According to the rules for taxon naming established by theInternational Committee on Taxonomy of Viruses (ICTV), the nameFiloviridae is always to becapitalized,italicized, never abbreviated, and to be preceded by the word "family". The names of its members (filoviruses or filovirids) are to be written in lower case, are not italicized, and used withoutarticles.[13][14]
Replication cycle of filoviruses and vectorsReplication cycle of filoviruses at and inside host cell
The filoviruslife cycle begins with virion attachment to specific cell-surfacereceptors, followed byfusion of the virion envelope with cellular membranes and the concomitant release of the virusnucleocapsid into thecytosol. The viralRNA-dependent RNA polymerase (RdRp, or RNA replicase) partially uncoats the nucleocapsid andtranscribes thegenes into positive-strandedmRNAs, which are thentranslated into structural and nonstructuralproteins. Filovirus RdRps bind to a singlepromoter 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 thenucleoprotein, whoseconcentration 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 thecell membrane. Virionsbud 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]
it forms nucleocapsids with a central axial channel (≈10–15 nm in width) surrounded by a dark layer (≈20 nm in width) and an outer helical layer (≈50 nm in width) with a cross striation (periodicity of ≈5 nm)
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 sequenced filovirus variants was estimated to be 1971 (1960–1976) for Ebola virus, 1970 (1948–1987) for Reston virus, and 1969 (1956–1976) for Sudan virus, with the most recent common ancestor among the four species included in the analysis (Ebola virus, Tai Forest virus, Sudan virus, and Reston virus) estimated at 1000–2100 years.[16] 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 (~16–23 million or so years ago).[17]
Paleoviral elements are known from each of the four main divergent clades of filoviruses. While orthologous elements in mammal genomes support a minimum age for filoviruses of tens of millions of years, the existence of filoviruses and their elements in divergent lineages of fishes suggests that the virus family is hundreds of millions of years old.[20] Paleoviruses that appear to be derived from filovirus-like viruses have been identified in the genomes of many small-bodied species includingbats,rodents,shrews,tenrecs,tarsiers,marsupials[21][22][23] and fishes.[24] Although most filovirus-like elements appear to bepseudogenes, evolutionary and structural analyses suggest thatorthologs isolated from several species of the bat genusMyotis and the rodent family Spalacidae have been maintained by selection.[25][26]
There are presently very limited vaccines for known filovirus.[27] An effective vaccine against EBOV, developed in Canada,[28] was approved for use in 2019 in the US and Europe.[29][30] Similarly, efforts to develop a vaccine against Marburg virus are under way.[31]
There has been a pressing concern that a very slight genetic mutation to a filovirus such asEBOV could result in a change in transmission system from direct body fluid transmission to airborne transmission, as was seen in Reston virus (another member of genus Ebolavirus) between infected macaques. A similar change in the current circulating strains of EBOV could greatly increase the infection and disease rates caused by EBOV. However, there is no record of any Ebola strain ever having made this transition in humans.[32]
^US Animal and Plant Health Inspection Service (APHIS) and US Centers for Disease Control and Prevention (CDC)."National Select Agent Registry (NSAR)". Retrieved2011-10-16.
^McCormick, J. B. (1991). "Family Filoviridae". In Francki, R. I. B.; Fauquet, C. M.; Knudson, D. L.; et al. (eds.).Classification and Nomenclature of Viruses-Fifth Report of the International Committee on Taxonomy of Viruses. Archives of Virology Supplement. Vol. 2. Vienna, Austria: Springer. pp. 247–49.ISBN0-387-82286-0.
^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. (eds.).Virus Taxonomy—Sixth Report of the International Committee on Taxonomy of Viruses. Archives of Virology Supplement. Vol. 10. Vienna, Austria: Springer. pp. 289–92.ISBN3-211-82594-0.
^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. (eds.).Virus Taxonomy—Seventh Report of the International Committee on Taxonomy of Viruses. San Diego, USA: Academic Press. pp. 539–48.ISBN0-12-370200-3.
^abFeldmann, 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. (eds.).Virus Taxonomy—Eighth Report of the International Committee on Taxonomy of Viruses. San Diego, USA: Elsevier/Academic Press. pp. 645–653.ISBN0-12-370200-3.
Klenk, Hans-Dieter (1999).Marburg and Ebola Viruses. Current Topics in Microbiology and Immunology. Vol. 235. Berlin, Germany: Springer-Verlag.ISBN978-3-540-64729-4.
Klenk, Hans-Dieter; Feldmann, Heinz (2004).Ebola and Marburg Viruses—Molecular and Cellular Biology. Wymondham, Norfolk, UK: Horizon Bioscience.ISBN978-0-9545232-3-7.
Kuhn, Jens H. (2008).Filoviruses—A Compendium of 40 Years of Epidemiological, Clinical, and Laboratory Studies. Archives of Virology Supplement. Vol. 20. Vienna, Austria: Springer.ISBN978-3-211-20670-6.
Ryabchikova, Elena I.; Price, Barbara B. (2004).Ebola and Marburg Viruses—A View of Infection Using Electron Microscopy. Columbus, Ohio, USA: Battelle Press.ISBN978-1-57477-131-2.
