. Very high-resolution interpolated climate surfaces for global land areas. International Journal of Climatology. 2005; 25 :1965-1978
• 61. Mackensie J, Mills J, editors. Review. In: Wildlife and Emerging Zoonotic Diseases. Springer-Verelag CRC Press. Advances in Virology ch20
• 62. Shaman J, Day JF, Stieglitz M. Drought-induced amplification of Saint Louis encephalitis virus Florida. Emerging Infectious Diseases. 2002; 8 :575-580
• 63. Pourrut X, Kumulungui B, Wittmann T, Moussavou G, Delicat A, Yaba P, et al. The natural history of Ebola virus in Africa. Microbes and Infection. 2005; 7 (7-8):1005-1014
• 64. Gonzalez JP, Souris M, Valdivia-Granda W. Global spread of hemorrhagic fever viruses: Predicting pandemics. Methods in Molecular Biology. 2018; 1604 :3-31. DOI: 10.1007/978-1-4939-6981-4_1

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 3.0 License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Most Popular

11 days ago

Inspiration vs Plagiarism

How to write a synthesis essay.

12 days ago

How to Cite a Bill

How to write a 5 paragraph essay, openai prepares to launch web search feature for chatgpt, rivaling google and perplexity, symptoms of the ebola virus essay sample, example.

Ebola was first discovered 1976 in Africa, on the banks of the Ebola river, after which the virus has been named. Back then, there were two major outbreaks of the virus, and this is how people learned about it. There exist several strains of the Ebola virus, some of them are deadly to people, and some are not.

The main symptoms of Ebola can appear in a period between the second and the 21st days of contamination, but usually it happens on the eighth through 10th day (CDC). Among the symptoms that appear in the first turn, one should mention fever and chills, strong headaches, pain in joints and muscles, and general weakness. These symptoms are not too different from those that people usually experience when catching a severe cold, or flu, so victims may even ignore these symptoms, or try to treat them as a common sickness. However, as the virus keeps progressing, a patient develops nausea with vomiting, diarrhea, chest and stomach pains, red eyes and rashes over the body, severe weight loss, and bleeding from almost all bodily orifices (Mayo Clinic).

The virus is usually transmitted either through blood or through waste. Contagion through blood usually takes place if a person consumes infested meat, or even touches it (for example, butchering can also lead to contamination). Also, there were cases when people got infected after stepping in feces of infected mammals, mostly bats (Mayo Clinic). The other ways of getting infected is through skin by receiving bodily fluids through pores.

Even though there is no specific cure from Ebola, doctors still try to treat it. In order to diagnose Ebola, doctors usually take tests on such diseases as cholera or malaria, because it is difficult to diagnose Ebola based solely on symptoms. After the diagnosis has been made, doctors start treating the symptoms, which includes eliminating infected cells, electrolytes, blood pressure medication, blood transfusions, oxygen therapy, and so on (WebMD).

Though Ebola is a highly dangerous disease, it is not likely that it will spread globally. It is most deadly in anti-sanitary conditions, which many African countries are notorious for. As for first world countries, even though there is still no universal cure, they are at much lesser risk than African countries. Though the symptoms of Ebola are severe and getting infected is not difficult, with the correct handling of an outbreak, the virus should not be able to spread.

“Signs and Symptoms.” Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, 03 Oct. 2014. Web. 05 Oct. 2014. .

“Ebola Virus and Marburg Virus.” Causes. N.p., n.d. Web. 06 Oct. 2014. .

“Ebola Virus: Symptoms, Treatment, and Prevention.” WebMD. WebMD, n.d. Web. 05 Oct. 2014. .

Follow us on Reddit for more insights and updates.

Comments (0)

Welcome to A*Help comments!

We’re all about debate and discussion at A*Help.

We value the diverse opinions of users, so you may find points of view that you don’t agree with. And that’s cool. However, there are certain things we’re not OK with: attempts to manipulate our data in any way, for example, or the posting of discriminative, offensive, hateful, or disparaging material.

Comments are closed.

More from Expository Essay Examples and Samples

Nov 23 2023

Why Is Of Mice And Men Banned

Nov 07 2023

Pride and Prejudice Themes

May 10 2023

Remote Collaboration and Evidence Based Care Essay Sample, Example

Related writing guides, writing an expository essay.

Remember Me

What is your profession ? Student Teacher Writer Other

Forgotten Password?

Username or Email

Expository Essay on Ebola Virus

Jump ahead to:

Here you have an Expository Essay on Ebola Virus, Lets start with the introduction.

Introduction

The Ebola virus is one of the most dangerous and deadly viruses known to humans. The Ebola epidemic since its discovery in 1976 came from the Democratic Republic of Congo, formerly known as Zaire, but the largest Ebola outbreak known to date is still ongoing at the time of writing, in the West Africa. An estimated 550 000 reported incidents from Sierra Leone and Liberia took place on January 20, 2015.

The virus is prevalent in many countries including Guinea, Liberia, Sierra Leone, Nigeria as well as occasional reported cases in the USA, Canada. The Netherlands and India show the potential for infection to spread globally. Despite the fact that the disease is highly contagious, life-threatening, and no specific treatment is available, it can be prevented through the use of appropriate measures to prevent and control infection. The study of the Ebola virus is important as such knowledge will pave the way for the reduction of victims, the development of an effective drug and will be useful in controlling the same epidemic.

The Ebola virus is a member of the Philoviridae family. As the name implies the virus has a filamentous shape. Marburg virus and Ebolavirus are two major generations of the virus family that are important in medicine. Bacteria of these two species are studied and presented together due to their many similarities in the life cycle, water storage areas, transmission methods, clinical presentation, treatment and prevention measures. The only difference is that Marburgvirus is still distributed by forest-dwelling bats such as the savannah while Ebolavirus is distributed by bats species accustomed to deep rain forests.

Five subspecies of Ebolavirus, namely, Ebolavirus Zaire, Ebolavirus Sudan, Ebolavirus reston, Ebolavirus cote d’Ivore, and Ebolavirus bugs, have been identified and named after the place where they were first discovered. Of these E. Zaire was the first to be isolated and studied and is responsible for a large number of outbreaks  including recent outbreaks in 2014 before that E. Sudan accounted for ¼ of all Ebolavirus deaths. With the exception of a slightly lower mortality rate, E. Sudan is almost identical to E. Zaire. E death rate of E case. Sudan is reported as 40-60% and E. Zaire as 60-90%.

Ebola was originally transmitted to humans as a zoonosis. Different species of bats are found throughout sub-Saharan Africa such as. Contact with bats by biting and scratching or exposure to their discharges and discharges through broken skin or mucous membranes can cause infection in humans. The infection can also be spread to other end users. Those recorded in Africa are deer, wildebeests, chimpanzees, chimpanzees, gorillas, monkeys, and other non-humans. Attacks during the hunting of these animals or handling carcasses of infected animals have led to the introduction of the virus to humans from the wild. Outbreaks appear to be exacerbated during pregnancy and in childbirth. Records show that outbreaks appear to be exacerbated by the presence of multiple pathogens.

EVD is highly contagious. Infection can be spread in the community and in a hospital setting by direct contact with infected body fluids such as blood, fluid and discharge or the patient’s tissues or by direct contact with contaminants such as clothing and bed linen. One of the main reasons for the rapid spread of the epidemic is traditional funeral rites, which include cadaver cleaning, removal of fingernails, toenails and clothing. Caregivers, including health workers, are also at greater risk of contracting the disease. In addition the sperm of the surviving male is said to remain infected for up to 82 days after the onset of symptoms. As long as the virus stays in the body fluids a person stays infected. The spread of the Ebola virus is highly suspected but has not been proven by experiments.

Clinical Introduction

EVD caused by different types of Ebola virus brings different clinical features. The incubation period of Ebola virus is generally considered to be 2 – 21 days. Ebola virus disease shows a variety of symptoms that develop deep in the prodromal constitution leading to various diagnoses including not only other viral hemorrhagic diseases, but also malaria, typhoid, cholera, and others. bacterial rickettsia and non-infectious causes of bleeding.

The onset of the disease is similar to that of severe hemorrhagic fever. Patients have high fever, fever reaching 39-400C, body aches and fatigue. Subsequent abdominal symptoms such as epigastric pain, vomiting and / or bloodless diarrhea appear if the fever persists throughout the day. 3-5.

After 4 – 5 days of illness macular degeneration may be visible but may not be clearly visible on dark skin. After this stage the bleeding from different areas begins. Bleeding in both the upper and lower digestive tract, the respiratory tract, the urinary tract, the vagina in women can be detected. Continuous petechial in the buccal mucosa, skin and conjunctivae grow. Repeated cleansing bumps that prevent any oral fluid intake and a large amount of wet diarrhea (five liters or more per day) contribute to the loss of excess fluid leading to dehydration. If fluid changes are not enough, bending, extreme fatigue and hypovolemic shock eventually.

Hypovolemic shock was reported in 60% of cases. Despite high body temperature, patients experience cold edges due to peripheral vasoconstriction. Rapid and cord pulses, tachypnea, oliguria or anuria can be detected. At the same time features such as asthma and abdominal pain, muscle and joint pain and headache increase. Although in some cases coughing and dyspnoea occur as a result of pulmonary haemorrhage, other respiratory symptoms are uncommon. Conjunctival injection is a common clinical feature. The most common neurologic symptoms are hypoactive and hyperactive delirium characterized by decreased mental function, confusion, dizziness and unusual tremors. As the disease changes the internal bleeding may also begin but more often by this time the patients are already in a coma.

It is reported that only 5% of patients have bleeding from the gastrointestinal tract before death. Most of the reported deaths occurred as a result of shock during the 7th to 12th day of illness. Symptoms of 40% of patients have improved by day 10 although symptoms such as mouth sores and thrush have already appeared. Most patients who survived until day 13 showed a high chance of finally recovering. Some patients who showed early improvement in symptoms have had stiff necks and reduced cognitive levels associated with late death.

Post-mortem examinations and post-mortem biopsies are very useful in the study of the pathology of the Ebola virus disease. Because of the biosafety risk in autopsy staff when handling models, pathological explanations of only a limited number of available conditions.

The most common findings of Haematoxylin and eosine-stained tissue components are oval-shaped or filamentous eosinophilic intracellular inclusions formed by a combination of viral nucleobases. These implants can be found in macrophages, hepatocytes, endothelial cells, fibroblasts of connective tissue etc. Immunohistochemically stains express viral antigens to various infected tissue cells including macrophages, dendritic cells, epithelial cells and sweat glands, intermediate cells and kidney tubes. , seminiferous tubes, endothelial cells and endocardial cells. In addition necrotic cells and cellular waste contain antigens in abundance. Electron microscopy shows an abundance of free viral particles in the alveolar glands, liver sinusoids, and connective tissue cells of the testis and dermal collagen. Karyorrhexis and apoptosis are found in portal triads cells, macrophages of the red spleen pulp and epithelial cells of the tubular kidneys.

Liver tissue exhibits histopathological symptoms including concentrated or widespread necrosis of hepatocytes and central steatosis. Although inflammation is usually mild, hyperplasia of kupfer cells and infiltration of mononuclear inflammatory cells is observed. The infected lung shows congestion, bleeding and intra-alveolar edoema but inflammation is not significant. Concentrated infiltration of mononuclear inflammatory cells is known to occur in the lamina propria of the small intestine and colon. Skin biopsies reveal dermal edoema, concentrated bleeding, petechiae, ecchymosis, and macular rashes. Spleen and lymph nodes show widespread lymphoid depletion due to apoptosis and necrosis. Inflammation of the kidneys is undetectable although acute tubular necrosis is more common. Even if the heart endocardium contains viral antigens, the myocardium does not show significant damage. Brain histology shows panencephalitis and perivascular infiltration of lymphocytes.

The World Health Organization (WHO) has recommended a set of measures to prevent and control infection in health workers, including safety measures to be taken in the various stages of EVD patient management.

1. General precautionary measures

Regardless of the disease, it is recommended that health professionals take precautionary measures when treating all patients, as it is difficult to diagnose EVD patients at the onset of the disease. These are,

2. Doing hand hygiene

Use disposable gloves before handling items that may be infected w ear eye protection and a coat before engaging in procedures that body fluids may predict.

3. Hand hygiene

Hand hygiene should be done using soap and water or an alcohol-based hand sanitizer solution, in accordance with WHO guidelines, before wearing gloves and protective equipment (PPE) after exposure to a patient’s body fluids after contact with a dirty area or equipment after extracting PPE. if the hands appear dirty.

4. Personal Protective Equipment (PPE)

PPE should be worn before entering EVD patient care facilities in accordance with the WHO-recommended order and removed before leaving the care facility. Contact with used PPE on any part of the face or fragile skin should be avoided. PPE covers,

• Non-sterile gloves are the right size
• Non-slip and long-sleeved dress
• Face shield
• Locked shoes that prevent piercing and intrusion

5. Patient placement and management

Suspected or certified EVD patients should be kept in isolation and if possible kept in a single room. Otherwise they must be placed in beds with a gap of at least 1m in between. Visitors should have no restrictions other than those necessary for the patient’s well-being as a parent.

Management of used equipment and other items

It is recommended that equipment such as stethoscopes be refined and disinfected before reuse, if different equipment is not available. Parental equipment, surgical blades, syringes and needles should not be reused. They should be discarded in barrels that are resistant to piercing. All solid non-solid waste should be disposed of in non-leaky bags or bins.

Used linen should be collected from non-perishable bags stored during use. They should be washed with water and detergent, rinsed, soaked in 0.05% chlorine for 30 minutes and then dried.

All barrels must remain upright and must be closed when ¾ is full. Before being removed from the wards the outer surfaces of these containers should be disinfected using 0.5% chlorine.

1. Clean the environment

Cleaners should wear heavy rubber gloves, and non-slip, non-slip rubber boots over PPE. Water and cleaning should be used to clean work areas and the floor of the hospital. This should be done at least once a day. Some dirty areas and contaminants should be cleaned and disinfected using 0.5% chlorine.

2. Biological management

Performing autopsies, post-mortem biopsies and other laboratory tests of certified EVD tissue samples or suspected patients should be minimized and should only be performed by qualified personnel. Full PPE should be worn during template handling. All specimens should be submitted with clearly marked, non-leaky, non-breakable containers, with an antiseptic exterior.

Carcasses should never be washed or embalmed. They should be sealed in two bags, disinfected with 0.5% chlorine and buried immediately. Some cultural and religious practices can be changed if necessary, but body care should be kept to a minimum and full PPE should be worn at all times.

3. In the case of exposure to infected body fluids

All current operations should be safe and dry immediately and PPE should be safely removed. Affected skin should be washed with soap and water and any affected pores such as conjunctiva should be washed with plenty of running water. The person should be tested for fever and other symptoms for 21 days.

4. Pathogenesis

The pathogenesis of the Ebola virus shows similarity to that of most other filo viruses that include immunosuppression, increased vascular permeability and coagulopathy. The Ebola virus enters the scrotum even through skin scratches, either through mucous membranes or by accidental injection. The virus enters monocytes, macrophages and dendritic cells and is carried by lymphatics to circulation. It then spreads to the liver and spleen to infect tissue macrophages and fibroblastic reticular cell. The main cellular targets of this virus are macrophages, dendritic cells and kupfer cells. The Ebola virus shows an interaction between a variety of cellular proteins which is why the infection is characterized by broad tissue and organ tropism.

5. Immunopathology

In many cases of the virus, the immune system plays a key role in controlling the spread of the virus. However the tissues and organs of the fatal EVD cases show less inflammation, which raises the damage to the immune response.

It has been found that the proteins of the structure of filo viruses e.g. VP24 (Virion protein) and VP35 inhibit interferon reactions and thus avoid the host’s natural defences. As previously mentioned, apoptosis of natural killer cells and T lymphocytes was revealed in histopathology describing the suppression of dynamic immune responses.

As with most complex phones, the Ebola virus infection also causes significant release of pro-inflammatory and vasoactive substances. Even if pro-inflammatory mediators promote inflammation and inflammation, the spread of the infection system is not effectively controlled. This is due to vasodilation connected by active ingredients.

6. Endothelial dysfunction and coagulopathy

The virus attacks endothelial cells and endocardial cells and causes injury (18). This causes internal bleeding, fluid and electrolyte imbalance and cardiovascular failure. Endothelial damage leads to platelet aggregation and use. The increased level of inflammatory factors and increased production of surface tissue factor protein in infected monocytes and macrophages promotes coagulation decay. As a result of hepatocellular damage the production of coagulation factors, fibrinogen, protein C and S also decreases. Other social and economic problems associated with the Ebola virus epidemic

In view of the current outbreak, in addition to the large number of lives that have been claimed by the disease, it has created many other serious problems not only in Ebola-affected countries, but also in other African countries.

Agriculture contributes significantly to the African economy. As more and more farmers die of the disease and many leave their farms for fear of contracting the disease, there is a severe shortage of workers in these countries and a decline in food production. The emergence of food shortages in the near future is predicted by experts.

Chocolate companies and many other industries are particularly affected by the shortage of workers. Nigeria and Ivory Coast are the largest cork producing countries but most of the workers are from Liberia and Guinea. International companies such as Nestle and Mars have introduced education and fundraising programs to prevent the spread of the virus to cork workers.

Many schools have been closed because of a deadly epidemic that has swept across the country. Apart from the impact on education, the child support system in government has stalled as a result.

Tourism is another area affected by the epidemic. Although Africa is a larger continent than Europe, the USA and China combined; visitors often see it as a single country since the Ebola epidemic broke out. For example, Tanzania, a popular wildlife sanctuary, is an East African country, located more than 6,000 miles from the Ebola-affected area. Tanzanian hotels reportedly lost 50% of bookings in 2015.

Many African countries refused to host international events and conferences because of the risk of the Ebola outbreak. For example, Morocco, the host of the Africa Cup of Nations, scheduled for January 2015, is calling for a postponement. The government says, “There is no way we can be serious about the health and safety of Moroccan citizens.”

Download Expository Essay on Ebola Virus

If you want to Download the PDF of the Expository Essay on Ebola Virus you can simply click on the given link it is free of cost.

• Expository Essay on Leadership in 800-850 words | for 6-12 | Free Pdf
• Expository Essay on Science and Technology in 900-1000 words | Free Pdf

1 thought on “Expository Essay on Ebola Virus | 800-1000 words | Free PDF”

Thank you for taking the time to read our blog! We hope that you found it helpful. If so, please leave a comment or rating below, and share this blog with your friends on social media. Thank you again for reading!

Leave a Comment Cancel Reply

Your email address will not be published. Required fields are marked *

Save my name, email, and website in this browser for the next time I comment.

Notify me of follow-up comments by email.

Notify me of new posts by email.

Home — Essay Samples — Nursing & Health — Infectious Diseases — Ebola Virus

Essays About Ebola Virus

Ebola virus essay topics and outline examples, essay title 1: unmasking ebola: origins, transmission, and global response.

Thesis Statement: This essay provides an in-depth analysis of the Ebola virus, including its origins, modes of transmission, symptoms, and the global efforts in containing and managing Ebola outbreaks.

• Introduction
• Understanding Ebola: History, Types, and the Zaire Ebola Virus
• Transmission and Symptoms: How Ebola Spreads and Its Impact on the Human Body
• Outbreaks and Epidemics: Notable Ebola Outbreaks and Their Consequences
• Global Response: International Organizations, Research, and Medical Interventions
• Lessons Learned: Preparing for Future Ebola Outbreaks and Emerging Diseases
• Conclusion: The Ongoing Battle Against Ebola and Infectious Disease Preparedness

Essay Title 2: Ebola's Socioeconomic Impact: Health Systems, Communities, and Resilience

Thesis Statement: This essay explores the broader socioeconomic implications of Ebola outbreaks, examining their impact on healthcare systems, affected communities, and the resilience strategies employed in response to the crisis.

• Healthcare Infrastructure: Vulnerabilities and Challenges During Ebola Outbreaks
• Community Resilience: Coping Strategies and Local Responses to Ebola
• Economic Consequences: Impact on Livelihoods, Trade, and Economic Stability
• Psychosocial Effects: Stigma, Trauma, and Mental Health Considerations
• Global Aid and Assistance: International Support for Affected Regions
• Recovery and Rebuilding: Post-Ebola Rehabilitation and Strengthening Systems
• Conclusion: Beyond the Epidemic - Long-term Recovery and Strengthening Resilience

Essay Title 3: Ebola Vaccines and Therapeutics: Advances, Challenges, and Future Prospects

Thesis Statement: This essay delves into the development of Ebola vaccines and therapeutics, discussing recent advancements, challenges in deployment, and the potential for future innovations in combating Ebola.

• The Race for a Vaccine: Historical Context and the Quest for Immunization
• Therapeutics and Treatment: Experimental Drugs, Blood Plasma, and Supportive Care
• Vaccine Development: Progress in Vaccine Trials and Their Efficacy
• Challenges in Deployment: Ethical Considerations, Access, and Distribution
• Future Prospects: Potential Innovations in Ebola Prevention and Treatment
• Global Health Security: Ebola Preparedness and Pandemic Response
• Conclusion: Advancing Science and Preparedness in the Fight Against Ebola

Evaluation of The Issues Related to The Ebola Virus

Assessment of the ebola virus as a severe problem and ways to stop the disease, made-to-order essay as fast as you need it.

Each essay is customized to cater to your unique preferences

+ experts online

Review on African Virus Ebola

The main problems and suggestions regarding the spread of the ebola disease in africa, the importance of community engagement in eradication of the ebola virus, let us write you an essay from scratch.

• 450+ experts on 30 subjects ready to help
• Custom essay delivered in as few as 3 hours

Relevant topics

• Yellow Fever
• Infectious Disease
• Dengue Fever

By clicking “Check Writers’ Offers”, you agree to our terms of service and privacy policy . We’ll occasionally send you promo and account related email

No need to pay just yet!

We use cookies to personalyze your web-site experience. By continuing we’ll assume you board with our cookie policy .

• Instructions Followed To The Letter
• Deadlines Met At Every Stage
• Unique And Plagiarism Free

Ebola Virus Disease Analysis Essay

Gaps in the system that may contribute to the spread of ebola, strategy for addressing ebola within the structure of the health system, options for financing the strategy.

The Ebola virus disease (EVD) outbreak emerged as a significant threat to the lives and safety of both the countries of West Africa and the overall global community. The deaths of a significant number of citizens of West African countries might have been averted if several systematic and organizational issues have been implemented promptly. Unlike countries of equatorial Africa, West African states had never experienced EVD before 2014 and were unprepared to identify, treat, or epidemic management of the disease (World Health Organization [WHO], 2015a).

The overall underdeveloped and underfinanced system of health care in these countries significantly contributes to the spread of the illness. In particular, the public health system lacks funding, a scientific base, and experts. Also, “ineffective diagnostic and case management services” obstruct the opportunity to detect the first cases of EVD in time and prevent its international spread (Shrivastava, 2016, p. 105). Also, the unproductive cooperation of facilities and organizations at the community level complicates the possibility of united adherence to the same pattern of dealing with an outbreak and threatens the success of the implemented interventions.

Considering the factors that contribute to the spread of EVD in West African countries, the strategy for addressing the disease should be concentrated on the elimination of the identified problems. In general, the overall health care infrastructure of the developing countries has to be improved by means of international support and governmental programs. Firstly, scientific evidence-based health care needs to be advanced, which may be achieved through the attraction of foreign experts and the improvement of educational efforts. Secondly, better management and technology implementation is needed to ensure effective diagnostics and disease management.

For that matter, new laboratories need to be launched, as well as the number of facilities specializing in infectious diseases should be increased. Thirdly, community-based initiatives need to be implemented to ensure sufficient local work on the identification and treatment of EVD.

Fourthly, the countries of Western Africa need to develop an effective preventative program. All countries must be “ready to safely and effectively detect, investigate, manage and report potential Ebola cases” and act within the coordinated guidelines (WHO, 2015b, p. 12). Finally, an effective technology-driven and internationally supported monitoring program is required to ensure virus transmission surveillance (WHO, 2015a). All these steps are aimed at the strategic restructuring of the current health system of the countries significantly inclined to Ebola outbreaks. The implementation of the strategy requires proper financing for the effective achievement of anticipated results.

The issue of Ebola outbreaks in countries with ineffective health care systems imposes significant safety concerns for the whole global community due to the high level of transmission of EVD. Therefore, it is in the interests of international organizations to supply necessary resources for West African countries to enforce the strategy implementation. One of the options to attract financial aid to the region is via the Multi-Partner Trust Fund (WHO, 2015b). Also, the funding might be provided via national donations of the developed countries, as well as the World Bank and CDC fund (WHO, 2016). As for the community-based interventions, the governments of the countries of West Africa need to allocate the necessary budget to ensure effective local work.

Shrivastava, S. R., Shrivastava, P. S., & Ramasamy, J. (2016). Ebola outbreak in West Africa: Bridging the gap between the public health authorities and the community. Iranian Journal of Nursing and Midwifery Research, 21 (1), 105-106.

World Health Organization. (2015a). Factors that contributed to the undetected spread of the Ebola virus and impeded rapid containment . Web.

World Health Organization. (2016). West Africa Ebola outbreak: Funding. Web.

World Health Organization. (2015b). WHO strategic response plan: West Africa Ebola outbreak . Web.

• Global Health Funding Proposal
• Cultural Attitudes Complicate Ebola Treatment
• Ebola Control and Management
• The Outcomes of Appliance Digital Therapeutics in Healthcare
• Hyper Granulation Tissue: Capstone Project
• Telehealth: A Mind Map and Telehealth Implementation
• Opioid Disease Prevention: Levels of Disease Prevention
• Patient Education: Congestive Heart Failure
• Chicago (A-D)
• Chicago (N-B)

IvyPanda. (2022, February 11). Ebola Virus Disease Analysis. https://ivypanda.com/essays/ebola-virus-disease-analysis/

"Ebola Virus Disease Analysis." IvyPanda , 11 Feb. 2022, ivypanda.com/essays/ebola-virus-disease-analysis/.

IvyPanda . (2022) 'Ebola Virus Disease Analysis'. 11 February.

IvyPanda . 2022. "Ebola Virus Disease Analysis." February 11, 2022. https://ivypanda.com/essays/ebola-virus-disease-analysis/.

1. IvyPanda . "Ebola Virus Disease Analysis." February 11, 2022. https://ivypanda.com/essays/ebola-virus-disease-analysis/.

Bibliography

IvyPanda . "Ebola Virus Disease Analysis." February 11, 2022. https://ivypanda.com/essays/ebola-virus-disease-analysis/.

Ebola Virus - Essay Samples And Topic Ideas For Free

The Ebola virus causes an acute, serious illness which is often fatal if untreated. It was first discovered near the Ebola River in what is now the Democratic Republic of Congo in 1976. Essays could explore the history of Ebola outbreaks, efforts to combat the disease, the biological characteristics of the virus, or the social and economic impact of outbreaks. We have collected a large number of free essay examples about Ebola Virus you can find in Papersowl database. You can use our samples for inspiration to write your own essay, research paper, or just to explore a new topic for yourself.

History of Ebola Virus Disease

Imagine being isolated from your own family and feeling unsure as to weather or not you will ever see them again.The don't want to go anywhere near you because you are a threat to their health, that's what The Ebola Virus does to you. Ebola Virus Disease is a severe disease that causes internal bleeding and extremely high fever.In 1976 Ebola first emerged in Sudan and Zaire. The first outbreak of ebola infected over 284 people, with a mortality rate […]

Ebola Virus Epidemic

In 2014, the world was horrified when an unknown outbreak occurred and caused a major epidemic worldwide. The world was terrified especially when the outbreak occurred in Guinea and traveled West to the United States and many other countries without knowing what kind of disease that was killing people and infecting our healthcare workers. The virus was later known to be a Zaire Ebolavirus outbreak declared by the World Health Organization (CDC). The Ebola virus is a rare but deadly […]

Ebola: a Devastating Disease

It all began as a normal day for Macire Soumah, of Alassoya, Guinea. Busy with raising her six-year-old son, she hadn't thought much of the headaches and fatigue she had experienced over the past few days. However, this particular morning, she felt so ill that she decided to be examined by the town doctor. At her appointment, Macire was shocked to discover that she was suffering from a relatively new disease called Ebola, a disease for which there was no […]

We will write an essay sample crafted to your needs.

Ebola Virus Disease – Uncommon and Dangerous Illness

Ebola Virus Disease (EVD) is an uncommon and dangerous illness, most commonly affecting humans and nonhuman primates (monkeys, gorillas, and chimpanzees). It is caused by an infection with five categories of viruses within the genus Ebolavirus: Taï Forest virus (species Taï Forest ebolavirus, formerly Côte d'Ivoire ebolavirus), Bundibugyo virus (species Bundibugyo ebolavirus), Ebola virus (species Zaire ebolavirus), Sudan virus (species Sudan ebolavirus), Reston virus (species Reston ebolavirus), and Bombali virus (species Bombali ebolavirus). Of these, only four (Ebola, Sudan, Taï […]

The Spread of Ebola Virus

The Ebola Virus Disease is a disease that has existed for many years. It was first discovered in 1976 near the Ebola River that we know now as the Democratic Republic of Congo. The virus has been contaminating people since than leading it to spread to several African countries. It is a very rare and deadly disease affecting people and nonhumans. Such as monkeys, chimpanzees and gorillas and many more animals. It's a disease being transmitted to people from wild […]

Ebola Research Paper

Ebola is a rare and deadly disease that harvests in people and in-non human primates. Ebola is classified as a virus as it needs a host to survive. Ebola was first discovered in 1976 near the Ebola River in what is now Democratic Republic of Congo. Since then the virus has been infecting people from time to time and causing outbreaks in several african countries. There were 2 major outbreaks of Ebola. The first epidemic happened in 2014 and ended […]

Ebola Outbreak in West Africa

Introduction The 2014-2016 Ebola epidemic in West Africa exposed a divide between the planning of the global health community and the reality of controlling an infectious disease outbreak. Public health planners planned, prepared, and strategized about combating emerging infectious diseases and bioterrorism attacks, yet as the reality of the containment effort set in, the infection rate climbed out of control as the disease migrated from the rural area of origin to major urban centers in West Africa. Front-line doctors and […]

Global Response to the 2013 Ebola Outbreak

The aim of this essay is to present the global response to the epidemic of Ebola virus disease that spread in West Africa from the end of the year 2013. Ebola virus (EBOV, formerly designated Zaire ebolavirus) is one of five known viruses within the genus Ebolavirus and the Ebola Virus Disease is a viral haemorrhagic fever, a rare and deadly disease most commonly affecting people and nonhuman primates. (1) The epidemic started in 2013 was the largest ever seen […]

Ebola – Worst Virus in West Africa

Ebola is the number one worst virus in West Africa but this disease has not been a problem until the biggest outbreak during 2014 where many African residents caught the disease but how did it start and what happens when you catch Ebola. This disease has been around since 1976 it occured in a village near the Ebola River of West Africa this disease was discovered by a man named Barron Peter Karel Piot he recorded the disease the same […]

Research on Ebola

Abstract In the United States of America there was an outbreak in 2014. Many of the hospitals and staff members were unaware of the symptoms and transmission of this virulent virus until it was too late and it spread among patients and staff members. This paper serves as an overview of the virus, including symptoms, diagnosis, and treatments. Also, including how health care has changed to accommodate treating Ebola, and other viruses similar in severity. Introduction Viruses can be very […]

Ebola Epidemic in West Africa

The most recent Ebola epidemic in West Africa in 2014 - 2015 had a weak international response and was a moment of crisis in global health leadership. Certainly, the outbreak was catastrophic, with a total of 28,000 cases and 11,000 deaths, which totaled more than all previous outbreaks (Camacho, 2014). As a result, there was a downturn in the economy and the impact of those lives lost was felt by those who survived the epidemic. As argued by Piot, the […]

The Comparative Structure of Zika and Ebola

Background Information Viruses are microscopic parasites, must smaller than bacteria. They lack the skill to thrive and reproduced outside a host. Viruses are generally classified by the organisms they infect such as animals and plants. Zika and Ebola are two commonly known viruses that have infected a widespread of humans and animals. The Zika virus, ZIKV/Flaviviridae, also known as a flavivirus, is a virus infection that originated from the Zika Forest, Urganda, in 1947. This virus was commonly mistaken for […]

Ebola Infection Control

Abstract You should be able to see what the Ebola virus is. Where it came from. What the symptoms are.Whether or not there is a cure or there will become one. How it spreads. How infection control plays a part in this deadly Virus.Ebola is described as a rare and deadly virus. It is also believed to be a Ribonucleic acid virus. It affects wild animals such as primates, fruit bats and humans. There are five strains of the virus […]

The Black Death and Ebola

In the 1300's a mysterious disease struck Europe, this disease was unknown to the people of Europe which left many people terrified. This mysterious disease spread throughout Europe like a wildfire and between 1347-1375 it infected European cities numerous times and virtually wiped out the European population (Fiero). Similar to this tragic ailment, a mysterious disease erupted in West Africa. In 2014 when this mysterious disease began to spread like the mystic disease in the 1300's it left many people […]

1. Tell Us Your Requirements

2. Pick your perfect writer

3. Get Your Paper and Pay

Hi! I'm Amy, your personal assistant!

Don't know where to start? Give me your paper requirements and I connect you to an academic expert.

short deadlines

100% Plagiarism-Free

Certified writers

Transparency through our essay writing service

Transparency is unique to our company and for my writing essay services. You will get to know everything about 'my order' that you have placed. If you want to check the continuity of the order and how the overall essay is being made, you can simply ask for 'my draft' done so far through your 'my account' section. To make changes in your work, you can simply pass on your revision to the writers via the online customer support chat. After getting ‘my’ initial draft in hand, you can go for unlimited revisions for free, in case you are not satisfied with any content of the draft. We will be constantly there by your side and will provide you with every kind of assistance with our best essay writing service.

How to Write an Essay For Me

Finished Papers

The first step in making your write my essay request is filling out a 10-minute order form. Submit the instructions, desired sources, and deadline. If you want us to mimic your writing style, feel free to send us your works. In case you need assistance, reach out to our 24/7 support team.

Business Enquiries

Niamh Chamberlain

Customer Reviews

Customer Reviews

• On-schedule delivery
• Compliance with the provided brief
• Chat with your helper
• Ongoing 24/7 support
• Real-time alerts
• Free revisions
• Free quality check
• Free title page
• Free bibliography
• Any citation style

Charita Davis

Earl M. Kinkade

Cookies! We use them. Om Nom Nom ...

Viola V. Madsen

My Custom Write-ups

Finished Papers

An official website of the United States government

The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

• Publications
• Account settings

Preview improvements coming to the PMC website in October 2024. Learn More or Try it out now .

• Advanced Search
• Journal List
• J Infect Dis
• PMC10651193

The Multiple Origins of Ebola Disease Outbreaks

Seth d judson.

Division of Infectious Diseases, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

Vincent J Munster

Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA

Associated Data

The origins of Ebola disease outbreaks remain enigmatic. Historically outbreaks have been attributed to spillover events from wildlife. However, recent data suggest that some outbreaks may originate from human-to-human transmission of prior outbreak strains instead of spillover. Clarifying the origins of Ebola disease outbreaks could improve detection and mitigation of future outbreaks.

We reviewed the origins of all Ebola disease outbreaks from 1976 to 2022 to analyze the earliest cases and characteristics of each outbreak. The epidemiology and phylogenetic relationships of outbreak strains were used to further identify the likely source of each outbreak.

From 1976 to 2022 there were 35 Ebola disease outbreaks with 48 primary/index cases. While the majority of outbreaks were associated with wildlife spillover, resurgence of human-to-human transmission could account for roughly a quarter of outbreaks caused by Ebola virus. Larger outbreaks were more likely to lead to possible resurgence, and nosocomial transmission was associated with the majority of outbreaks.

Conclusions

While spillover from wildlife has been a source for many Ebola disease outbreaks, multiple outbreaks may have originated from flare-ups of prior outbreak strains. Improving access to diagnostics as well as identifying groups at risk for resurgence of ebolaviruses will be crucial to preventing future outbreaks.

Despite global advancements in vaccines, diagnostics, and therapeutics for ebolaviruses, devastating outbreaks of Ebola disease (EBOD) continue to occur across Africa. Understanding where and when ebolaviruses emerge in human populations could enhance preparedness for future outbreaks. Since ebolaviruses were first detected in humans in 1976, it has been widely thought that all EBOD outbreaks originate from spillover of ebolaviruses from wildlife into humans [ 1 ], but recent outbreaks have changed our understanding of the emergence of ebolaviruses [ 2 ]. Therefore, reassessing historic EBOD outbreaks through modern epidemiologic and phylogenetic lenses could reveal patterns for preventing further outbreaks.

Ebolaviruses are members of the family Filoviridae, and viruses from 4 Ebolavirus species are known to cause disease in humans ( Table 1 ). We now generally refer to the disease caused by all ebolaviruses in humans as EBOD, ever since the International Classification of Disease for filoviruses (ICD-11) in 2019 [ 3 ]. These different ebolaviruses likely have distinct reservoir hosts and ecological niches [ 4 ]. Ebola virus (EBOV) RNA has been detected in 3 fruit bat species [ 5 ], whereas Sudan virus (SUDV), Bundibugyo virus (BDBV), and Taï Forest virus (TAFV) have not been detected in any potential wildlife reservoirs. While no ebolavirus that is known to be pathogenic in humans has ever been isolated from a putative reservoir host, multiple bat species have been considered possible reservoir hosts and other mammals have been deemed likely incidental hosts [ 4 ]. Spillover from these reservoir hosts or incidental hosts has been historically determined to be the likely source of EBOD outbreaks.

Ebolaviruses Known to Cause Disease in Humans

However, recent findings have changed how we think about the emergence of ebolaviruses in humans. During the West Africa Ebola virus disease (EVD) epidemic, a male survivor infected his female partner 179 days after being diagnosed with EVD, likely through sexual transmission [ 6 ]. Towards the end of the West Africa epidemic, a new cluster of EVD cases were found in Guinea and Liberia, which were linked to sexual transmission from a survivor that occurred about 470 days after he had symptoms [ 7 ]. Subsequent cohort studies have demonstrated prolonged EBOV persistence in the semen of EVD survivors, further indicating risk for delayed sexual transmission [ 8 ]. EBOV was also found to persist in aqueous humor as well as cerebrospinal fluid in survivors who developed uveitis and meningoencephalitis after their initial convalescence [ 9 , 10 ]. Therefore, the testes, eyes, central nervous system, as well as placenta and potentially breast milk were deemed immune-privileged sites where EBOV can persist and evade the immune system [ 11 ].

Another potential source for EVD outbreaks was identified after a survivor had relapse of infection 149 days after leaving an Ebola treatment unit, which caused a new chain of transmission [ 12 ]. Although risk factors for relapse of infection remain unknown, it was noted that the survivor had received antibody-based therapies during their initial treatment [ 12 ]. Researchers also found EBOV persistence in the central nervous system and recrudescence of infection in nonhuman primates who were treated with monoclonal antibody-based therapies, leading to concerns such therapies may contribute to relapse of EVD in humans [ 13 ].

Recently, phylogenetic analyses of EBOV genomes from the 2021 outbreak in Guinea showed that the outbreak strain was genetically similar to the Makona strain from the West Africa epidemic from 2013 to 2016 [ 2 ]. It was postulated that this outbreak may have originated from delayed sexual transmission, reactivation of latent infection, or unrecognized chains of transmission among humans instead of spillover from wildlife. Hereon we refer to outbreaks originating from such sources as flare-ups or resurgence events of human-to-human transmission. Unpublished sequences from the 2020 Equateur, 2021 North Kivu, and 2022 North Kivu outbreaks were also shown to be similar to sequences from prior outbreaks in those regions, and it is thought that these outbreaks were resurgence events, while the 2022 Equateur outbreak has been recognized to be likely a separate spillover event [ 14–18 ].

Investigating the spatiotemporal and phylogenetic relationships of prior EBOD outbreaks could further elucidate how outbreaks originate. While reviewing the exposure history and contexts of initial cases could help identify the sources of EBOD outbreaks, additional insights can be gained through phylogenetic analyses. During initial EVD outbreaks researchers found little genetic variation within the same epidemic chain and that the glycoprotein (GP) gene was conserved [ 19–22 ]. Rapid sequencing in the field during the West Africa EVD epidemic also initially revealed that EBOV sequences from human-to-human transmission had few mutations that were mostly synonymous or in noncoding regions [ 23 ]. However, as the outbreak grew and became the largest and longest EVD epidemic in history, multiple EBOV lineages were subsequently found, and a higher amount of genetic diversity was found in the GP gene [ 24 ]. The mean EBOV evolutionary rate from human-to-human transmission during this outbreak was estimated at approximately 1.2 × 10 −3 nucleotide substitutions/site/year [ 24 ]. The EBOV genome is approximately 19 kb so this is roughly 23 substitutions per year.

While less is known about the evolutionary rate during persistent EBOV infection, researchers found low genetic divergence in reemerged strains from persistently infected individuals [ 25 ]. In samples from acutely infected individuals, researchers found an evolutionary rate of 0.96 × 10 −3 nucleotide substitutions/site/year and similar or reduced evolutionary rates in semen, aqueous humor, and urine during persistent infection [ 26 ]. In fact, the virus from the EVD survivor who infected his partner through sexual transmission 470 days after symptom onset had an evolutionary rate of 0.19 × 10 −3 substitutions/site/year, or approximately 4 substitutions per year [ 7 ]. Therefore, these evolutionary rates provide rough estimates of the expected variation one might see from very prolonged human-to-human transmission versus relapse of persistent infection as the origin of a new outbreak.

The evolutionary rate in the natural reservoir host for EBOV remains unknown. However, there was found to be significant sequence variation between EBOV strains from separate spillover events from wildlife [ 20 , 22 ]. Because spillover events from wildlife occur with viruses from different populations, host species, and locations, it is expected that there would be greater genetic variation between viruses from different spillover events. Therefore, considering both epidemiologic and phylogenetic patterns is necessary to characterize the origins of EBOD outbreaks.

Knowing how EBOD outbreaks originate and whether they are more likely to occur from spillover or resurgence of human-to-human transmission could change the way that we prepare for future outbreaks. Therefore, the goal of this study is to identify the origins of all EBOD outbreaks from 1976 to 2022. Through comparing epidemiologic and phylogenetic relationships, we aim to determine the origins and characteristics of each EBOD outbreak. Additionally, we aim to analyze if the detection of ebolaviruses and EBOD outbreaks has changed, and what gaps remain in detecting and preventing future outbreaks.

We investigated the epidemiology of all known EBOD outbreaks from 1976 to 2022. The US Centers for Disease Control and Prevention's chronology of EBOD outbreaks was used as a guide to determine outbreaks (excluding laboratory-acquired and exported cases) [ 27 ]. We then reviewed the primary literature as well as World Health Organization (WHO) and international outbreak reports. For each outbreak, we sought to determine the earliest infected individual, known as the primary case. If this was not possible, we identified the first case recognized by health care authorities, the index case. We labeled some individuals as both primary and index cases if they fulfilled both of these criteria. In certain circumstances, we identified multiple primary/index cases from the same outbreak (if multiple individuals were exposed to the same animal or if there was an epizootic event). We categorized each primary/index case as confirmed, probable, or suspected according to WHO Integrated Disease Surveillance and Response EVD case definitions [ 28 ]. We created a dataset of all primary/index cases from 1976 to 2022 along with their associated locations, dates of onset, demographics, suspected sources, and diagnostics [ 29 ]. We also made a dataset of all EBOD outbreaks from 1976 to 2022, including locations, most likely origins, cases, deaths, case fatality rates, and factors associated with transmission [ 29 ].

To determine whether EBOD outbreaks originated from spillover or resurgence of human-to-human transmission, we conducted a phylogenetic analysis with representative sequences from each outbreak ( Supplementary Table 1 ). We then compared epidemiological contexts with phylogenetic relationships to determine the most likely origin of each outbreak. We aligned 26 ebolavirus whole-genome sequences from 1976 to 2021 using MAFFT [ 30 ] with the default parameters in Geneious Prime version 2023.0 ( https://www.geneious.com ) and constructed a maximum likelihood tree from PhyML [ 31 ] using the GTR nucleotide substitution model with 100 bootstraps in Geneious Prime. Given representative sequence similarities, we also performed separate alignments of multiple EBOV whole-genome sequences from the 1976 and 1977 outbreaks, as well as the 2007 and 2008 outbreaks in the Democratic Republic of the Congo ( Supplementary Table 2 ). We used a distance matrix to compare the number of nucleotide differences between aligned sequences. We considered the previously described EBOV evolutionary rates in humans when comparing nucleotide differences, with 23 nucleotide substitutions/year as the upper boundary in variation one might expect from an outbreak originating from sustained human-to-human transmission. Therefore, genome sequences from consecutive years that had alignment differences of less than 23 nucleotide substitutions and no epidemiologic evidence of spillover were considered to potentially originate from resurgence of human transmission.

We created a map of the initial locations of each outbreak using QGIS ( http://www.qgis.org ). We used the point coordinates from prior analyses [ 4 , 32 ], as well as where initial cases were treated for the 2017–2022 outbreaks. For outbreaks that were possibly from resurgence events, we calculated the number of days from the first case of a possible flare-up to the date that the previous zoonotic outbreak was declared to be over. We also performed a logistic regression analysis to determine the association between the number of cases in an outbreak and whether that outbreak strain was associated with a subsequent flare-up. We conducted statistical analyses using GraphPad Prism 9 ( https://www.graphpad.com/ ).

We identified a total of 35 EBOD outbreaks ( Table 2 ); 24 of 35 (68.5%) of EBOD outbreaks were due to EVD. If a primary case seemed more likely due to spillover and there was an epidemiologic association with particular wildlife exposure, we included these wildlife species as suspected sources ( Supplementary Table 3 ). Only outbreaks of EVD were recognized as potentially originating from resurgence of prior outbreak strains. TAFV, BDBV, and SUDV have not been associated with transmission via relapse or epizootic events, so outbreaks from these viruses were characterized as separate spillover events, likely from different wildlife hosts. The potential origins of EBOD outbreaks included a single spillover event from a wildlife host, multiple spillover events from a wildlife host, epizootic events with spillover from multiple different wildlife hosts, and resurgence of human-to-human transmission/flare-ups from previous outbreaks. At least one EVD outbreak may have originated from both a spillover event and a resurgence event. Seven of 24 (25.9%) of EVD outbreaks were found to possibly originate from resurgence events, 5 of which occurred after the 2013–2016 epidemic. The initial locations and origins for each outbreak are shown in Figure 1 .

Locations of Ebolavirus emergence 1976–2022. The locations and potential origins of each Ebola disease outbreak are shown. Potential resurgence of human-to-human transmission generally occurred in close proximity to the locations of prior outbreaks.

Ebola Disease Outbreak Origins 1976–2022

Abbreviations: CFR, case fatality rate; DRC, Republic of the Congo; EBOV, Ebola virus; ROC, Republic of the Congo; SUDV, Sudan virus; TAFV, Taï Forest virus.

a Potential resurgence.

Forty-eight primary/index cases were identified for the 35 EBOD outbreaks. The mean age of these cases was 32 years (range, 2–65 years). Thirty of 48 (62.5%) primary/index cases had available demographic information: of these thirty, 9 (30%) were hunters, 6 (20%) were children, 2 (6.67%) were health care workers, and 3 (10%) were pregnant. One primary/index case had a husband who was an EVD survivor. Full case details are available in our Index and Primary Cases dataset [ 29 ] and demographic details are included in Supplementary Table 4 . The initial diagnoses for index cases included: malaria, unknown viral hemorrhagic fever, yellow fever, dysentery/gastroenteritis, and salmonellosis. Thirty-six of 48 (75%) were diagnosed only via clinical review of signs/symptoms and epidemiological history, whereas the other cases were diagnosed via reverse transcription polymerase chain reaction (RT-PCR), serology, and/or virus isolation. From 2021 to 2022 all 6 index cases were confirmed via RT-PCR.

Thirty-one of 35 (88.6%) EBOD outbreaks involved multiple cases, for which there were documented chains of transmission. Of these 31 outbreaks, 25 (80.6%) had reported nosocomial transmission, 14 (45.1%) had transmission from burial practices, and 11 (35.5%) were associated with bushmeat contact. An average of 637 days (range, 222–1690 days) occurred between the end of an original zoonotic outbreak and a potential subsequent flare-up. A logistic regression analysis showed that the odds of an EVD outbreak being associated with a future flare-up increased as the total cases increased (odds ratio, 1.013; 95% confidence interval, 1.002–1.028).

The maximum likelihood phylogenetic tree was constructed from 26 ebolavirus whole-genome sequences (16 EBOV, 7 SUDV, 2 BDBV sequences, and 1 TAFV) ( Figure 2 ). There were multiple outbreaks in which phylogenetic and epidemiologic evidence supported the presumption of spillover as the etiology. The 1994, 1995, 1996, 2002, 2003, 2013, 2014, 2017, and 2018 EBOV genomes all had greater sequence variation and/or suspected wildlife sources, so these outbreaks likely started from different spillover events. Only sequences from the EBOV GP or nucleoprotein were available for some of the 2001–2003 outbreaks in the Republic of the Congo (ROC) and Gabon, so these were not included in our phylogenetic tree. Reviewing previous analyses of these sequences and their contexts revealed that there were 4 separate outbreaks during this period due to multiple epizootic and spillover events [ 33–35 ]. For each of these outbreaks there were multiple suspected primary/index cases in the context of different spillover sources, chains of transmission, and sequences. We were also unable to find a whole-genome sequence for the 2005 ROC outbreak, where the primary/index cases were 2 hunters with bushmeat contact [ 36 ]. We also found that the representative sequences from the 2013–2016 epidemic and the 2021 outbreak in Guinea were closely related (28 nucleotide differences), which was consistent with prior analyses [ 2 ].

Maximum likelihood phylogenetic tree of ebolavirus whole genomes. Representative whole-genome sequences of EBOV, SUDV, TAFV, and BDBV from 1976 to 2021 were used to construct the phylogenetic tree. Numbers above the main nodes are bootstrap values (100 replicates). Each tip is labeled by the ebolavirus, year of onset, and initial country or province/district of each outbreak. Abbreviations: BDBV, Bundibugyo virus; DRC, Republic of the Congo; EBOV, Ebola virus; ROC, Republic of the Congo; SUDV, Sudan virus; TAFV, Taï Forest virus

There were a few historic outbreaks that may have originated from resurgence of prior outbreak strains based on phylogenetic and epidemiologic evidence. The 1977 sequence from Tandala/Bonduni was 99.97%–99.99% similar (2–5 nucleotide differences) to the 3 sequences from the 1976 outbreak in Yambuku (isolates named Mayinga, deRoover, and Ecran). In fact, the Bonduni sequence was more similar to the deRoover isolate (2 nucleotide differences) than all the 1976 isolates were to each other (5 nucleotide differences). Given this sequence similarity, it is possible that the 1977 outbreak may have originated from a resurgence event instead of spillover. The locations of the index cases are roughly 390 kilometers apart and there was no clear epidemiologic chain of transmission. However, during the 1976 outbreak cases were detected within 120 kilometers of Yambuku, and an additional cluster occurred via even further travel by a nurse to Kinshasa [ 37 ]. Therefore, a human origin of the 1977 outbreak could not be ruled out.

Given close similarities between the 2007 and 2008 Luebo strains, an additional alignment was done for the 2008 sequence with 5 sequences from the 2007 outbreak in the same location. The sequence from the 2008 Luebo outbreak had 99.9%–99.94% sequence similarity (11–19 nucleotide differences) to the 2007 viruses that occurred in the same location. A prior analysis of the nucleotide substitutions between these outbreak strains postulated that the 2008 virus could be a direct descendent of the 2007 strain [ 38 ]. Given the sequence similarities and epidemiologic relationships between these outbreaks, it is possible that the 2008 outbreak originated from resurgence of human-to-human transmission instead of spillover.

The 1979 SUDV sequence from Nzara was 99.75% similar (46 nucleotide differences) to the 1976 outbreak in the same region. The 2004 SUDV strain from Yambio was 99.6% similar (70 nucleotide differences) to the nearby 1976 Nzara sequence. The 2000, 2011, and 2012 SUDV sequences were more divergent, and the preliminary 2022 sequence was not included in our phylogenetic analysis [ 39 ]. The evolutionary rate of SUDV from sustained human-to-human transmission or persistent infection has not been determined, and it is unknown whether SUDV can cause flare-ups, so it was assumed that these outbreaks were all separate spillover events. The 2012 Isiro BDBV sequence was 98.6% similar (252 nucleotide differences) to the 2007 Uganda BDBV sequence; there were no identified sources for these outbreaks, and given the sequence differences it was assumed that they occurred from separate spillover events.

We identified multiple origins for EBOD outbreaks. While wildlife spillover seemed the likely etiology for the majority of outbreaks, there are both recent and historical outbreaks that may have emerged from human-to-human transmission of prior outbreak strains instead of spillover from wildlife. We identified 2 historic outbreaks (1977 Tandala/Bonduni and 2008 Luebo) that were previously deemed due to spillover events, but it now seems difficult to exclude resurgence of human-to-human transmission as the potential origin for these outbreaks. Since the 2013–2016 West Africa epidemic, 5 EBOD outbreaks have been considered to originate from possible flare-ups of previous outbreak strains. Given these findings we must reconsider the ways that we prepare for future outbreaks.

Previous research on ebolaviruses has focused on mitigating spillover through reducing contact with wildlife and bushmeat. While roughly a third of all EBOD outbreaks and primary/index cases involved suspected bushmeat contact, this is not the only source that we must consider. Identifying which human populations are at risk for reemergence of outbreak strains and increasing surveillance among these populations will also be key to outbreak prevention. Additionally, understanding risk factors for resurgence, such as whether certain antibody-based therapies increase the likelihood of viral persistence, will also be important to determining populations at risk for future outbreaks.

We found that as cases increase during a particular EVD outbreak, there appear to be greater odds of subsequent resurgence. Therefore, early detection and mitigation of EBOD outbreaks is not only critical for stopping current outbreaks but also for preventing future outbreaks. Identifying regions that have had high numbers of survivors from prior outbreaks could help target surveillance and improve early detection of future outbreaks. While we found that there were fewer historical outbreaks that seemed to originate from delayed sexual transmission or relapse of infection, a potential confounding factor is that detection of flare-ups may have increased recently due to enhanced diagnostic methods.

We also found that the majority of EBOD outbreaks were associated with nosocomial transmission. Equipping and training responders with personal protective equipment and the appropriate resources to quickly diagnose and isolate patients will be crucial to stopping health care-acquired transmission. Additionally, multiple transmission events occurred among family groups during burials and by sexual transmission from survivors. Community-based approaches are therefore essential for educating about ebolavirus transmission while also mitigating stigma.

Our epidemiologic and phylogenetic analyses provide a rough estimation of what outbreaks could plausibly occur from resurgence of prior strains, but there are multiple limitations. Given limited sequence data from wildlife, the genetic diversity in wildlife reservoirs remains unknown. Although it has been observed that there are greater differences between strains from separate spillover events compared to human-to-human transmission, further wildlife and human sequences are needed to clarify these relationships and the degree of genetic variation. We also used representative whole-genome sequences from each outbreak to estimate phylogenetic relationships because of limited availability of multiple sequences from different outbreaks. We used previously published estimates of EBOV evolutionary rates as a guide, but estimates may vary depending on the outbreak strain and size of the outbreak. Additionally, ebolaviruses may exhibit heterogeneous evolutionary rates during persistent infection [ 26 ], and further studies among survivors are needed to determine these phylogenetic relationships.

Another limitation in our phylogenetic analysis is that methods for sequencing and virus isolation have changed over time, which could influence comparisons of evolutionary relationships. The ability to detect genetic variation within and between outbreaks has improved, making it difficult to compare sequences determined multiple decades ago to those from recent outbreaks. Virus isolates used to go through plaque purification prior to sequencing, which could introduce cell-adapted mutations and clonal selection, which could minimize nucleotide variations. Resequencing archived samples using newer methods and as well as more in-depth phylogenetic analyses including evolutionary rate estimations could provide further information about genetic relationships between ebolaviruses.

The evolutionary rates of SUDV, BDBV, and TAFV are less characterized, and it is also unknown whether these viruses can cause resurgent outbreaks through sexual transmission or relapse of infection. Additional phylogenetic analyses and cohort studies of survivors from infections from these other ebolaviruses are needed to determine genetic variation and the risk for resurgence. A recent genomic analysis of BDBV sequences from the 2012 outbreak supports the hypothesis that multiple spillover events could have contributed to this outbreak, but further epidemiologic and phylogenetic data are needed [ 40 ].

Ebolaviruses can emerge in human populations in multiple ways. Recently, there have been large EBOD outbreaks, which create the potential for future resurgence. Therefore, we need additional research and resources dedicated to improving risk assessment and early detection in human populations. Improving the rapid detection and isolation of primary and index cases will be essential to preventing further EBOD outbreaks.

Supplementary Data

Supplementary materials are available at The Journal of Infectious Diseases online. Consisting of data provided by the authors to benefit the reader, the posted materials are not copyedited and are the sole responsibility of the authors, so questions or comments should be addressed to the corresponding author.

Supplementary Material

Jiad352_supplementary_data, contributor information.

Seth D Judson, Division of Infectious Diseases, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

Vincent J Munster, Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA.

Author contributions . S. D. J. contributed conceptualization, analysis, and figures, and wrote the original draft. S. D. J. and V. J. M. reviewed and edited the manuscript.

Disclaimer. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

Data availability. All relevant data are within the manuscript and its online files. Datasets and analyses are available online ( https://github.com/sethdjudson/ebola-origins ) and can be cited at https://doi.org/10.6084/m9.figshare.22257433.v4 .

Financial support . This work was supported by the National Institute of Health (grant number T32 {"type":"entrez-nucleotide","attrs":{"text":"AI007291","term_id":"3215368","term_text":"AI007291"}} AI007291 –27 to S. D. J.). V. J. M. is supported by the Intramural Research Program of the National Institute of Allergy and Infectious Diseases, National Institutes of Health.

Supplement sponsorship. This article appears as part of the supplement “10 th International Symposium on Filoviruses.”

Please don't hesitate to contact us if you have any questions. Our support team will be more than willing to assist you.

Standard essay helper

Orders of are accepted for more complex assignment types only (e.g. Dissertation, Thesis, Term paper, etc.). Special conditions are applied to such orders. That is why please kindly choose a proper type of your assignment.

Customer Reviews

Who will write my essay?

On the website are presented exclusively professionals in their field. If a competent and experienced author worked on the creation of the text, the result is high-quality material with high uniqueness in all respects. When we are looking for a person to work, we pay attention to special parameters:

• work experience. The longer a person works in this area, the better he understands the intricacies of writing a good essay;
• work examples. The team of the company necessarily reviews the texts created by a specific author. According to them, we understand how professionally a person works.
• awareness of a specific topic. It is not necessary to write a text about thrombosis for a person with a medical education, but it is worth finding out how well the performer is versed in a certain area;
• terms of work. So that we immediately understand whether a writer can cover large volumes of orders.

Only after a detailed interview, we take people to the team. Employees will carefully select information, conduct search studies and check each proposal for errors. Clients pass anti-plagiarism quickly and get the best marks in schools and universities.

Finished Papers

is here to help you!

Student years are the best time of one’s life. You are in the prime of your life and hopeful about the bright future ahead. This is the period that leaves the funniest photos, the sweetest memories, and gives you the most faithful friends. However, there is one thing that spoils all the fun – assignment writing. Have you ever struggled to write an essay or prepare a speech only to find that the deadline is getting closer, and the work is not ready yet? Are you desperate for someone to have your paper done? Ordering it online is a really convenient option, but you must be sure that the final product is worth the price. is one of the leading online writing centers that deliver only premium quality essays, term papers, and research papers.

Once you place an order and provide all the necessary instructions, as well as payment, one of our writers will start working on it. Be sure we won’t choose a person to do your paper at random. The writer assigned will hold an academic degree in the respective area of expertise, which makes it possible for him/her to find the relevant information, carry out exhaustive research, and develop a comprehensible and well-organized document. The final product will meet all your specifications regarding the content and formatting style. What is more, you will not have to proofread it for any grammatical or spelling errors, because our professionals have a really good command of the English language.

Need a personal essay writer? Try EssayBot which is your professional essay typer.

• EssayBot is an essay writing assistant powered by Artificial Intelligence (AI).
• Given the title and prompt, EssayBot helps you find inspirational sources, suggest and paraphrase sentences, as well as generate and complete sentences using AI.
• If your essay will run through a plagiarism checker (such as Turnitin), don’t worry. EssayBot paraphrases for you and erases plagiarism concerns.
• EssayBot now includes a citation finder that generates citations matching with your essay.

If you can’t write your essay, then the best solution is to hire an essay helper. Since you need a 100% original paper to hand in without a hitch, then a copy-pasted stuff from the internet won’t cut it. To get a top score and avoid trouble, it’s necessary to submit a fully authentic essay. Can you do it on your own? No, I don’t have time and intention to write my essay now! In such a case, step on a straight road of becoming a customer of our academic helping platform where every student can count on efficient, timely, and cheap assistance with your research papers, namely the essays.

Can I pay someone to write my essay?

Time does not stand still and the service is being modernized at an incredible speed. Now the customer can delegate any service and it will be carried out in the best possible way.

Writing essays, abstracts and scientific papers also falls into this category and can be done by another person. In order to use this service, the client needs to ask the professor about the topic of the text, special design preferences, fonts and keywords. Then the person contacts the essay writing site, where the managers tell him about the details of cooperation. You agree on a certain amount that you are ready to give for the work of a professional writer.

A big bonus of such companies is that you don't have to pay money when ordering. You first receive a ready-made version of the essay, check it for errors, plagiarism and the accuracy of the information, and only then transfer funds to a bank card. This allows users not to worry about the site not fulfilling the agreements.

Go to the website and choose the option you need to get the ideal job, and in the future, the best mark and teacher's admiration.

Laura V. Svendsen

Our Professional Writers Are Our Pride

EssayService boasts its wide writer catalog. Our writers have various fields of study, starting with physics and ending with history. Therefore we are able to tackle a wide range of assignments coming our way, starting with the short ones such as reviews and ending with challenging tasks such as thesis papers. If you want real professionals some of which are current university professors to write your essays at an adequate price, you've come to the right place! Hiring essay writers online as a newcomer might not be the easiest thing to do. Being cautious here is important, as you don't want to end up paying money to someone who is hiring people with poor knowledge from third-world countries. You get low-quality work, company owners become financial moguls, and those working for such an essay writing service are practically enduring intellectual slavery. Our writing service, on the other hand, gives you a chance to work with a professional paper writer. We employ only native English speakers. But having good English isn't the only skill needed to ace papers, right? Therefore we require each and every paper writer to have a bachelor's, master's, or Ph.D., along with 3+ years of experience in academic writing. If the paper writer ticks these boxes, they get mock tasks, and only with their perfect completion do they proceed to the interview process.

Finished Papers

Calculate the price

Minimum Price

2269 Chestnut Street, #477 San Francisco CA 94123

Can you write my essay fast?

Our company has been among the leaders for a long time, therefore, it modernizes its services every day. This applies to all points of cooperation, but we pay special attention to the speed of writing an essay.

Of course, our specialists who have extensive experience can write the text quickly without losing quality. The minimum lead time is three hours. During this time, the author will find the necessary information, competently divide the text into several parts so that it is easy to read and removes unnecessary things. We do not accept those customers who ask to do the work in half an hour or an hour just because we care about our reputation and clients, so we want your essay to be the best. Without the necessary preparation time, specialists will not be able to achieve an excellent result, and the user will remain dissatisfied. For the longest time, we write scientific papers that require exploratory research. This type of work takes up to fourteen days.

We will consider any offers from customers and advise the ideal option, with the help of which we will competently organize the work and get the final result even better than we expected.