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Zaire ebolavirus is one of six known type of Ebolavirus.[1] Four of the six, including EBOV, cause a severe and often fatal hemorrhagic fever in humans and other mammals, known as Ebola virus disease .[2]


EBOV carries a negative-sense RNA genome in virions that are cylindrical and tubular, and contain viral envelope, matrix, and nucleocapsid components. The overall cylinders are generally approximately 80 nanometers in diameter, and have a virally encoded glycoprotein projecting as 7 to 10 nanometer long spikes from its lipid bilayer surface.[3]

Genome 1

Each virion contains one molecule of linear, single-stranded, negative-sense RNA, 18,959 to 18,961 nucleotides in length.[4] The 3 prime terminus is not polyadenylated and the 5 prime end is not capped.[5] [6][7]

Genome 2

This viral genome codes for seven structural proteins and one non-structural protein. The gene order is 3 prime – leader – NP – VP35 – VP40 – GP/sGP – VP30 – VP24 – L – trailer – 5 prime; with the leader and trailer being non-transcribed regions, which carry important signals to control transcription, replication, and packaging of the viral genomes into new virions. Sections of the NP, VP35 and the L genes from filoviruses have been identified as endogenous in the genomes of several groups of small mammals.[5][6][7]

Viral entry

There are two candidates for host cell entry proteins. The first is a cholesterol transporter protein, the host-encoded Niemann–Pick C1 NPC1, which appears to be essential for entry of Ebola virions into the host cell and for its ultimate replication.[8][9] The second candidate is T-cell immunoglobulin and mucin domain 1.[10]


Being acellular, viruses such as Ebola do not replicate through any type of cell division, rather, they use a combination of host- and virally encoded enzymes, alongside host cell structures, to produce multiple copies of themselves. These then self-assemble into viral macromolecular structures in the host cell.[11]


Ebola virus disease kills between 25 percent and 90 percent of those that are infected.[12] Death is often due to shock from fluid loss, and occurs between 6 and 16 days after the first symptoms appear.[13]


The name Ebola virus is derived from the Ebola River a river that was at first thought to be in close proximity to the area in Democratic Republic of Congo, previously called Zaire, where the 1976 Zaire Ebola virus outbreak occurred.[14][15]


Zaire ebolavirus diverged from its ancestors between 1960 and 1976.[16] The genetic diversity of Ebolavirus remained constant before 1900.[16][17] Then, around 1960 , most likely due to climate change or human activities, the genetic diversity of the virus dropped rapidly and most lineages became extinct.[17]A recombination event between Zaire ebolavirus lineages likely took place between 1996 and 2001 in wild apes giving rise to recombinant progeny viruses.[18]


  1. Kuhn, Jens H.; Becker, Stephan; Ebihara, Hideki; Geisbert, Thomas W.; Johnson, Karl M.; Kawaoka, Yoshihiro; Lipkin, W. Ian; Negredo, Ana I.; Netesov, Sergey V.; Nichol, Stuart T.; Palacios, Gustavo; Peters, Clarence J.; Tenorio, Antonio; Volchkov, Viktor E.; Jahrling, Peter B. (December 2010). "Proposal for a revised taxonomy of the family Filoviridae: classification, names of taxa and viruses, and virus abbreviations". Archives of virology. 155 (12): 2083–2103. doi:10.1007/s00705-010-0814-x. ISSN 0304-8608. Retrieved 20 February 2022.
  2. Na, Woonsung; Park, Nanuri; Yeom, Minju; Song, Daesub (4 December 2016). "Ebola outbreak in Western Africa 2014: what is going on with Ebola virus?". Clinical and Experimental Vaccine Research. 4 (1): 17–22. doi:10.7774/cevr.2015.4.1.17. ISSN 2287-3651. PMC 4313106. PMID 25648530.
  3. Klenk, H.-D.; Feldmann, H., eds. (2004). Ebola and Marburg Viruses – Molecular and Cellular Biology. Wymondham, Norfolk, UK: Horizon Bioscience. p. 28. ISBN 978-0-9545232-3-7.
  4. Zaire ebolavirus isolate H.sapiens-wt/GIN/2014/Makona-Kissidougou-C15, complete genome, GenBank
  5. 5.0 5.1 Taylor D, Leach R, Bruenn J (2010). "Filoviruses are ancient and integrated into mammalian genomes". BMC Evolutionary Biology. 10: 193. doi:10.1186/1471-2148-10-193. PMC 2906475. PMID 20569424.
  6. 6.0 6.1 Belyi, V. A.; Levine, A. J.; Skalka, A. M. (2010). Buchmeier, Michael J. (ed.). "Unexpected Inheritance: Multiple Integrations of Ancient Bornavirus and Ebolavirus/Marburgvirus Sequences in Vertebrate Genomes". PLOS Pathogens. 6 (7): e1001030. doi:10.1371/journal.ppat.1001030. PMC 2912400. PMID 20686665.
  7. 7.0 7.1 Taylor DJ, Ballinger MJ, Zhan JJ, Hanzly LE, Bruenn JA (2014). "Evidence that ebolaviruses and cuevaviruses have been diverging from marburgviruses since the Miocene". PeerJ. 2: e556. doi:10.7717/peerj.556. PMC 4157239. PMID 25237605.
  8. Carette JE, Raaben M, Wong AC, Herbert AS, Obernosterer G, Mulherkar N, Kuehne AI, Kranzusch PJ, Griffin AM, Ruthel G, Dal Cin P, Dye JM, Whelan SP, Chandran K, Brummelkamp TR (September 2011). "Ebola virus entry requires the cholesterol transporter Niemann-Pick C1". Nature. 477 (7364): 340–3. Bibcode:2011Natur.477..340C. doi:10.1038/nature10348. PMC 3175325. PMID 21866103. Lay summaryNew York Times. {{cite journal}}: Cite uses deprecated parameter |lay-url= (help)
  9. Côté M, Misasi J, Ren T, Bruchez A, Lee K, Filone CM, Hensley L, Li Q, Ory D, Chandran K, Cunningham J (September 2011). "Small molecule inhibitors reveal Niemann-Pick C1 is essential for Ebola virus infection". Nature. 477 (7364): 344–8. Bibcode:2011Natur.477..344C. doi:10.1038/nature10380. PMC 3230319. PMID 21866101. Lay summaryNew York Times. {{cite journal}}: Cite uses deprecated parameter |lay-url= (help)
  10. Kondratowicz, Andrew S.; Lennemann, Nicholas J.; Sinn, Patrick L.; Davey, Robert A.; Hunt, Catherine L.; Moller-Tank, Sven; Meyerholz, David K.; Rennert, Paul; Mullins, Robert F.; Brindley, Melinda; Sandersfeld, Lindsay M.; Quinn, Kathrina; Weller, Melodie; McCray, Paul B.; Chiorini, John; Maury, Wendy (17 May 2011). "T-cell immunoglobulin and mucin domain 1 (TIM-1) is a receptor for Zaire Ebolavirus and Lake Victoria Marburgvirus". Proceedings of the National Academy of Sciences of the United States of America. 108 (20): 8426–8431. doi:10.1073/pnas.1019030108. ISSN 1091-6490. Retrieved 22 February 2022.
  11. Biomarker Database. Ebola virus. Korea National Institute of Health. Archived from the original on 2008-04-22. Retrieved 2009-05-31.
  12. "WHO | Ebola virus disease". 14 December 2014. Retrieved 24 February 2022.
  13. Singh SK, Ruzek D, eds. (2014). Viral hemorrhagic fevers. Boca Raton: CRC Press, Taylor & Francis Group. p. 444. ISBN 9781439884294. Archived from the original on 29 April 2016.
  14. Bowen ETW, Lloyd G, Harris WJ, Platt GS, Baskerville A, Vella EE (1977). "Viral haemorrhagic fever in southern Sudan and northern Zaire. Preliminary studies on the aetiological agent". Lancet. 309 (8011): 571–573. doi:10.1016/s0140-6736(77)92001-3. PMID 65662. S2CID 3092094.
  15. Johnson KM, Webb PA, Lange JV, Murphy FA (1977). "Isolation and partial characterisation of a new virus causing haemorrhagic fever in Zambia". Lancet. 309 (8011): 569–71. doi:10.1016/s0140-6736(77)92000-1. PMID 65661. S2CID 19368457.
  16. 16.0 16.1 Carroll, S.A. (2012). "Molecular Evolution of Viruses of the Family Filoviridae Based on 97 Whole-Genome Sequences". Journal of Virology. 87 (5): 2608–2616. doi:10.1128/JVI.03118-12. PMC 3571414. PMID 23255795.
  17. 17.0 17.1 Li, Y.H. (2013). "Evolutionary history of Ebola virus". Epidemiology and Infection. 142 (6): 1138–1145. doi:10.1017/S0950268813002215. PMID 24040779. S2CID 9873900.
  18. Wittmann TJ, Biek R, Hassanin A, Rouquet P, Reed P, Yaba P, Pourrut X, Real LA, Gonzalez JP, Leroy EM. Isolates of Zaire ebolavirus from wild apes reveal genetic lineage and recombinants. Proc Natl Acad Sci U S A. 2007 Oct 23;104(43):17123-7. Epub 2007 Oct 17. Erratum in: Proc Natl Acad Sci U S A. 2007 Dec 4;104(49):19656. PMID: 17942693