Simian foamy virus: Difference between revisions
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==Description== |
==Description== |
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Although the simian foamy virus is [[Endemic (epidemiology)|endemic]] in African apes and monkeys, there are extremely high infection rates in captivity, ranging from 70% to 100% in adult animals.<ref name=":0" /> As humans are in close proximity to infected individuals, people who have had contact with primates can become infected with SFV.<ref name="pmid15043960">{{cite journal|date=March 2004|title=Naturally acquired simian retrovirus infections in central African hunters|url=|journal=Lancet|volume=363|issue=9413|pages=932–7|doi=10.1016/S0140-6736(04)15787-5|pmid=15043960|vauthors=Wolfe ND, Switzer WM, Carr JK, etal}}</ref> Its ability to cross over to humans was proven in 2004 by a joint [[United States]] and [[Cameroon]]ian team which found the [[retrovirus]] in [[gorilla]]s, [[mandrill]]s, and [[guenon]]s; unexpectedly, they also found it in 10 of 1,100 local Cameroon residents. Of those found infected, the majority are males who had been bitten by a primate. While this only accounts for 1% of the population, this detail alarms some who fear the outbreak of another [[zoonotic]] [[epidemic]].<ref>{{cite news|url=http://www.newyorker.com/magazine/2010/12/20/the-doomsday-strain|title=The Doomsday Strain|last=Specter|first=Michael|date=20 December 2010|newspaper=New Yorker|department=Letter from Cameroon}}</ref> |
Although the simian foamy virus is [[Endemic (epidemiology)|endemic]] in African apes and monkeys, there are extremely high infection rates in captivity, ranging from 70% to 100% in adult animals.<ref name=":0" /> As humans are in close proximity to infected individuals, people who have had contact with primates can become infected with SFV.<ref name="pmid15043960">{{cite journal|date=March 2004|title=Naturally acquired simian retrovirus infections in central African hunters|url=|journal=Lancet|volume=363|issue=9413|pages=932–7|doi=10.1016/S0140-6736(04)15787-5|pmid=15043960|vauthors=Wolfe ND, Switzer WM, Carr JK, etal}}</ref> Its ability to cross over to humans was proven in 2004 by a joint [[United States]] and [[Cameroon]]ian team which found the [[retrovirus]] in [[gorilla]]s, [[mandrill]]s, and [[guenon]]s; unexpectedly, they also found it in 10 of 1,100 local Cameroon residents. Of those found infected, the majority are males who had been bitten by a primate. While this only accounts for 1% of the population, this detail alarms some who fear the outbreak of another [[zoonotic]] [[epidemic]].<ref>{{cite news|url=http://www.newyorker.com/magazine/2010/12/20/the-doomsday-strain|title=The Doomsday Strain|last=Specter|first=Michael|date=20 December 2010|newspaper=New Yorker|department=Letter from Cameroon}}</ref> |
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SFV causes [[Cell (biology)|cell]]s to fuse with each other to form so-called [[syncytium|syncytia]], or more figurative, "giant cells", which look, on a slide, like foamy bubbles, hence its name. It has been tentatively linked to several diseases, but without any real evidence. |
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== Structure == |
== Structure == |
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=== Replication and Transcription === |
=== Replication and Transcription === |
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As both ssRNA(+) and dsDNA enter the cell, the remaining ssRNA is copied into dsDNA through reverse transcriptase. Nuclear entry of the viral dsDNA is covalently integrated into the cell’s genome by the viral [[integrase]], forming a provirus. The integrated provirus utilizes the promoter elements in the 5’LTR to drive transcription. This gives rise to the unspliced full length mRNA that will serve as genomic RNA to be packaged into virions or used as a template for translation of ''gag''.<ref name=":1" /> The spliced mRNAs encode pol (PR, RT, RnaseH, IN) and env (Leader peptide, SU, TM). The subsequent mRNA from the transcribed genes are translated to create the polypeptide chains that will be modified into viral proteins. |
As both ssRNA(+) and dsDNA enter the cell, the remaining ssRNA is copied into dsDNA through reverse transcriptase. Nuclear entry of the viral dsDNA is covalently integrated into the cell’s genome by the viral [[integrase]], forming a provirus. The integrated provirus utilizes the promoter elements in the 5’LTR to drive transcription. This gives rise to the unspliced full length mRNA that will serve as genomic RNA to be packaged into virions or used as a template for translation of ''gag''.<ref name=":1" /> The spliced mRNAs encode pol (PR, RT, RnaseH, IN) and env (Leader peptide, SU, TM). The subsequent mRNA from the transcribed genes are translated to create the polypeptide chains that will be modified into viral proteins. |
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=== Assembly and Release === |
=== Assembly and Release === |
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The SFV capsid is assembled in the cytoplasm as a result of multimerization of Gag molecules, but unlike other related viruses, SFV Gag lacks an N-terminal myristylation signal and capsids are not targeted to the plasma membrane (PM). They require expression of the envelope protein for budding of intracellular capsids from the cell, suggesting a specific interaction between the Gag and Env proteins. Evidence for this interaction was discovered in 2001 when a deliberate mutation a conserved [[arginine]] (Arg) residue at position 50 to alanine of the SFV cpz(hu) inhibited proper capsid assembly and abolished viral budding even in the presence of the envelope (Env) glycoproteins.<ref>{{Cite journal|last=Eastman|first=Scott W.|last2=Linial|first2=Maxine L.|date=2001-08-01|title=Identification of a Conserved Residue of Foamy Virus Gag Required for Intracellular Capsid Assembly|url=http://jvi.asm.org/content/75/15/6857|journal=Journal of Virology|language=en|volume=75|issue=15|pages=6857–6864|doi=10.1128/JVI.75.15.6857-6864.2001|issn=0022-538X|pmid=11435565}}</ref> |
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FV capsid assembly, which results from multimerization of Gag molecules, occurs in the cytoplasm of infected cells. |
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Assembly of the virion and packaging of the viral RNA genome. |
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Budding predominantly into the endoplasmic reticulum (ER) and occasionally through the plasma membrane, most viral particles remain in the cell. |
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Proteolytic processing of the precursors polyproteins by viral protease and maturation of the virions. |
Proteolytic processing of the precursors polyproteins by viral protease and maturation of the virions. |
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== Transmission & Pathogenicity == |
== Transmission & Pathogenicity == |
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SFV causes [[Cell (biology)|cell]]s to fuse with each other to form so-called [[syncytium|syncytia]], or more figurative, "giant cells", which look, on a slide, like foamy bubbles, hence its name. The first case of a spumavirus being isolated from a primate was in 1955 ''(Rustigan et al., 1955)'' from the kidneys.<ref>{{Cite book|url=https://link.springer.com/chapter/10.1007/978-1-4899-1627-3_6|title=The Retroviridae|last=Loh|first=Philip C.|date=1993|publisher=Springer, Boston, MA|isbn=9781489916297|series=The Viruses|pages=361–397|language=en|doi=10.1007/978-1-4899-1627-3_6}}</ref> |
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The transmission of SFV is believed to spread through a saliva vector, because large quantities of viral RNA, indicative of SFV gene expression and replication, are present in cells of the oral mucosa.<ref name=":0" /> Aggressive behaviors such as bites, to nurturing ones such as a mother licking and infant all have the ability to spread the virus. However, little is known about the prevalence and transmission patterns of SFV in wild-living primate populations. |
The transmission of SFV is believed to spread through a saliva vector, because large quantities of viral RNA, indicative of SFV gene expression and replication, are present in cells of the oral mucosa.<ref name=":0" /> Aggressive behaviors such as bites, to nurturing ones such as a mother licking and infant all have the ability to spread the virus. However, little is known about the prevalence and transmission patterns of SFV in wild-living primate populations. |
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Revision as of 21:14, 2 November 2017
| Simian foamy virus | |
|---|---|
| Virus classification | |
| Group: | Group VI (ssRNA-RT)
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| Family: | |
| Subfamily: | Spumaretrovirinae
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| Genus: | |
| Species: | Simian foamy virus
|
The Simian Foamy Virus (SFV) is species of the genus Spumavirus, which belongs to the family of Retroviridae. It has been identified in a wide variety of primates, including pro-simians, New World and Old World monkeys as well as apes, and each species has been shown to harbor a unique (species-specific) strain of SFV, including African green monkeys, baboons, macaques and chimpanzees.[1] As it is related to the more well known retrovirus Human Immunodeficiency Virus (HIV), its discovery in primates has led to some speculation that HIV may have been spread to the human species in Africa through contact with blood from apes, monkeys, and other primates, most likely through bushmeat hunting practices.
Description
Although the simian foamy virus is endemic in African apes and monkeys, there are extremely high infection rates in captivity, ranging from 70% to 100% in adult animals.[1] As humans are in close proximity to infected individuals, people who have had contact with primates can become infected with SFV.[2] Its ability to cross over to humans was proven in 2004 by a joint United States and Cameroonian team which found the retrovirus in gorillas, mandrills, and guenons; unexpectedly, they also found it in 10 of 1,100 local Cameroon residents. Of those found infected, the majority are males who had been bitten by a primate. While this only accounts for 1% of the population, this detail alarms some who fear the outbreak of another zoonotic epidemic.[3]
Structure
The SFV is a spherical, enveloped virus that ranges from 80-100 nm in diameter.
Genome
As a retrovirus, the genomic material is monopartite, linear, positive single strand RNA that forms a double stranded DNA intermediate through the use of the enzyme reverse transcriptase. The RNA strand is approximately 12kb's in length, with a 5'-cap and a 3’poly-A tail. There are two long terminal repeats (LTRs) of about 600nt long at the 5' and 3' ends. The LTRs contain the U3, R, and U5 regions that are characteristic of retroviruses. There are also a primer binding site (PBS) at the 5’end and a polypurine tract (PPT) at the 3’end.[4]
In December 2016 the first, full genome annotation of a proviral SFV isolated from cynomolgus macaque (Macaca fascicularis) had been performed. It revealed two regulatory sequences, tas and bet, in addition to the structural sequences of gag, pol and env.[5]
Replication Cycle
Entry into Cell
The virus attaches to host receptors through the surface (SU) glycoprotein, and the transmembrane (TM) glycoprotein mediates fusion with cell membrane. Once the virus has entered the interior of the cell, the retroviral core undergoes structural transformations through the activity of viral proteases. Studies have revealed that there are three internal protease-dependent cleavage sites that are critical for the virus to be infectious. One mutation within the gag gene had caused a structural change to the first cleavage site, preventing subsequent cleavage at the two other sites by the viral PR, reflecting its prominent role.[6] Once disassembled, the genetic material and enzymes are free within the cytoplasm to proceed with the infection. Whereas most retroviruses deposit ssRNA(+) into the cell, SFV and other related species are different in that up to 20% of of released viral particles already contains dsDNA genomes. This is due to an unique feature of spumaviruses in which the onset of reverse transcription of genomic RNA occurs before release rather than after entry of the new host cell like in other retroviruses.[4]
Replication and Transcription
As both ssRNA(+) and dsDNA enter the cell, the remaining ssRNA is copied into dsDNA through reverse transcriptase. Nuclear entry of the viral dsDNA is covalently integrated into the cell’s genome by the viral integrase, forming a provirus. The integrated provirus utilizes the promoter elements in the 5’LTR to drive transcription. This gives rise to the unspliced full length mRNA that will serve as genomic RNA to be packaged into virions or used as a template for translation of gag.[4] The spliced mRNAs encode pol (PR, RT, RnaseH, IN) and env (Leader peptide, SU, TM). The subsequent mRNA from the transcribed genes are translated to create the polypeptide chains that will be modified into viral proteins.
Assembly and Release
The SFV capsid is assembled in the cytoplasm as a result of multimerization of Gag molecules, but unlike other related viruses, SFV Gag lacks an N-terminal myristylation signal and capsids are not targeted to the plasma membrane (PM). They require expression of the envelope protein for budding of intracellular capsids from the cell, suggesting a specific interaction between the Gag and Env proteins. Evidence for this interaction was discovered in 2001 when a deliberate mutation a conserved arginine (Arg) residue at position 50 to alanine of the SFV cpz(hu) inhibited proper capsid assembly and abolished viral budding even in the presence of the envelope (Env) glycoproteins.[7]
Proteolytic processing of the precursors polyproteins by viral protease and maturation of the virions.
Modulation and Interaction of Host Cell
Transmission & Pathogenicity
SFV causes cells to fuse with each other to form so-called syncytia, or more figurative, "giant cells", which look, on a slide, like foamy bubbles, hence its name. The first case of a spumavirus being isolated from a primate was in 1955 (Rustigan et al., 1955) from the kidneys.[8]
The transmission of SFV is believed to spread through a saliva vector, because large quantities of viral RNA, indicative of SFV gene expression and replication, are present in cells of the oral mucosa.[1] Aggressive behaviors such as bites, to nurturing ones such as a mother licking and infant all have the ability to spread the virus. However, little is known about the prevalence and transmission patterns of SFV in wild-living primate populations.
With little evidence to suggest that SFV infection causes illness, some scientists believe that it has a commensal relationship to simians.[9]
Tropism
Cospeciation of SFV and primates
The phylogenetic tree analysis of SFV polymerase and mitochondrial cytochrome oxidase subunit II (COII has been shown as a powerful marker used for primate phylogeny) from African and Asian monkeys and apes provides very similar branching order and divergence times among the two trees, supporting the cospeciation. Also, the substitution rate in the SFV gene was found to be extremely slow, i.e. the SFV has evolved at a very low rate (1.7×10−8 substitutions per site per year). These results suggest SFV has been cospeciated with Old World primates for about 30 million years, making them the oldest known vertebrate RNA viruses.[10]
The SFV sequence examination of species and subspecies within each clade of the phylogenetic tree of the primates indicated cospeciation of SFV and the primate hosts, as well. A strong linear relationship was found between the branch lengths for the host and SFV gene trees, which indicated synchronous genetic divergence in both data sets.[10]
By using the molecular clock, it was observed that the substitution rates for the host and SFV genes were very similar. The substitution rates for host COII gene and the SFV gene were found out to be (1.16±0.35)×10−8 and (1.7±0.45)×10−8 respectively. This is the slowest rate of substitution observed for RNA viruses and is closer to that of DNA viruses and endogenous retroviruses. This rate is quite different from that of exogenous RNA viruses such as HIV and influenza A virus (10−3 to 10−4 substitutions per site per year).[10]
Prevalence
Researchers in Cameroon, the Democratic Republic of the Congo, France, Gabon, Germany, Japan, Rwanda, the United Kingdom, and the United States have found that simian foamy virus is widespread among wild chimpanzees throughout equatorial Africa.[11]
Humans exposed to wild primates, including chimpanzees, can acquire SFV infections.[2][12] Since the long-term consequences of these cross-species infections are not known, it is important to determine to what extent wild primates are infected with simian foamy viruses. In this study, researchers tested this question for wild chimpanzees by using novel noninvasive methods. Analyzing over 700 fecal samples from 25 chimpanzee communities across sub-Saharan Africa, the researchers obtained viral sequences from a large proportion of these communities, showing a range of infection rates from 44% to 100%.
Major disease outbreaks have originated from cross-species transmission of infectious agents between primates and humans, making it important to learn more about how these cross-species transfers occur. The high SFV infection rates of chimpanzees provide an opportunity to monitor where humans are exposed to these viruses. Identifying the locations may help determine where the highest rates of human–chimpanzee interactions occur. This may predict what other pathogens may jump the species barrier next.
References
- ^ a b c Liu, Weimin; Worobey, Michael; Li, Yingying; Keele, Brandon F.; Bibollet-Ruche, Frederic; Guo, Yuanyuan; Goepfert, Paul A.; Santiago, Mario L.; Ndjango, Jean-Bosco N. (2008-07-04). "Molecular Ecology and Natural History of Simian Foamy Virus Infection in Wild-Living Chimpanzees". PLOS Pathogens. 4 (7): e1000097. doi:10.1371/journal.ppat.1000097. ISSN 1553-7374.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ a b Wolfe ND, Switzer WM, Carr JK, et al. (March 2004). "Naturally acquired simian retrovirus infections in central African hunters". Lancet. 363 (9413): 932–7. doi:10.1016/S0140-6736(04)15787-5. PMID 15043960.
- ^ Specter, Michael (20 December 2010). "The Doomsday Strain". Letter from Cameroon. New Yorker.
- ^ a b c "Spumavirus". viralzone.expasy.org. SIB Swiss Institute of Bioinformatics. Retrieved 2017-11-02.
{{cite web}}: Cite has empty unknown parameter:|dead-url=(help) - ^ Sakai, Koji; Ami, Yasushi; Suzaki, Yuriko; Matano, Tetsuro (2016-12-29). "First Complete Genome Sequence of a Simian Foamy Virus Isolate from a Cynomolgus Macaque". Genome Announcements. 4 (6): e01332–16. doi:10.1128/genomeA.01332-16. ISSN 2169-8287. PMID 27908992.
- ^ Lehmann-Che, Jacqueline; Giron, Marie-Lou; Delelis, Olivier; Löchelt, Martin; Bittoun, Patricia; Tobaly-Tapiero, Joelle; Thé, Hugues de; Saïb, Ali (2005-07-01). "Protease-Dependent Uncoating of a Complex Retrovirus". Journal of Virology. 79 (14): 9244–9253. doi:10.1128/JVI.79.14.9244-9253.2005. ISSN 0022-538X. PMID 15994819.
- ^ Eastman, Scott W.; Linial, Maxine L. (2001-08-01). "Identification of a Conserved Residue of Foamy Virus Gag Required for Intracellular Capsid Assembly". Journal of Virology. 75 (15): 6857–6864. doi:10.1128/JVI.75.15.6857-6864.2001. ISSN 0022-538X. PMID 11435565.
- ^ Loh, Philip C. (1993). The Retroviridae. The Viruses. Springer, Boston, MA. pp. 361–397. doi:10.1007/978-1-4899-1627-3_6. ISBN 9781489916297.
- ^ "Foamy Virus (Spumavirus) Infection | CARTA". carta.anthropogeny.org. Retrieved 2017-11-02.
- ^ a b c Switzer WM, Salemi M, Shanmugam V, et al. (March 2005). "Ancient co-speciation of simian foamy viruses and primates". Nature. 434 (7031): 376–80. doi:10.1038/nature03341. PMID 15772660.
- ^ Liu W, Worobey M, Li Y, Keele BF, Bibollet-Ruche F, Guo Y, Goepfert PA, Santiago ML, Ndjango JB, Neel C, Clifford SL, Sanz C, Kamenya S, Wilson ML, Pusey AE, Gross-Camp N, Boesch C, Smith V, Zamma K, Huffman MA, Mitani JC, Watts DP, Peeters M, Shaw GM, Switzer WM, Sharp PM, Hahn BH (2008). "Molecular ecology and natural history of simian foamy virus infection in wild-living chimpanzees". PLoS Pathog. 4 (7): e1000097. doi:10.1371/journal.ppat.1000097. PMC 2435277. PMID 18604273.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ Switzer WM, Bhullar V, Shanmugam V, et al. (March 2004). "Frequent simian foamy virus infection in persons occupationally exposed to nonhuman primates". J. Virol. 78 (6): 2780–9. doi:10.1128/JVI.78.6.2780-2789.2004. PMC 353775. PMID 14990698.
External links
- "ARCHIVED — Simian Foamy Virus (SFV): Questions and Answers". Infectious Diseases. Public Health Agency of Canada. 2008-01-08.
- "Topic I. Potential concerns for Simian Foamy virus (SFV) transmission by Blood and Blood Products". Blood Products Advisory Committee Meeting. U.S. Food and Drug Administration. 13 December 2001.
{{cite web}}: Missing or empty|url=(help) - Simian+foamy+virus at the U.S. National Library of Medicine Medical Subject Headings (MeSH)