The primary targets of HIV-1 (T lymphocytes, macrophages, and monocytes) are able to limit HIV-1 replication by expressing the restriction factors APOBEC3F and APOBEC3G (A3F/G). These two proteins have cytidine deaminase activity and induce mutations during reverse transcription of the genomic RNA that could be lethal for the virus. A3F/G also interfere with the reverse transcription and integration processes independently from this deaminase activity. To counteract this restriction, HIV-1 has evolved the viral infectivity factor (Vif), a multifunctional protein that is able to reduce the cellular A3F/G expression level through two major mechanisms: (1) Vif induces degradation of A3F/G by the proteasome by recruiting an E3 ubiquitin ligase complex, and (2) Vif inhibits A3F/G translation by interacting with the 5′ untranslated region (UTR) of their mRNAs. These two mechanisms ultimately reduce the packaging of A3F/G into virions. The intimate relationship between Vif and...
- Zinc Finger Motif
- Equine Infectious Anemia Virus
- Ubiquitin Ligase Complex
- APOBEC3 Protein
- Reverse Transcription Complex
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Libre, C., Batisse, J., Guerrero, S., Marquet, R., Paillart, JC. (2015). APOBEC3F/G and Vif: Action and Counteractions. In: Hope, T., Stevenson, M., Richman, D. (eds) Encyclopedia of AIDS. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-9610-6_376-1
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