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 or filovirids) are to be written in lower case, are not italicized, and used without
articles.[13][14]
Life cycle
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]
Family inclusion criteria
A virus that fulfills the criteria for being a member of the order Mononegavirales is a member of the family Filoviridae if:[13][14]
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]
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.[20][21][22] 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.[23]
Vaccines
There are presently very limited vaccines for known filovirus.[24] An effective vaccine against EBOV, developed in Canada,[25] was approved for use in 2019 in the US and Europe.[26][27] Similarly, efforts to develop a vaccine against Marburg virus are under way.[28]
Mutation concerns and pandemic potential
There has been a pressing concern that a very slight genetic mutation to a filovirus such as
EBOV 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.[29]
^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.
^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.
External links
Wikimedia Commons has media related to Filoviridae.