A conflict of interest: the evolutionary arms race between mammalian APOBEC3 and lentiviral Vif
Abstract Apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3 (APOBEC3) proteins are mammalian-specific cellular deaminases and have a robust ability to restrain lentivirus replication. To antagonize APOBEC3-mediated antiviral action, lentiviruses have acquired viral infectivity factor...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
BMC
2017-05-01
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| Series: | Retrovirology |
| Subjects: | |
| Online Access: | http://link.springer.com/article/10.1186/s12977-017-0355-4 |
| _version_ | 1818067742853431296 |
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| author | Yusuke Nakano Hirofumi Aso Andrew Soper Eri Yamada Miyu Moriwaki Guillermo Juarez-Fernandez Yoshio Koyanagi Kei Sato |
| author_facet | Yusuke Nakano Hirofumi Aso Andrew Soper Eri Yamada Miyu Moriwaki Guillermo Juarez-Fernandez Yoshio Koyanagi Kei Sato |
| author_sort | Yusuke Nakano |
| collection | DOAJ |
| description | Abstract Apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3 (APOBEC3) proteins are mammalian-specific cellular deaminases and have a robust ability to restrain lentivirus replication. To antagonize APOBEC3-mediated antiviral action, lentiviruses have acquired viral infectivity factor (Vif) as an accessory gene. Mammalian APOBEC3 proteins inhibit lentiviral replication by enzymatically inserting G-to-A hypermutations in the viral genome, whereas lentiviral Vif proteins degrade host APOBEC3 via the ubiquitin/proteasome-dependent pathway. Recent investigations provide evidence that lentiviral vif genes evolved to combat mammalian APOBEC3 proteins. In corollary, mammalian APOBEC3 genes are under Darwinian selective pressure to escape from antagonism by Vif. Based on these observations, it is widely accepted that lentiviral Vif and mammalian APOBEC3 have co-evolved and this concept is called an “evolutionary arms race.” This review provides a comprehensive summary of current knowledge with respect to the evolutionary dynamics occurring at this pivotal host-virus interface. |
| first_indexed | 2024-12-10T15:28:31Z |
| format | Article |
| id | doaj.art-dd78050a680e415cb625feaf9c1ea460 |
| institution | Directory Open Access Journal |
| issn | 1742-4690 |
| language | English |
| last_indexed | 2024-12-10T15:28:31Z |
| publishDate | 2017-05-01 |
| publisher | BMC |
| record_format | Article |
| series | Retrovirology |
| spelling | doaj.art-dd78050a680e415cb625feaf9c1ea4602022-12-22T01:43:28ZengBMCRetrovirology1742-46902017-05-0114111210.1186/s12977-017-0355-4A conflict of interest: the evolutionary arms race between mammalian APOBEC3 and lentiviral VifYusuke Nakano0Hirofumi Aso1Andrew Soper2Eri Yamada3Miyu Moriwaki4Guillermo Juarez-Fernandez5Yoshio Koyanagi6Kei Sato7Laboratory of Systems Virology, Department of Biosystems Science, Institute for Frontier Life and Medical Sciences, Kyoto UniversityLaboratory of Systems Virology, Department of Biosystems Science, Institute for Frontier Life and Medical Sciences, Kyoto UniversityLaboratory of Systems Virology, Department of Biosystems Science, Institute for Frontier Life and Medical Sciences, Kyoto UniversityLaboratory of Systems Virology, Department of Biosystems Science, Institute for Frontier Life and Medical Sciences, Kyoto UniversityLaboratory of Systems Virology, Department of Biosystems Science, Institute for Frontier Life and Medical Sciences, Kyoto UniversityLaboratory of Systems Virology, Department of Biosystems Science, Institute for Frontier Life and Medical Sciences, Kyoto UniversityLaboratory of Systems Virology, Department of Biosystems Science, Institute for Frontier Life and Medical Sciences, Kyoto UniversityLaboratory of Systems Virology, Department of Biosystems Science, Institute for Frontier Life and Medical Sciences, Kyoto UniversityAbstract Apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3 (APOBEC3) proteins are mammalian-specific cellular deaminases and have a robust ability to restrain lentivirus replication. To antagonize APOBEC3-mediated antiviral action, lentiviruses have acquired viral infectivity factor (Vif) as an accessory gene. Mammalian APOBEC3 proteins inhibit lentiviral replication by enzymatically inserting G-to-A hypermutations in the viral genome, whereas lentiviral Vif proteins degrade host APOBEC3 via the ubiquitin/proteasome-dependent pathway. Recent investigations provide evidence that lentiviral vif genes evolved to combat mammalian APOBEC3 proteins. In corollary, mammalian APOBEC3 genes are under Darwinian selective pressure to escape from antagonism by Vif. Based on these observations, it is widely accepted that lentiviral Vif and mammalian APOBEC3 have co-evolved and this concept is called an “evolutionary arms race.” This review provides a comprehensive summary of current knowledge with respect to the evolutionary dynamics occurring at this pivotal host-virus interface.http://link.springer.com/article/10.1186/s12977-017-0355-4VifAPOBEC3LentivirusMammalEvolutionary arms race |
| spellingShingle | Yusuke Nakano Hirofumi Aso Andrew Soper Eri Yamada Miyu Moriwaki Guillermo Juarez-Fernandez Yoshio Koyanagi Kei Sato A conflict of interest: the evolutionary arms race between mammalian APOBEC3 and lentiviral Vif Retrovirology Vif APOBEC3 Lentivirus Mammal Evolutionary arms race |
| title | A conflict of interest: the evolutionary arms race between mammalian APOBEC3 and lentiviral Vif |
| title_full | A conflict of interest: the evolutionary arms race between mammalian APOBEC3 and lentiviral Vif |
| title_fullStr | A conflict of interest: the evolutionary arms race between mammalian APOBEC3 and lentiviral Vif |
| title_full_unstemmed | A conflict of interest: the evolutionary arms race between mammalian APOBEC3 and lentiviral Vif |
| title_short | A conflict of interest: the evolutionary arms race between mammalian APOBEC3 and lentiviral Vif |
| title_sort | conflict of interest the evolutionary arms race between mammalian apobec3 and lentiviral vif |
| topic | Vif APOBEC3 Lentivirus Mammal Evolutionary arms race |
| url | http://link.springer.com/article/10.1186/s12977-017-0355-4 |
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