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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5 Key excerpts on "Ebola Virus"

  • Biology And Pathogenesis Of Rhabdo- And Filoviruses
    • Asit K Pattnaik, Michael A Whitt(Authors)
    • 2014(Publication Date)
    • WSPC
      (Publisher)
    Filoviruses, including Ebola and Marburg, are among the deadliest viruses known and are capable of causing severe hemorrhagic fever outbreaks with case fatality rates as high as 90%, depending on the virus. Almost all filovirus outbreaks have so far originated and occurred in Africa, with a frequency that has been increasing since the first outbreak was recorded in 1967. Mounting ecological and epidemiological evidence now implicates several species of bats as at least one reservoir for filoviruses. Studies suggest that contact with these animals, as well as certain other susceptible hosts, including primates, plays a significant role in transmitting virus to humans. Indeed, it is thought that human filovirus outbreaks originate from multiple spillover events from a widely distributed reservoir or host, an assertion that is supported by serological evidence indicating a potentially large geographic distribution of these viruses. In humans, most filoviruses cause severe hemorrhagic fever that often results in death precipitated by multi-organ failure and shock. Early infection of phagocytic cells permits rapid and systemic virus replication that elicits the formation of a cytokine storm and a critically dysfunctional immune system. The defective immune response, in conjunction with massive virus replication, results in the coagulation and vascular abnormalities that are hallmarks of filovirus hemorrhagic fevers, as well as the extreme organ and tissue damage that, in many cases, overwhelms the patient. Despite the increasing frequency of filovirus outbreaks, and the risk of importation or bioterrorism, there are still no licensed vaccines or therapeutics to treat filovirus infections.
    1.   Introduction
    Filoviruses are among the most deadly viruses known, causing large hemorrhagic fever outbreaks in humans and primates with case fatality rates that can reach as high as 90%.
    1 ,2
    To date, there are no licensed vaccines or therapeutics to treat filovirus infections, making outbreaks a significant public health concern. For these reasons, filoviruses are considered Tier 1 Select Agents and Category A bioterrorism agents by the US Centers for Disease Control and Prevention, and all experimental work with these viruses must be performed under biosafety level 4 (BSL4) conditions. Filoviruses have a characteristically filamentous morphology, and their name is ultimately derived from the Latin filum, meaning thread-like. The virions range in length from 800 to 1200 nm and have a consistent diameter of about 80 nm. The single, negative sense RNA genome is approximately 19 kb long and contains seven genes, encoding up to nine proteins depending on the virus.
    1 ,2
    The viruses are taxonomically grouped into the family Filoviridae, which belongs to the order Mononegavirales and is comprised of two genera, Marburgvirus and Ebolavirus. Within the latter genus are five species, each made up of a single virus: the type species Zaire ebolavirus contains Ebola Virus (EBOV), Sudan ebolavirus contains Sudan virus (SUDV), Reston ebolavirus contains Reston virus (RESTV), Taï Forest ebolavirus contains Taï Forest virus (TAFV), and Bundibugyo ebolavirus contains Bundibugyo virus (BDBV). The genus Marburgvirus is comprised of only a single species, Marburg marburgvirus, which contains two closely related viruses, Marburg virus (MARV) and Ravn virus (RAVV). A proposed third genus, Cuevavirus, is comprised of the species Lloviu cuevavirus and the putative Lloviu virus (LLOV), although the virus itself has not yet been isolated.3
  • Emerging Infectious Diseases
    eBook - ePub

    Emerging Infectious Diseases

    A Guide to Diseases, Causative Agents, and Surveillance

    • Lisa A. Beltz(Author)
    • 2011(Publication Date)
    • Jossey-Bass
      (Publisher)
    1. Marburg and Ebola Viruses are members of the Filoviridae family of the order Mononegavirales. Their closest relatives are the paramyxoviruses and rhabdoviruses. Identify pathogenic viruses that belong to these latter viral groups and the symptoms of the diseases that they produce in humans and domestic animals.
    2. Filoviruses actively suppress protective antiviral activities of B, CD4+ T helper, and CD8+ T killer lymphocytes as well as NK cells. These viruses also induce production of a pathogenic proinflammatory innate immune response. Discuss ways in which the pathogenic immune responses might be minimized and protective immunity maximized.
    3. Fruit bats appear to be at least one of the reservoir hosts for filoviruses. Discuss affordable protective measures that might be implemented to decrease transmission of the viruses from bats to mine workers and tourists. Your answer may involve ways of decreasing human contact with infectious bat materials, decreasing the infection rate in bats, or decreasing infectivity of bat-derived material.
    4. Limited ability to rapidly transport regional, national, and international health care teams and proper protective equipment and supplies into remote regions during filovirus outbreaks hampers efforts to control epidemics. Limited access to communication with the global medical and health care agencies inhibits rapid identification and response to initial stages of a hemorrhagic fever epidemic and decreases the ability of local clinicians and public health personnel to easily learn of the most recent advances in prevention and treatment of serious microbial infections, including filovirus infections. Suggest ways in which transportation and communications might be improved, keeping in mind relevant local economic circumstances, civil unrest and refugee migrations, and environmental and climatic conditions.
    Resources
    Ascenzi, P., and others. “Ebolavirus and Marburgvirus: Insight the Filoviridae family.” Molecular Aspects of Medicine,
  • BSL3 and BSL4 Agents
    eBook - ePub

    BSL3 and BSL4 Agents

    Epidemiology, Microbiology and Practical Guidelines

    • Mandy Elschner, Sally Cutler, Manfred Weidmann, Patrick Butaye(Authors)
    • 2012(Publication Date)
    • Wiley-Blackwell
      (Publisher)
    Chapter 13 Filoviruses: Hemorrhagic Fevers Victoria Wahl-Jensen, Sheli R. Radoshitzky, Sina Bavari, Peter B. Jahrling, and Jens H. Kuhn

    13.1 Characteristics

    The family Filoviridae (order Mononegavirales ) contains three genera. Marburg virus (MARV) and Ravn virus (RAVV) are members of the genus Marburgvirus and are assigned to the same species (Marburg marburgvirus ). Bundibugyo virus (BDBV), Ebola Virus (EBOV), Reston virus (RESTV), Sudan virus (SUDV), and Taï Forest virus (TAFV) are members of individual species (Bundibugyo ebolavirus , Zaire ebolavirus , Reston ebolavirus , Sudan ebolavirus , and Taï Forest ebolavirus , respectively) in the genus Ebolavirus . Finally, Lloviu virus (LLOV) is the sole member of the tentative species “Lloviu cuevavirus” in the tentative genus “Cuevavirus” (Table13.1 ) [1]. The genomic sequences of the individual filoviruses are rather divergent. However, their genomic organization and the morphology of their virions are strikingly similar. A filovirus genome is a linear nonsegmented single-stranded negative-sense RNA molecule approximately 19 kb in length. It contains seven genes in the order 3-NP-VP35-VP40-GP-VP30-VP24-L -5. One distinguishing feature of marburgviruses, ebolaviruses, and “cuevaviruses” is the number and location of gene overlaps. The genes, respectively, encode seven structural proteins, the nucleoprotein (NP), RNA-dependent RNA polymerase cofactor (VP35), matrix protein (VP40), spike glycoprotein (GP1,2 ), transcriptional activator (VP30), potential secondary matrix protein (VP24), and the RNA-dependent RNA polymerase (L) [2–4]. NP helically encapsidates the genome and associates with VP30, VP35, and L to form the tubule-like ribonucleoprotein (RNP) complex [5–7]. VP40 and VP24 surround the RNP and are surrounded by a lipid envelope derived from the host cell during virion egress [8, 9]. GP1,2 is found inserted into the membrane, protruding from the virion surface [10]. Mature virions are 80 nm in diameter but differ in average length (≈800–1100 nm). The filaments can branch, or form shapes resembling Us, 6s, or toroids [11]. Ebolavirus and “cuevavirus”, but not marburgvirus, GP
  • Emerging Infections 10
    • 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
  • The Soviet Biological Weapons Program
    The Byelorussian Institute of Epidemiology and Microbiology, which was mostly an open institute, supplied the variant that was studied, Ebola Virus Mayinga. It had received this variant from the Virology Unit at the Institute of Tropical Medicine, Antwerp, Belgium. The Byelorussian scientists had been performing a diagnostic project involving Marburg virus, Ebola Virus, Machupo virus, and Lassa virus as part of Problem 5. Samples of the virus were secretly transported as military shipments from the Byelorussian Institute of Epidemiology and Microbiology to Vector under the supervision of Vector biosafety experts. The major goals of Ebola Virus R&D were to investigate the growth characteristics of Ebola Virus in order to develop methods for optimizing growth rates; to clarify the action of immunoglobulins against Ebola Virus; and to develop vaccines against Ebola Virus disease. Due to the deadliness of Ebola Virus, vaccine development was given the highest priority. At first Vector scientists tried to develop a killed vaccine, but it had no effect. They then tried to develop an attenuated form of Ebola Virus. For this purpose, the Zagorsk Institute sent Vector an Ebola Virus variant that supposedly was less pathogenic for humans than a wild-type virus. 33 Officials tasked Vector scientists with developing vaccines and immunoglobulins using this variant. However, as there was no animal model for doing this kind of developmental research, Vector scientists first sought to increase the strain’s virulence in order to be able to use an existing animal model for vaccine testing. They attempted to do this through the selective passage of Ebola Virus through guinea pigs, but they were unsuccessful. Next they tried to attenuate the variant by growing viruses in a cell line from embryo lung cells (diploid cells) and to use the attenuated viruses as vaccines
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