For the genus, see Ebolavirus. For other uses, see Ebola.
Ebola virus (EBOV)

Virus classification
Group: Group V ((-)ssRNA)
Order: Mononegavirales
Family: Filoviridae
Genus: Ebolavirus
Species: Zaire ebolavirus
Ebola virus (EBOV, formerly designated Zaire ebolavirus) is one of five known viruses within the genus Ebolavirus.[1] Four of the five known ebolaviruses, including EBOV, cause a severe and often fatal hemorrhagic fever in humans and other mammals, known as Ebola virus disease (EVD). Ebola virus has caused the majority of human deaths from EVD, and is the cause of the 2013–2014 Ebola virus epidemic in West Africa, which has resulted in at least 9,693 suspected cases and 4,811 confirmed deaths.[2][3][4][5]

Ebola virus and its genus were both originally named for Zaire (now the Democratic Republic of Congo), the country where it was first described,[1] and was at first suspected to be a new “strain” of the closely related Marburg virus.[6][7] The virus was renamed “Ebola virus” in 2010 to avoid confusion. Ebola virus is the single member of the species Zaire ebolavirus, which is the type species for the genus Ebolavirus, family Filoviridae, order Mononegavirales.[8][1] The natural reservoir of Ebola virus is believed to be bats, particularly fruit bats, and it is primarily transmitted between humans and from animals to humans through body fluids.

The EBOV genome is a single-stranded RNA approximately 19,000 nucleotides long. It encodes seven structural proteins: nucleoprotein (NP), polymerase cofactor (VP35), (VP40), GP, transcription activator (VP30), VP24, and RNA polymerase (L).[9]

Because of its high mortality rate, EBOV is also listed as a select agent, World Health Organization Risk Group 4 Pathogen (requiring Biosafety Level 4-equivalent containment), a U.S. National Institutes of Health/National Institute of Allergy and Infectious Diseases Category A Priority Pathogen, U.S. CDC Centers for Disease Control and Prevention Category A Bioterrorism Agent, and listed as a Biological Agent for Export Control by the Australia Group.

Ebola virus disease
History and nomenclature
Virus inclusion criteria
External links

Phylogenetic tree comparing ebolaviruses and marburgviruses. Numbers indicate percent confidence of branches.
EBOV carries a negative-sense RNA genome in virions that are cylindrical/tubular, and contain viral envelope, matrix, and nucleocapsid components. The overall cylinders are generally approx. 80 nm in diameter, and having a virally encoded glycoprotein (GP) projecting as 7-10 nm long spikes from its lipid bilayer surface.[10] The cylinders are of variable length, typically 800 nm, but sometimes up to 1000 nm long. The outer viral envelope of the virion is derived by budding from domains of host cell membrane into which the GP spikes have been inserted during their biosynthesis.[citation needed] Individual GP molecules appear with spacings of about 10 nm.[citation needed] Viral proteins VP40 and VP24 are located between the envelope and the nucleocapsid (see following), in the matrix space.[11] At the center of the virion structure is the nucleocapsid, which is composed of a series of viral proteins attached to a 18–19 kb linear, negative-sense RNA without 3′-polyadenylation or 5′-capping (see following);[citation needed] the RNA is helically wound and complexed with the NP, VP35, VP30, and L proteins;[12][better source needed] this helix has a diameter of 80 nm and contains a central channel of 20–30 nm in diameter.

The overall shape of the virions after purification and visualization (e.g., by ultracentrifugation and electron microscopy, respectively) varies considerably; simple cylinders are far less prevalent than structures showing reversed direction, branches, and loops (e.g., U-, shepherd’s crook-, 9- or eye bolt-shapes, or other or circular/coiled appearances), the origin of which may be in the laboratory techniques applied.[13] The characteristic “threadlike” structure is, however, a more general morphologic characteristic of filoviruses (alongside their GP-decorated viral envelope, RNA nucleocapsid, etc.).[13]


Each virion contains one molecule of linear, single-stranded, negative-sense RNA, 18,959 to 18,961 nucleotides in length. The 3′ terminus is not polyadenylated and the 5′ end is not capped. This viral genome codes for seven structural proteins and one non-structural protein. The gene order is 3′ – leader – NP – VP35 – VP40 – GP/sGP – VP30 – VP24 – L – trailer – 5′; 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.[14][15][16]

It was found that 472 nucleotides from the 3′ end and 731 nucleotides from the 5′ end are sufficient for replication of a viral “minigenome”, though not sufficient for infection.[13] The minigenome’s genetic material by itself is not infectious, because viral proteins, among them the RNA-dependent RNA polymerase, are necessary to transcribe the viral genome into mRNAs because it is a negative sense RNA virus, as well as for replication of the viral genome.

Sequencing of 99 different Ebola isolates from patients in the 2014 West African outbreak of Ebola showed the virus to be rapidly mutating,[17] with a mutation rate of 2.0 x 10-3 substitutions per site per year making it as fast changing as seasonal influenza.[18] This is likely to represent rapid adaptation to human hosts as the virus is repeatedly passed from human to human (as opposed to usually being passed between fruit bats and only occasionally crossing over into humans), and may pose challenges for the development of a vaccine to the virus.[19][20]


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.[21][22] In one study, mice with one copy of the NPC1 gene removed showed an 80 percent survival rate fifteen days after exposure to mouse-adapted Ebola virus, while only 10 percent of unmodified mice survived this long.[jargon][21] In another study, small molecules were shown to inhibit Ebola virus infection by preventing viral envelope glycoprotein (GP) from binding to NPC1.[22][23] Hence, NPC1 was shown to be critical to entry of this filovirus, because it mediates infection by binding directly to viral GP.[22]

When cells from Niemann Pick Type C patients lacking this transporter were exposed to Ebola virus in the laboratory, the cells survived and appeared impervious to the virus, further indicating that Ebola relies on NPC1 to enter cells;[21] mutations in the NPC1 gene in humans were conjectured as a possible mode to make some individuals resistant to this deadly viral disease.[citation needed][speculation?] The same studies described similar results regarding NPC1’s role in virus entry for Marburg virus, a related filovirus.[21] A further study has also presented evidence that NPC1 is critical receptor mediating Ebola infection via its direct binding to the viral GP, and that it is the second “lysosomal” domain of NPC1 that mediates this binding.[24]

The second candidate is TIM-1 (aka HAVCR1).[25] TIM-1 was shown to bind to the receptor binding domain of the EBOV glycoprotein, to increase the receptivity of Vero cells. Silencing its effect with siRNA prevented infection of Vero cells. TIM1 is expressed in tissues known to be seriously impacted by EBOV lysis (trachea, cornea, and conjunctiva). A monoclonal antibody against the IgV domain of TIM-1, ARD5, blocked EBOV binding and infection.

Together, these studies suggest NPC1 and TIM-1 may be potential therapeutic targets for an Ebola anti-viral drug and as a basis for a rapid field diagnostic assay.[citation needed]


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.[12][better source needed] The virus completes a set of steps when infecting each individual cell:[citation needed]

The virus begins its attack by attaching to host receptors through the glycoprotein (GP) surface peplomer and is endocytosed into macropinosomes in the host cell.[26][non-primary source needed] To penetrate the cell, the viral membrane fuses with vesicle membrane, and the nucleocapsid is released into the cytoplasm. Encapsidated, negative-sense genomic ssRNA is used as a template for the synthesis (3′-5′) of polyadenylated, monocistronic mRNAs and, using the host cell’s ribosomes, tRNA molecules, etc., the mRNA is translated into individual viral proteins.

These viral proteins are processed, a glycoprotein precursor (GP0) is cleaved to GP1 and GP2, which are then heavily glycosylated using cellular enzymes and substrates. These two molecules assemble, first into heterodimers, and then into trimers to give the surface peplomers. Secreted glycoprotein (sGP) precursor is cleaved to sGP and delta peptide, both of which are released from the cell.[citation needed] As viral protein levels rise, a switch occurs from translation to replication. Using the negative-sense genomic RNA as a template, a complementary +ssRNA is synthesized; this is then used as a template for the synthesis of new genomic (-)ssRNA, which is rapidly encapsidated.

The newly formed nucleocapsids and envelope proteins associate at the host cell’s plasma membrane; budding occurs, destroying the cell.


Ebola virus is a zoonotic pathogen. Intermediary hosts have been reported to be “various species of fruit bats … throughout central and sub-Saharan Africa”. Evidence of infection in bats has been detected through molecular and serologic means. However, ebolaviruses have not been isolated in bats.[27] End hosts are humans and great apes, infected through bat contact or through other end hosts. Pigs on the Philippine islands have been reported to be infected with Reston virus, so other interim or amplifying hosts may exist.[27]

Ebola virus disease

Main article: Ebola virus disease
Ebola virus is one of the four ebolaviruses known to cause disease in humans. It has the highest case-fatality rate of these ebolaviruses, averaging 83 percent since the first outbreaks in 1976, although fatality rates up to 90 percent have been recorded in one epidemic (2002–03). There have also been more outbreaks of Ebola virus than of any other ebolavirus. The first outbreak occurred on 26 August 1976 in Yambuku.[28] The first recorded case was Mabalo Lokela, a 44‑year-old schoolteacher. The symptoms resembled malaria, and subsequent patients received quinine. Transmission has been attributed to reuse of unsterilized needles and close personal contact, body fluids and places where the person has touched.

History and nomenclature

See also: Zaire ebolavirus § Nomenclature
During the 1976 Ebola outbreak in Zaire, Ngoy Mushola travelled from Bumba to Yambuku, where he recorded the first clinical description of the virus in his daily log:[29]

“The illness is characterized with a high temperature of about 39°C, hematemesis, diarrhea with blood, retrosternal abdominal pain, prostration with “heavy” articulations, and rapid evolution death after a mean of three days.”

Ebola virus (/ε’boʊlə vaɪrəs/)[1] was first identified as a possible new “strain” of Marburg virus in 1976.[6][7][30] At the same time, a third team introduced the name “Ebola virus”.[31][6][7][31] The International Committee on Taxonomy of Viruses lists Ebola virus as the single member of the species Zaire ebolavirus, which is included into the genus Ebolavirus, family Filoviridae, order Mononegavirales. 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—and the taxonomic suffix virus.[1]

In 2000, the virus name was changed to Zaire Ebola virus,[32][33] and in 2002 to Zaire ebolavirus.[34][35] However, most scientific articles continued to refer to Ebola virus or used the terms Ebola virus and Zaire ebolavirus in parallel Consequently, in 2010, the name Ebola virus was reinstated.[1] Previous abbreviations for the virus were EBOV-Z (for Ebola virus Zaire) and ZEBOV (for Zaire Ebola virus or Zaire ebolavirus). In 2010, EBOV was reinstated as the abbreviation for the virus.[1]

The prototype Ebola virus, variant Mayinga (EBOV/May), was named for Mayinga N’Seka, a nurse who died during the 1976 Zaire outbreak.[36][1][37]


Inactivated Ebola virus vaccines were shown to not promote enough of an immune response to the real pathogen. Recently, however, new techniques are being used; creating vaccines with the viral subunits. These subunit vaccines are showing promise in lab animals for protecting against Ebola infection.[11]

Virus inclusion criteria

See also: Zaire ebolavirus § Species inclusion criteria
A virus of the species Zaire ebolavirus is an Ebola virus (EBOV) if it has the properties of Zaire ebolaviruses and if its genome diverges from that of the prototype Ebola virus, Ebola virus variant Mayinga (EBOV/May), by ten percent or less at the nucleotide level.[1]


Robin Cook’s 1987 novel Outbreak

William Close’s 1995 Ebola: A Documentary Novel of Its First Explosion and 2002 Ebola: Through the Eyes of the People focused on individuals’ reactions to the 1976 Ebola outbreak in Zaire.[38]

Tom Clancy’s 1996 novel, Executive Orders, involves a Middle Eastern terrorist attack on the United States using an airborne form of a deadly Ebola virus named “Ebola Mayinga”.[39]


Recent advances in genomic technologies have been applied to the analysis of blood samples from those infected in the 2014 outbreak. A massively parallel viral sequencing of genetic material collected from 78 patients with confirmed Ebola virus disease, representing more than 70% of cases diagnosed in Sierra Leone from late May to mid-June, 2014 was carried out.[40][41] This work provided near–real-time insights into the transmission dynamics and genetic evolution, shedding light on the origins of the virus causing the 2014 outbreak in West Africa, and whether the 2014 outbreak is still being fed by new contacts with its natural reservoir (no such evidence was found). As is typical of RNA-coded viruses,[40] the Ebola virus was found to mutate rapidly, both within a person during the progression of disease and in the reservoir among the local human population.[41]


Kuhn, Jens H.; Becker, Stephan; Ebihara, Hideki; Geisbert, Thomas W.; Johnson, Karl M.; Kawaoka, Yoshihiro; Lipkin, W. Ian; Negredo, Ana I et al. (2010). “Proposal for a revised taxonomy of the family Filoviridae: Classification, names of taxa and viruses, and virus abbreviations”. Archives of Virology 155 (12): 2083–103. doi:10.1007/s00705-010-0814-x. PMC 3074192. PMID 21046175.
“Guinea: Ebola Virus Disease (EVD) Outbreak”. 17 October 2014. Retrieved 20 October 2014.
“Sierra Leone: EBOLA VIRUS DISEASE – SITUATION REPORT (Sit-Rep) – 18 October, 2014”. 17 October 2014. Retrieved 20 October 2014.
“Liberia Ebola SitRep no. 155”. 17 October 2014. Retrieved 20 October 2014.
Pattyn, S.; Jacob, W.; van der Groen, G.; Piot, P.; Courteille, G. (1977). “Isolation of Marburg-like virus from a case of haemorrhagic fever in Zaire”. Lancet 309 (8011): 573–4. doi:10.1016/s0140-6736(77)92002-5. PMID 65663.
Bowen, E. T. W.; Lloyd, G.; Harris, W. J.; Platt, G. S.; Baskerville, A.; Vella, E. E. (1977). “Viral haemorrhagic fever in southern Sudan and northern Zaire. Preliminary studies on the aetiological agent”. Lancet 309 (8011): 571–3. doi:10.1016/s0140-6736(77)92001-3. PMID 65662.
WHO. “Ebola virus disease”.
Nanbo, Asuka; Watanabe, Shinji; Halfmann, Peter; Kawaoka, Yoshihiro (4 Feb 2013). “The spatio-temporal distribution dynamics of Ebola virus proteins and RNA in infected cells”. Nature 3: 1206. Bibcode:2013NatSR…3E1206N. doi:10.1038/srep01206.
Klenk & Feldmann 2004, p. 28.
Feldmann, H. K. (1993). “Molecular biology and evolution of filoviruses”. Archives of virology. Supplementum 7: 81–100. ISSN 0939-1983. PMID 8219816. edit
Biomarker Database. Ebola virus. Korea National Institute of Health. Retrieved 2009-05-31.
Klenk, H-D; Feldmann, H (editor) (2004). Ebola and Marburg Viruses: Molecular and Cellular Biology. Horizon Bioscience. ISBN 978-1-904933-49-6.
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. edit
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. edit
Taylor, D. J.; Ballinger, M. J.; Zhan, J. J.; Hanzly, L. E.; Bruenn, J. A. (2014). “Evidence that ebolaviruses and cuevaviruses have been diverging from marburgviruses since the Miocene”. PeerJ 2: e556. doi:10.7717/peerj.556. edit
Gire, S. K.; Goba, A; Andersen, K. G.; Sealfon, R. S.; Park, D. J.; Kanneh, L; Jalloh, S; Momoh, M; Fullah, M; Dudas, G; Wohl, S; Moses, L. M.; Yozwiak, N. L.; Winnicki, S; Matranga, C. B.; Malboeuf, C. M.; Qu, J; Gladden, A. D.; Schaffner, S. F.; Yang, X; Jiang, P. P.; Nekoui, M; Colubri, A; Coomber, M. R.; Fonnie, M; Moigboi, A; Gbakie, M; Kamara, F. K.; Tucker, V et al. (2014). “Genomic surveillance elucidates Ebola virus origin and transmission during the 2014 outbreak”. Science 345 (6202): 1369–72. doi:10.1126/science.1259657. PMID 25214632. edit
Jenkins, G. M.; Rambaut, A; Pybus, O. G.; Holmes, E. C. (2002). “Rates of molecular evolution in RNA viruses: A quantitative phylogenetic analysis”. Journal of Molecular Evolution 54 (2): 156–65. doi:10.1007/s00239-001-0064-3. PMID 11821909. edit
Tracking a Serial Killer: Could Ebola Mutate to Become More Deadly? David Quammen, National Geographic News, 15 October 2014
Ebola 2014 is Mutating as Fast as Seasonal Flu. Operonlabs.com, 16 October 2014
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; Raaben; Wong; Herbert; Obernosterer; Mulherkar; Kuehne; Kranzusch; Griffin; Ruthel; Dal Cin; Dye; Whelan; Chandran; Brummelkamp (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 summary – New York Times.
Côté M, Misasi J, Ren T, Bruchez A, Lee K, Filone CM, Hensley L, Li Q, Ory D, Chandran K, Cunningham J; Misasi; Ren; Bruchez; Lee; Filone; Hensley; Li; Ory; Chandran; Cunningham (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 summary – New York Times.
Flemming A (October 2011). “Achilles heel of Ebola viral entry”. Nat Rev Drug Discov 10 (10): 731. doi:10.1038/nrd3568. PMID 21959282.
Miller EH, Obernosterer G, Raaben M, Herbert AS, Deffieu MS, Krishnan A, Ndungo E, Sandesara RG, Carette JE, Kuehne AI, Ruthel G, Pfeffer SR, Dye JM, Whelan SP, Brummelkamp TR, Chandran K; Obernosterer; Raaben; Herbert; Deffieu; Krishnan; Ndungo; Sandesara; Carette; Kuehne; Ruthel; Pfeffer; Dye; Whelan; Brummelkamp; Chandran (March 2012). “Ebola virus entry requires the host-programmed recognition of an intracellular receptor”. EMBO Journal 31 (8): 1947–60. doi:10.1038/emboj.2012.53. PMC 3343336. PMID 22395071.
Kondratowicz AS, Lennemann NJ, Sinn PL et al. (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): 8426–31. doi:10.1073/pnas.1019030108. PMC 3100998. PMID 21536871.
Saeed, M. F.; Kolokoltsov, A. A.; Albrecht, T.; Davey, R. A. (2010). Basler, Christopher F., ed. “Cellular Entry of Ebola Virus Involves Uptake by a Macropinocytosis-Like Mechanism and Subsequent Trafficking through Early and Late Endosomes”. PLoS Pathogens 6 (9): e1001110. doi:10.1371/journal.ppat.1001110. PMC 2940741. PMID 20862315. edit
Feldmann H (May 2014). “Ebola — A Growing Threat?”. N. Engl. J. Med. 371 (15): 1375–8. doi:10.1056/NEJMp1405314. PMID 24805988.
Isaacson, M; Sureau, P; Courteille, G; Pattyn, SR;. “Clinical Aspects of Ebola Virus Disease at the Ngaliema Hospital, Kinshasa, Zaire, 1976”. Retrieved 2014-06-24.
Bardi, Jason Socrates. “Death Called a River”. The Scripps Research Institute. Retrieved 9 October 2014.
Johnson, K. M.; Webb, P. A.; Lange, J. V.; Murphy, F. A. (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.
Netesov, S. V.; Feldmann, H.; Jahrling, P. B.; Klenk, H. D.; Sanchez, A. (2000). “Family Filoviridae”. In van Regenmortel, M. H. V.; Fauquet, C. M.; Bishop, D. H. L.; Carstens, E. B.; Estes, M. K.; Lemon, S. M.; Maniloff, J.; Mayo, M. A.; McGeoch, D. J.; Pringle, C. R.; Wickner, R. B. Virus Taxonomy—Seventh Report of the International Committee on Taxonomy of Viruses. San Diego, USA: Academic Press. pp. 539–48. ISBN 0-12-370200-3{{inconsistent citations}}
Pringle, C. R. (1998). “Virus taxonomy-San Diego 1998”. Archives of Virology 143 (7): 1449–59. doi:10.1007/s007050050389. PMID 9742051.
Feldmann, H.; Geisbert, T. W.; Jahrling, P. B.; Klenk, H.-D.; Netesov, S. V.; Peters, C. J.; Sanchez, A.; Swanepoel, R.; Volchkov, V. E. (2005). “Family Filoviridae”. In Fauquet, C. M.; Mayo, M. A.; Maniloff, J.; Desselberger, U.; Ball, L. A. Virus Taxonomy—Eighth Report of the International Committee on Taxonomy of Viruses. San Diego, USA: Elsevier/Academic Press. pp. 645–653. ISBN 0-12-370200-3.
Mayo, M. A. (2002). “ICTV at the Paris ICV: results of the plenary session and the binomial ballot”. Archives of Virology 147 (11): 2254–60. doi:10.1007/s007050200052.
Wahl-Jensen, V.; Kurz, S. K.; Hazelton, P. R.; Schnittler, H.-J.; Stroher, U.; Burton, D. R.; Feldmann, H. (2005). “Role of Ebola Virus Secreted Glycoproteins and Virus-Like Particles in Activation of Human Macrophages”. Journal of Virology 79 (4): 2413. doi:10.1128/JVI.79.4.2413-2419.2005. PMID 15681442.
Kesel, A. J.; Huang, Z; Murray, M. G.; Prichard, M. N.; Caboni, L; Nevin, D. K.; Fayne, D; Lloyd, D. G.; Detorio, M. A.; Schinazi, R. F. (2014). “Retinazone inhibits certain blood-borne human viruses including Ebola virus Zaire”. Antiviral Chemistry and Chemotherapy 23 (5): 197–215. doi:10.3851/IMP2568. PMID 23636868.
(1) Close, William T. (1995). Ebola: A Documentary Novel of Its First Explosion. New York: Ivy Books. ISBN 0804114323. OCLC 32753758. At Google Books.
(2) Grove, Ryan (2006-06-02). “More about the people than the virus”. Review of Close, William T., Ebola: A Documentary Novel of Its First Explosion. Amazon.com. Retrieved 2014-09-17.
(3) Close, William T. (2002). Ebola: Through the Eyes of the People. Marbleton, Wyoming: Meadowlark Springs Productions. ISBN 0970337116. OCLC 49193962. At Google Books.
(4) Pink, Brenda (2008-06-24). “A fascinating perspective”. Review of Close, William T., Ebola: Through the Eyes of the People. Amazon.com. Retrieved 2014-09-17.
(1) Clancy, Tom (1996). Executive Orders. New York: Putnam. ISBN 0399142185. OCLC 34878804. At Google Books.
(2) Line, Matt; Jeremy; Dan. “Executive Orders book reviews”. AllReaders.com. Archived from the original on 2014-08-01. Retrieved 2014-09-10.
(3) Stone, Oliver (1996-09-02). “Who’s That in the Oval Office?”. Books News & Reviews. The New York Times Company. Archived from the original on 2009-04-10. Retrieved 2014-09-10.
Richard Preston (27 October 2014). “The Ebola Wars”. The NewYorker (New York: Condé Nast). Retrieved 20 October 2014.
Stephen K. Gire with 57 others (2014). “Genomic surveillance elucidates Ebola virus origin and transmission during the 2014 outbreak”. Science (journal) 345 (6202): 1369–1372. doi:10.1126/science.1259657.

Klenk, Hans-Dieter; Feldmann, Heinz (2004). Ebola and Marburg Viruses – Molecular and Cellular Biology. Wymondham, Norfolk, UK: Horizon Bioscience. ISBN 978-0-9545232-3-7.
External links

ICTV Files and Discussions — Discussion forum and file distribution for the International Committee on Taxonomy of Viruses
Genomic data on Ebola virus isolates and other members of the Filoviridae family
ViralZone: Ebola-like viruses – Virological repository from the Swiss Institute of Bioinformatics
U.C. Santa Cruz Ebola genome browser
The Ebola Virus 3D model of the Ebola virus, prepared by Visual Science, Moscow.
ICTV Files and Discussions — Discussion forum and file distribution for the International Committee on Taxonomy of Viruses
FILOVIR — scientific resources for research on filoviruses
“Zaire ebolavirus”. NCBI Taxonomy Browser. 186538.
“Ebola virus sp.”. NCBI Taxonomy Browser. 205488.
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About garyskeete

ASHWORTH MEDICINE-Professional Medical Assisting, Doctor of Science,Legal Assistant Diploma BSc Criminal Justice PhD Computational Neuroscience MD DSC Epigenetics
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