Filoviridae

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Family Filoviridae
Virus classification
Group: Group V ((-)ssRNA)
Order: Mononegavirales
Family: Filoviridae
Genera

The family and CDC Filoviridae (members are called Filovirus)[1] is the taxonomic home of several related viruses that form filamentous infectious viral particles (virions), and encode their genome in the form of single-stranded negative-sense RNA. Two members of the family that are commonly known are Ebola virus and Marburg virus. Both viruses, and some of their lesser known relatives, cause severe disease in humans and nonhuman primates in the form of viral hemorrhagic fevers.[2] All ebolaviruses and marburgviruses are Select Agents,[3] World Health Organization Risk Group 4 Pathogens (requiring Biosafety Level 4-equivalent containment),[4] National Institutes of Health/National Institute of Allergy and Infectious Diseases Category A Priority Pathogens,[5] Centers for Disease Control and Prevention Category A Bioterrorism Agents,[6] and listed as Biological Agents for Export Control by the Australia Group.[7] It is expected that cuevaviruses [8] will be classified in a similar way in the near future.

Use of term[edit]

The family Filoviridae is a virological taxon that was created in 1982[2] and emended in 1991,[9] 1998,[10] 2000,[11] 2005,[12] 2010[8] and 2011.[13] The family currently includes the three virus genera Cuevavirus, Ebolavirus, and Marburgvirus and is included in the order Mononegavirales.[8] The members of the family (i.e. the actual physical entities) are called filoviruses or filovirids.[8] The name Filoviridae is derived from the Latin noun filum (alluding to the filamentous morphology of filovirions) and the taxonomic suffix -viridae (which denotes a virus family).[2]

Note[edit]

Filoviridae is pronounced ˌfiːloʊ’viːrɨdɛ (IPA) or fee-loh-vee-ri-deh in English phonetic notation.[8] According to the rules for taxon naming established by the International Committee on Taxonomy of Viruses (ICTV), the name Filoviridae is always to be capitalized, italicized, never abbreviated, and to be preceded by the word "family". The names of its members (filoviruses/filovirids) are to be written in lower case, are not italicized, and used without articles.[8][13]

Family inclusion criteria[edit]

A virus that fulfills the criteria for being a member of the order Mononegavirales is a member of the family Filoviridae if[8][13]

Family organization[edit]

Family Filoviridae: genera, species, and viruses
Genus name Species name Virus name (Abbreviation)
Cuevavirus Lloviu cuevavirus* Lloviu virus (LLOV)
Ebolavirus Bundibugyo ebolavirus Bundibugyo virus (BDBV; previously BEBOV)
Reston ebolavirus Reston virus (RESTV; previously REBOV)
Sudan ebolavirus Sudan virus (SUDV; previously SEBOV)
Taï Forest ebolavirus Taï Forest virus (TAFV; previously CIEBOV)
Zaire ebolavirus* Ebola virus (EBOV; previously ZEBOV)
Marburgvirus Marburg marburgvirus* Marburg virus (MARV)
Ravn virus (RAVV)

Table legend: "*" denotes type species.

Nomenclature below species level[edit]

Recommendations have been made for the identification of these viruses below the species level.[14] These include the use of virus name / strain / isolation host-suffix / country of sampling / year of sampling / genetic variant designation / isolate designation. The use of the suffix "rec" is recommended if the virus has been identified via recombinant DNA.

Phylogenetics[edit]

The mutation rates in these genomes have been estimated to be between 0.46 × 10−4 and 8.21 × 10−4 nucleotide substitutions/site/year.[15] The most recent common ancestor of both the Reston and Zaire species has been estimated to be ~1960. The most recent common ancestor of the Marburg and Sudan species appears to have evolved 700 and 850 years before present respectively. Although mutational clocks placed the divergence time of extant filoviruses at ~10,000 years before the present, dating of orthologous endogenous elements (paleoviruses) in the genomes of hamsters and voles indicated that the extant genera of filovirids had a common ancestor at least as old as the Miocene.[16]

Life cycle[edit]

The filovirus life cycle begins with virion attachment to specific cell-surface receptors, followed by fusion of the virion envelope with cellular membranes and the concomitant release of the virus nucleocapsid into the cytosol. The viral RNA-dependent RNA polymerase (RdRp, or RNA replicase) partially uncoats the nucleocapsid and transcribes the genes into positive-stranded mRNAs, which are then translated into structural and nonstructural proteins. Filovirus RdRps bind to a single promoter located at the 3' end of the genome. Transcription either terminates after a gene or continues to the next gene downstream. This means that genes close to the 3' end of the genome are transcribed in the greatest abundance, whereas those toward the 5' end are least likely to be transcribed. The gene order is therefore a simple but effective form of transcriptional regulation. The most abundant protein produced is the nucleoprotein, whose concentration in the cell determines when the RdRp switches from gene transcription to genome replication. Replication results in full-length, positive-stranded antigenomes that are in turn transcribed into negative-stranded virus progeny genome copies. Newly synthesized structural proteins and genomes self-assemble and accumulate near the inside of the cell membrane. Virions bud off from the cell, gaining their envelopes from the cellular membrane they bud from. The mature progeny particles then infect other cells to repeat the cycle.[12]

Reston monkey outbreak[edit]

With the Ebola virus only being seen in Africa, it was beginning to be thought that it was a African problem, this would all change with a discovery in Reston, Virginia a town that is a few minutes outside of Washington D.C. In medical research, the use of monkeys is critical, and as a precaution, the government mandates a quarantine of all monkeys imported into this country. Monkeys are held in primate houses until they are cleared to be shipped to research facilities around the country. One such primate house is located in Reston, Virginia, called the Reston Primate Quarantine Unit. In 1989, this primate house had received a shipment of cynomolgus monkeys from the Philippines. The workers in the unit began to notice an abnormal amount of deaths in the monkeys. They realized they had a pathogen on their hands when entire rooms of monkeys began showing signs of illness. The veterinarians that worked at the facility thought they had a case of simian hemmoragic fever which is extremely lethal in primates, but doesn’t affect humans. They sent off a sample of the affected blood to USAMRIID at Fort Detrick. There, they discovered that it was the Ebola virus causing the monkeys to die.[12]

The Army and CDC quickly put together an operation to exterminate the monkeys and sterilize the monkey house. It was discovered that this was a unique variant of the virus, this virus had an Asian origin. This bug could be transmitted through the air via tiny droplets similar to the way the flu virus is spread. But there was a silver lining to this case, there were human exposures to the virus and none showed signs of the disease. The virus that caused this scare is known as Reston ebolavirus. Epidemics with the Reston strain continued through 1992 and again in 1996. Subsequent analysis of the Reston’s genome shows nearly no variation from that of Zaire ebolavirus, which is alarming considering the air path of transmission in the Reston case.[12]

Paleovirology[edit]

Filoviruses have a history that dates back several tens of million of years. Endogenous viral elements (EVEs) that appear to be derived from filovirus-like viruses have been identified in the genomes of bats, rodents, shrews, tenrecs, tarsiers, and marsupials.[17][18][19] Although most filovirus-like EVEs appear to be pseudogenes, evolutionary analyses suggest that orthologs isolated from several species of the bat genus Myotis have been maintained by selection.[20]

Vaccines and concerns[edit]

There are presently no vaccines for known filovirus.[21] There has been concern that a mutation to a filovirus such as EBOV could result in a change in transmission system from direct body fluid transmission to airborne transmission, which would greatly increase the infection and disease rates caused by EBOV. However, there is no record of any virus ever having made this transition and it is highly improbable.[22]

References[edit]

  1. ^ WHO. "Ebola virus disease". 
  2. ^ a b c Kiley MP, Bowen ET, Eddy GA, Isaäcson M, Johnson KM, McCormick JB, Murphy FA, Pattyn SR, Peters D, Prozesky OW, Regnery RL, Simpson DI, Slenczka W, Sureau P, van der Groen G, Webb PA, Wulff H (1982). "Filoviridae: A taxonomic home for Marburg and Ebola viruses?". Intervirology 18 (1–2): 24–32. doi:10.1159/000149300. PMID 7118520. 
  3. ^ US Animal and Plant Health Inspection Service (APHIS) and US Centers for Disease Control and Prevention (CDC). "National Select Agent Registry (NSAR)". Retrieved 2011-10-16. 
  4. ^ US Department of Health and Human Services. "Biosafety in Microbiological and Biomedical Laboratories (BMBL) 5th Edition". Retrieved 2011-10-16. 
  5. ^ US National Institutes of Health (NIH), US National Institute of Allergy and Infectious Diseases (NIAID). "Biodefense — NIAID Category A, B, and C Priority Pathogens". Retrieved 2011-10-16. 
  6. ^ US Centers for Disease Control and Prevention (CDC). "Bioterrorism Agents/Diseases". Retrieved 2011-10-16. 
  7. ^ The Australia Group. "List of Biological Agents for Export Control". Retrieved 2011-10-16. 
  8. ^ a b c d e f g Kuhn JH, Becker S, Ebihara H, Geisbert TW, Johnson KM, Kawaoka Y, Lipkin WI, Negredo AI, Netesov SV, Nichol ST, Palacios G, Peters CJ, Tenorio A, Volchkov VE, Jahrling PB (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. PMC 3074192. PMID 21046175. 
  9. ^ McCormick, J. B. (1991). "Family Filoviridae". In Francki, R. I. B.; Fauquet, C. M.; Knudson, D. L. et al. Classification and Nomenclature of Viruses-Fifth Report of the International Committee on Taxonomy of Viruses. Archives of Virology Supplement 2. Vienna, Austria: Springer. pp. 247–49. ISBN 0-387-82286-0. 
  10. ^ Jahrling, P. B.; Kiley, M. P.; Klenk, H.-D.; Peters, C. J.; Sanchez, A.; Swanepoel, R. (1995). "Family Filoviridae". In Murphy, F. A.; Fauquet, C. M.; Bishop, D. H. L.; Ghabrial, S. A.; Jarvis, A. W.; Martelli, G. P.; Mayo, M. A.; Summers, M. D. Virus Taxonomy—Sixth Report of the International Committee on Taxonomy of Viruses. Archives of Virology Supplement 10. Vienna, Austria: Springer. pp. 289–92. ISBN 3-211-82594-0. 
  11. ^ 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. 
  12. ^ a b c d 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. 
  13. ^ a b c Kuhn, J. H.; Becker, S.; Ebihara, H.; Geisbert, T. W.; Jahrling, P. B.; Kawaoka, Y.; Netesov, S. V.; Nichol, S. T.; Peters, C. J.; Volchkov, V. E.; Ksiazek, T. G. (2011). "Family Filoviridae". In King, Andrew M. Q.; Adams, Michael J.; Carstens, Eric B. et al. Virus Taxonomy—Ninth Report of the International Committee on Taxonomy of Viruses. London, UK: Elsevier/Academic Press. pp. 665–671. ISBN 978-0-12-384684-6. 
  14. ^ Kuhn JH, Bào Y, Bavari S, Becker S, Bradfute S, Brauburger K, Rodney Brister J, Bukreyev AA, Caì Y, Chandran K, Davey RA, Dolnik O, Dye JM, Enterlein S, Gonzalez JP, Formenty P, Freiberg AN, Hensley LE, Hoenen T, Honko AN, Ignatyev GM, Jahrling PB, Johnson KM, Klenk HD, Kobinger G, Lackemeyer MG, Leroy EM, Lever MS, Mühlberger E, Netesov SV, Olinger GG, Palacios G, Patterson JL, Paweska JT, Pitt L, Radoshitzky SR, Ryabchikova EI, Saphire EO, Shestopalov AM, Smither SJ, Sullivan NJ, Swanepoel R, Takada A, Towner JS, van der Groen G, Volchkov VE, Volchkova VA, Wahl-Jensen V, Warren TK, Warfield KL, Weidmann M, Nichol ST (November 2013). "Virus nomenclature below the species level: a standardized nomenclature for filovirus strains and variants rescued from cDNA". Arch. Virol. 159 (5): 1229–37. doi:10.1007/s00705-013-1877-2. PMID 24190508. 
  15. ^ Carroll SA, Towner JS, Sealy TK, McMullan LK, Khristova ML, Burt FJ, Swanepoel R, Rollin PE, Nichol ST (March 2013). "Molecular evolution of viruses of the family Filoviridae based on 97 whole-genome sequences". J. Virol. 87 (5): 2608–16. doi:10.1128/JVI.03118-12. PMC 3571414. PMID 23255795. 
  16. ^ 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
  17. ^ Taylor DJ, Leach RW, 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. 
  18. ^ Belyi VA, Levine AJ, Skalka AM (2010). Buchmeier, 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. 
  19. ^ Katzourakis A, Gifford RJ (2010). "Endogenous Viral Elements in Animal Genomes". PLoS Genetics 6 (11): e1001191. doi:10.1371/journal.pgen.1001191. PMC 2987831. PMID 21124940. 
  20. ^ Taylor DJ, Dittmar K, Ballinger MJ, Bruenn JA (2011). "Evolutionary maintenance of filovirus-like genes in bat genomes". BMC Evolutionary Biology 11 (336): 336. doi:10.1186/1471-2148-11-336. PMC 3229293. PMID 22093762. 
  21. ^ Peters CJ, LeDuc JW (February 1999). "An Introduction to Ebola: The Virus and the Disease". The Journal of Infectious Diseases 179 (Supplement 1): ix–xvi. doi:10.1086/514322. JSTOR 30117592. PMID 9988154. 
  22. ^ Kelland, Kate (19 September 2014). "Scientists see risk of mutant airborne Ebola as remote". Reuters. Retrieved 10 October 2014. 

Further reading[edit]

  • Klenk, Hans-Dieter (1999). Marburg and Ebola Viruses. Current Topics in Microbiology and Immunology 235. Berlin, Germany: Springer-Verlag. ISBN 978-3-540-64729-4. 
  • 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. 
  • Kuhn, Jens H. (2008). Filoviruses—A Compendium of 40 Years of Epidemiological, Clinical, and Laboratory Studies. Archives of Virology Supplement 20. Vienna, Austria: Springer. ISBN 978-3-211-20670-6. 
  • Ryabchikova, Elena I.; Price, Barbara B. (2004). Ebola and Marburg Viruses—A View of Infection Using Electron Microscopy. Columbus, Ohio, USA: Battelle Press. ISBN 978-1-57477-131-2. 

External links[edit]