Biological Sciences
Ebola Virus
Ebola virus is a highly contagious and often fatal virus that causes severe hemorrhagic fever in humans and nonhuman primates. It is transmitted through direct contact with the blood, body fluids, and tissues of infected individuals or animals. The virus can lead to symptoms such as fever, muscle pain, vomiting, and bleeding, and has caused several outbreaks in Africa.
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12 Key excerpts on "Ebola Virus"
eBook - PDF- Sunit K. Singh, Daniel Ruzek, Sunit K. Singh, Daniel Ruzek(Authors)
- 2016(Publication Date)
- CRC Press(Publisher)
The most recent identification of an Ebola Virus was confirmed in 2007; this virus was identified as Bundibugyo ebolavirus from the Bundibugyo district of Uganda (World Health Organization 2008a). Due to the high mortality rate of Ebola Virus infection, the lack of an approved treatment or vaccine and the ability to be transmitted in the laboratory and known human-to-human trans-mission, all filoviruses are classified as biosafety level 4 (BSL-4) pathogens by the World Health Organization (WHO 2008b) and the Centers for Disease Control and Prevention (CDC) and all work with filoviruses requires maximum containment (BMBL 5th edn, CDC). Ebola Virus , like Marburg virus , is classified as CDC Category A agents (http://www.bt.cdc.gov/agent/agentlist-category.asp#a). This classification is part of an ever-changing system for prioritizing initial public health preparedness risk and grading of the potential of these pathogens as biological weapons. Filoviruses are classified as select agents and are federally regulated within the United States by the CDC Select Agent Program (http://www.cdc.gov/of/sap/). 24.2 VIRUS STRUCTURE The electron micrographs of viruses appearing during the initial outbreak showed filamentous par-ticles that exhibited a variable length of between 300 nm and greater than 1500 nm, a diameter of 80 nm, and a 20–30 nm central axis running through the entire particle (Murphy et al. 1978). These studies noted that the particles were indistinguishable from Marburg virus particles, first described in 1968 (Kissling et al. 1968). Filovirus particles are pleomorphic and the unusual structures they form have become a defining characteristic. They may be long filaments, “U” shaped, “6” shaped, or circular (Bowen et al. 1977; Johnson et al. 1977; Pattyn et al. 1977; Murphy et al. 1978). The particle consists of a lipid envelope derived from host membranes decorated with membrane-bound peplomers of GP, which protrude approximately 10 nm.
eBook - PDFViruses
Agents of Evolutionary Invention
- Michael G. Cordingley(Author)
- 2017(Publication Date)
- Harvard University Press(Publisher)
· 248 · · 12 · EBOL AVIRUS The EBOV Makona outbreak, tragic though it was, provided a unique opportunity for scientists to accumulate empirical observations of Ebolavirus biology and evolution. Hard data could now replace mere speculation. We will begin by laying the groundwork and discussing the family Filoviridae that is made up of three genera: Ebolavirus , Marburg-virus , and Cuevavirus . Among these genera and among the five recog-nized Ebolavirus species, there is a wide spectrum of pathogenicity for humans and nonhuman primates. The storied Reston ebolavirus achieved repute after it caused a deadly outbreak of Ebola disease in monkeys housed in a U.S. animal facility. The fear of a deadly hemorrhagic fever virus threatening to emerge in the American heartland was tangible but ill-founded: the virus was not pathogenic in humans. The outbreaks that have come to our attention in central Africa are all associated with severe, often fatal disease in humans and in primates. Human outbreaks have been linked to wildlife die-offs (Leroy, Rouquet, et al. 2004). The out-breaks are so feared because of the ruthless efficiency with which the virus replicates and spreads systemically, apparently unchecked, resulting in renegade inflammatory responses causing the filovirus-typical disease symptoms: extremely high fevers, vascular leakage, and bleeding disor-ders. It is ironic that the rapidity with which the infection takes down its victims and the horrific symptomology of the disease are the very factors Ebolavirus · 249 that have restricted its capacity to establish extended chains of transmis-sion in man. It is simply too pathogenic to cause a pandemic. Direct physical contact with body fluids of the infected victim is required for transmission, so the combination of effective quarantine measures, con-tact tracing, and rigorous deployment of protective gear to health care workers has routinely brought a halt to outbreaks.
- Dongyou Liu(Author)
- 2014(Publication Date)
- CRC Press(Publisher)
65 7 7.1 INTRODUCTION Filoviruses, specifically the marburgviruses and ebolaviruses, cause hemorrhagic fevers with significant mortality in humans in sub-Saharan Africa. Outside of Africa, the viruses are less of a medical concern, but the potential for utilizing these viruses in biowarfare or bioterrorism has heightened the interests in understanding the viruses, the disease they cause, and its prevention. In developed countries, the dra-matic disease and high lethality of filoviruses with the serious social consequences of the ensuing anxiety and panic of an outbreak makes these viruses a major public health priority. Given the very rapid spread of the disease and the lack of a vaccine or effective therapy, the only medical countermea-sures remain the prevention and rapid control of outbreaks. 7.2 CLASSIFICATION AND MORPHOLOGY 7.2.1 T AXONOMY The family Filoviridae is comprised of enveloped, non-segmented, negative-stranded RNA viruses and includes two genera, Marburgvirus and Ebolavirus . 1 A third genus, Cuevavirus , is proposed for Lloviu virus (LLOV) identified in bats from Spain. 2 Filoviruses are members of the order Mononegavirales, which includes other families whose mem-bers have similar genomic characteristics and organization. The genus Ebolavirus has five members based on genetic divergence: Ebola Virus (EBOV), Sudan virus (SUDV), Taï Forest virus (TAFV), Reston virus (RESTV), and Bundibugyo virus (BDBV). Each virus is represented by multiple variants that emerged during outbreaks. Unlike ebolaviruses, which are quite divergent, there are only two marburgviruses, Marburg virus (MARV) and Ravn virus (RAVV). 3,4 The taxonomy of the family Filoviridae continues to evolve since the first char-acterizations of MARV (1947) and EBOV (1976).
eBook - ePubEbola Virus Disease
From Origin to Outbreak
- Adnan I. Qureshi(Author)
- 2016(Publication Date)
- Academic Press(Publisher)
Figure 3.1 )? The growing concerns, fears, and recent news about newly diagnosed patients in the United States and other countries have spread fear among many residents of these countries. The use of the word “pandemic” gives a face to people’s fears and provides hope that most humanity will unite together to fight against the disease. But where did it all start and were there ever other cases reported outside of Africa in the past?“Ebola Virus,” is a household term, but few recognize it as a filamentous virus that has a negative sense ribonucleic acid genome. The term “virus” originates from a Latin word simply meaning “slimy fluid.” Virions are cylindrical or tubular structure containing a viral envelope, matrix, and nucleocapsid component, and are approximately 80 nm in diameter and 800–1000 nm in length. Over a century, this definition has evolved from the first identified human virus, which caused yellow fever reported in 1901 by the US Army physician Walter Reed. The work followed after pioneering work in Cuba by Carlos Finlay, proving that mosquitoes transmitted the deadly disease. The Chamberland–Pasteur filter had been developed in 1884 in Paris by Charles Chamberland, who worked with Louis Pasteur. But it was Dmitri Ivanowski in St. Petersburg in Russia in 1892 who used porcelain filters to isolate and characterize what we now know to be a virus. The name Ebola is derived from the name of the Ebola River near a town called Yambuku in the Democratic Republic of Congo (previously Zaire) where the first outbreak was identified.2 There have been five subtypes identified, namely, Ebola-Zaire, Ebola-Sudan, Ebola-Bundibugyo, and Ebola-Taï Forest. The fifth which was called Ebola-Reston never actually infected any humans.2Figure 3.1 Geographic locations of Ebola Virus disease (1976–2008).Marburg virus disease emergence (1967–1975)
The Ebola Virus has characteristics that are very similar to another virus from filoviridae family of viruses called the Marburg virus. This virus was first described in summer of 1967 when an outbreak of unknown disease occurred in Germany and Yugoslavia. It was also a filamentous RNA virus source of which was traced to the vervet monkeys (Cercopithecus aethiops) imported from Uganda.3
eBook - PDF- Dongyou Liu(Author)
- 2016(Publication Date)
- CRC Press(Publisher)
559 50.1 INTRODUCTION 50.1.1 C LASSIFICATION , M ORPHOLOGY , AND B IOLOGY Ebola Viruses (EBOV) belong to the family Filoviridae of the order Mononegavirales . Filoviruses are enveloped, non-segmented, single-stranded, negative-sense RNA viruses [1]. The family name is derived from the morphology of the virus, which is characterized by a thin and elongated shape (filo, Latin for “filament”). EBOV was named after the Ebola River in Zaire, where the first recognized outbreak occurred. Five species of EBOV have been defined to date on the basis of genetic divergence: Zaire ebolavirus (ZEBOV), Sudan ebolavirus (SEBOV), Ivory Coast ebolavirus (CIEBOV: also known as Cote d’Ivoire ebolavirus ), Reston ebolavirus (REBOV), and Bundibugyo ebolavirus (BEBOV). ZEBOV, SEBOV, CIEBOV, and BEBOV cause clinical symptoms in humans and nonhuman primates, while REBOV causes dis-ease only in nonhuman primates, but not in humans. Electron microscopic studies revealed that the virions of EBOV are pleomorphic, appearing as either U-shaped, figure 6-shaped, or circular configurations, or as elongated filamentous forms of varying length (up to 14,000 nm). The virions are usually 80 nm in diameter and 800 – 1000 nm in length [2]. The virions are enveloped with a lipid bilayer (envelope), which is derived from the host cells, anchoring a glycoprotein that projects spikes 7–10 nm in length from its surface. The genome is 19 kb long and encodes the viral proteins in the order NP-VP35-VP40-GP/sGP-VP30-VP24-L (Figure 50.1). The extragenic sequence at the 3' end, which is called the leader, of EBOV is short, ranging from 50 to 70 bases in length, while the length of the 5' end sequence, which is called the trailer, is variable depending on the species, ranging from 25 to 677 bases (25 bases for REBOV and 677 bases for ZEBOV). The extreme 3' and 5' end sequences are conserved and potentially form stem-loop structures [3–5].
eBook - ePubEmerging Infectious Diseases
Clinical Case Studies
- Onder Ergonul, Fusun Can, Murat Akova, Lawrence Madoff(Authors)
- 2014(Publication Date)
- Academic Press(Publisher)
Chapter 9Ebola Virus Disease
Pierre Formenty, Emerging and Epidemic Zoonotic Diseases Team (CED/EZD), World Health OrganizationFive species of ebolavirus constitute the genus Ebolavirus , one member of the Filoviridae family. The Bundibugyo, Zaire, and Sudan ebolavirus species cause severe Ebola Virus disease (EVD) outbreaks in humans whereas the Reston and Taï Forest species do not. EVD is a febrile hemorrhagic illness, which causes death in 25–90% of all clinically ill cases. EVD outbreaks occur primarily in remote villages in Central and West Africa, near tropical rainforests. The virus is transmitted to people from wild animals and spreads in the human population through human-to-human transmission. Fruit bats of the Pteropodidae family are considered to be the natural host of the Ebola Virus. The laboratory diagnostic remains essential to confirm EVD cases. There is no treatment or vaccine available for either people or animals. Raising awareness of the risk factors of Ebola infection and the protective measures individuals can take is the only way to reduce human infection and death.Keywords
Ebolavirus; Bundibugyo virus; Ebola Virus; Sudan virus; Reston virus; Taï Forest virus; Africa; Asia; Ebola Virus disease (EVD) outbreaksCase Presentation
In the Taï National Park, Côte d’Ivoire, the behavior of a community of free-living chimpanzees has been studied since 19791 . In early November 1994, several decomposed corpses of chimpanzees were found and one chimpanzee that had died less than 12 hours previously was dissected on November 16 by three research workers. There were signs of hemorrhage and non-clotting blood. Eight days later, one of the researchers, a 34-year-old woman, became ill.Clinical Course
On November 24 (day 1), around 6 pm, the patient started shivering with fever (Figure 9.1
- Alfonso J. Rodriguez-Morales(Author)
- 2018(Publication Date)
- IntechOpen(Publisher)
It has also been identified in Pennsylvania, Texas and Siena, Italy. iv. Côte d ’ Ivoire Ebola Virus: Also referred to as Taï Forest Ebola Virus (TAFV), it was first discovered in chimpanzees from the Taï Forest in Ivory Coast in 1994 v. Bundibugyo Ebola Virus (BDBV): This virus species was discovered in 2007 in Uganda following the outbreak in Bundibugyo District which recorded 39 deaths with a mortality rate of 34%. 6. Ebola Virus morphology The genus Ebola are negative-sense, single stranded RNA viruses which are non-segmented belonging to the Filoviridae family. The negative-sense RNA genome is approximately 19 kb in size but varies among the various Ebola species and it is encapsulated in a lipid membrane used for the formation of new particles on the surfaces of their host cells [24, 25]. The core of the virus constitutes the genomic RNA surrounded by nucleoproteins (NP). The Ebola genome consists of seven genes that codes viral proteins (VPs) each of which differs in function [26]. Among these proteins, VP24 which constitutes the main matrix protein is the most abundant virion protein. VP30 is involved in the activation of RNA transcription while VP35 is involved in viral RNA synthesis. VP35 is also attributed to be responsible for varying degrees of viru-lence among different strains of Ebola Virus. VP40 is also a matrix protein of the negative stranded RNA and its roles is to assemble the lipid envelop of the virus by linking the nucleocapsid to the surrounding membrane. The virus also contains a transmembrane glyco-protein (GP) which is responsible for the formation of virion spikes which facilitates viral entry into cells. A section of this glycoprotein (GP1 and GP2) are responsible for immunosuppression Figure 1. Morphological representation of the Ebola Virus showing the various proteins: VP, virion protein; and GP, glycoprotein [28]. Current Topics in Tropical Emerging Diseases and Travel Medicine 132
No longer available |Learn more- (Author)
- 2014(Publication Date)
- Learning Press(Publisher)
________________________ WORLD TECHNOLOGIES ________________________ Chapter- 3 Ebola Ebola 1976 photograph of two nurses standing in front of Kinshasa case No. 3 (Mayinga N'Seka), who was treated and later died in Ngaliema Hospital in Kinshasa, Zaire ICD-10 A98.4 ________________________ WORLD TECHNOLOGIES ________________________ ICD-9 065.8 DiseasesDB 18043 MedlinePlus 001339 eMedicine med/626 MeSH D019142 Ebola Ebola Virus electron micrograph Virus classification Group: Group V ((-)ssRNA) Order: Mononegavirales Family: Filoviridae Genus: Ebolavirus Type species Zaire ebolavirus Species ________________________ WORLD TECHNOLOGIES ________________________ Ivory Coast ebolavirus Reston ebolavirus Sudan ebolavirus Ebola is the virus Ebolavirus (EBOV), a viral genus, and the disease Ebola hemor-rhagic fever (EHF), a viral hemorrhagic fever (VHF). The virus is named after the Ebola River Valley in the Democratic Republic of the Congo (formerly Zaire), which is near the site of the first recognized outbreak in 1976 at a mission hospital run by Flemish nuns. It remained largely obscure until 1989 when several widely publicized outbreaks occurred among monkeys in the United States. The virus interferes with the endothelial cells lining the interior surface of blood vessels and with coagulation. As the blood vessel walls become damaged and destroyed, the pla-telets are unable to coagulate, patients succumb to hypovolemic shock. Ebola is trans-mitted through bodily fluids, while conjunctiva exposure may also lead to transmission. There are five recognized species within the ebolavirus genus, which have a number of specific strains. The Zaire virus is the type species, which is also the first discovered and the most lethal. Electron micrographs show long filaments, characteristic of the Filoviridae viral family. Classification The genera Ebolavirus and Marburgvirus were originally classified as the species of the now-obsolete Filovirus genus.
eBook - PDF- Ming Luo(Author)
- 2011(Publication Date)
- World Scientific(Publisher)
Chapter 14 Ebolaviruses: What We Know and Where We Are on Potential Therapeutics Peter Halfmann ∗ , Gabriele Neumann ∗ and Yoshihiro Kawaoka ∗ , † , ‡ , § 1. An Introduction to Ebolavirus The first recorded outbreak of Ebolavirus occurred in 1976, when a mysterious disease killed 280 of 318 infected individuals in Zaire (now the Republic of Congo). This outbreak resulted in a case fatality rate of 88%, a figure that alarmed health care workers and scientists. The causative agent was eventually identified as Ebolavirus, named after the Ebola River that runs through Zaire. As then, there have been additional sixteen outbreaks of Ebolaviruses, resulting in 2299 confirmed cases with 1556 deaths. Ebolavirus belongs to the family Filoviridae (order Mononegavirales ) along with the closely related Marburgvirus. 1 Within the genus Ebolavirus , five species are currently recognized: Zaire ebolavirus , Sudan ebolavirus , Ivory Coast ebolavirus , Bundibugyo ebolavirus , and Reston ebolavirus . The recently discov-ered Bundibugyo ebolavirus (named after the Bundibugyo district of Uganda where the outbreak occurred in 2007) shows a 32% nucleotide difference from its clos-est phylogenetic relative, Ivory Coast ebolavirus , which is similar in nucleotide divergence to the other Ebolavirus species (which ranges from 35–45%). 2 ∗ Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison, WI 53706, USA. † Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan. ‡ International Research Center for Infectious Diseases, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan. § ERATO Infection-Induced Host Responses Project, Saitama 332-0012, Japan. 295 296 P. Halfmann, G. Neumann and Y. Kawaoka Table 1. Known Ebolavirus cases and outbreaks.
eBook - PDF- John I. Gallin, Anthony S. Fauci(Authors)
- 1998(Publication Date)
- Academic Press(Publisher)
D. Lessons from Clinical and Pathological Characteristics of Filovirus Infections in Humans An old truism states, Understanding the nature of a disease in the individual patient is a key to understanding the nature of the disease in the population. Ebola Virus ~ 8 7 This truism must stem from diseases where there is one host species, one host population involved. However, with recognition of the extra complexity added by multispecies zoonotic transmission cycles, especially an unknown zoonotic transmission cycle, precise lessons seem hard to come by. Nevertheless, a review of the clinical and pathological nature of filovirus infections is warranted. Marburg and Ebola Virus subtypes Zaire, Sudan, and C6te d'Ivoire cause severe hemorrhagic fever in humans--the evolution of disease often seems in- exorable and invariable (Piot et al., 1978). Following an incubation period of usually 4 to 10 days (extreme range 2 to 21 days for infection by the Zaire subtype of Ebola Virus), there is an abrupt onset of illness with initial nonspe- cific symptoms including fever, severe frontal headache, malaise, and myalgia. Early signs include bradycardia and conjunctivitis, and there may be a macro- papular rash most readily evident on white skin (Pattyn, 1978; Peters et al., 1994, 1996; Khan et al., 1996). Deterioration over the following 2 to 3 days is marked by pharyngitis, nausea, and vomiting, progressing to hematemeses and melena. There is prostration and bleeding which is manifested as petechiae, ec- chymoses, uncontrolled bleeding from venepuncture sites, and postmortem evi- dence of visceral hemorrhagic effusions. Death usually occurs 6 to 9 days after onset of clinical disease (range 1 to 21 days). Abortion is a common conse- quence of infection, and infants born to mothers dying of infection are fatally infected. Convalescence is slow and marked by prostration, weight loss, and often amnesia for the period of acute illness.
eBook - PDFViral Diagnostics
Advances and Applications
- Robert S. Marks, Leslie Lobel, Amadou Sall, Robert S. Marks, Leslie Lobel, Amadou Sall(Authors)
- 2014(Publication Date)
- Jenny Stanford Publishing(Publisher)
Due to its ability to develop new lethal strains, such as the recent one, 2007– 2008, 152 or to distinguish engineered strains from other pathogens that may produce similar symptoms, continuous efforts toward developing new, advanced assays, which will be quick and reliable with minimum sample handling and laboratory skill requirement, are a necessity. 98 Today, traditional detection systems, such as virus culture, electron microscopy, and IF, are still considered key elements in the confirmation and detection of Ebola and will continue to be so despite their risk to lab workers, the requirement for special facilities, and the high cost in time and labor intensity. It is clear that future diagnostics of viruses, such as Ebola, will evolve depending on new developments of cutting-edge technologies, as well as a greater understanding of Ebola immunology 155, 156 which will produce detection systems able to cope with and overcome difficulties existing today and in the future. References 1. Feldmann, H., et al. Ebola Virus ecology: a continuing mystery. 2004. Trends Microbiol ., 12 (10), 433–437. 2. Pringle, C. R. The Bunyaviridae and their genetics: an overview. 1991. Curr. Top. Microbiol. Immunol ., 169 , 1–25. 3. Feldmann, H., and H. D. Klenk. Marburg and Ebola Viruses. 1996. Adv. Virus Res ., 47 , 1–52. 4. Colebunders, R., and M. Borchert. Ebola haemorrhagic fever: a review. 2000. J. Infect ., 401 , 16–20. 5. Murphy, F. A., G., van der Groen, S. G. Whitfield, and J. V. Lange. 1978. Ebola and Marburg virus morphology and taxonomy, in Ebola Virus Haemorrhagic Fever (Pattyn, S. R., ed), Elsevier, Amsterdam, pp. 61–84. References 189 6. Kiley, M. P., et al. Filoviridae: a taxonomic home for Marburg and Ebola Viruses? 1982. Intervirology , 181 (2), 24–32. 7. Cox, N. J., et al. Evidence for two subtypes of Ebola Virus based on oligonucleotide mapping of RNA. 1983. J. Infect. Dis ., 147 (2), 272– 275. 8. Buchmeier, M.
eBook - ePub- W. Michael Scheld, James M. Hughes, Richard J. Whitley, W. Michael Scheld, James M. Hughes, Richard J. Whitley(Authors)
- 2016(Publication Date)
- ASM Press(Publisher)
[CrossRef]10. Centers for Disease Control and Prevention (CDC) . 2001. Outbreak of Ebola hemorrhagic fever Uganda, August 2000-January 2001. MMWR Morb Mortal Wkly Rep 50 : 73–77.[PubMed]11. Leroy EM , Epelboin A , Mondonge V , Pourrut X , Gonzalez J-P , Muyembe-Tamfum J-J , Formenty P . 2009. Human Ebola outbreak resulting from direct exposure to fruit bats in Luebo, Democratic Republic of Congo, 2007. Vector Borne Zoonotic Dis 9 : 723–728.[PubMed] [CrossRef]12. Sanchez A , Kiley MP , Holloway BP , Auperin DD . 1993. Sequence analysis of the Ebola Virus genome: organization, genetic elements, and comparison with the genome of Marburg virus. Virus Res 29 : 215–240.[PubMed] [CrossRef]13. Elliott LH , Kiley MP , McCormick JB . 1985. Descriptive analysis of Ebola Virus proteins. Virology 147 : 169–176.[PubMed] [CrossRef]14. Sanchez A , Trappier SG , Mahy BW , Peters CJ , Nichol ST . 1996. The virion glycoproteins of Ebola Viruses are encoded in two reading frames and are expressed through transcriptional editing. Proc Natl Acad Sci USA 93 : 3602–3607.[PubMed] [CrossRef]15. de La Vega M-A , Wong G , Kobinger GP , Qiu X . The multiple roles of sGP in Ebola pathogenesis. Viral Immunol [Epub ahead of print.] doi:10.1089/vim.2014.0068 . [PubMed] [CrossRef]16. Ramanan P , Shabman RS , Brown CS , Amarasinghe GK , Basler CF , Leung DW . 2011. Filoviral immune evasion mechanisms. Viruses 3 : 1634–1649.[PubMed] [CrossRef]17. Berman M , du Lac JF , Izadi E , Dennis B . 2014. As Ebola confirmed in U.S., CDC vows: ‘We’re stopping it in its tracks’. The Washington Post
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