Abstract
The viral infectivity factor (Vif) of HIV type-1 (HIV-1) is essential for efficient viral replication, yet was, until recently, enigmatic. This resulted from the complexity and cellular specificity of its function and the correspondingly complex systems that are required for its investigation. These limitations have been overcome and Vif function has been rapidly elucidated, with implications for the development of drugs to block its activity. These studies have revealed a novel component of the innate immune system, APOBEC3G, that lethally hypermutates retroviruses, including HIV-1. For HIV-1, the competition between the virus and APOBEC3G is tipped in favor of the invader by Vif, which binds to APOBEC3G and triggers its polyubiquitination and rapid degradation, thereby preventing its entry into progeny virions.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 291-297 |
| Number of pages | 7 |
| Journal | Trends in Molecular Medicine |
| Volume | 10 |
| Issue number | 6 |
| DOIs | |
| State | Published - Jun 1 2004 |
Funding
Our work on Vif and in preparation of this manuscript were supported by NIH grant AI49729 from the US Public Health Service.
| Funders | Funder number |
|---|---|
| US Public Health Service | |
| Author National Institutes of Health National Institutes of Health National Institutes of Health National Institutes of Health The Bev Hartig Huntington's Disease Foundation National Institutes of Health | |
| National Institute of Allergy and Infectious Diseases | R01AI049729 |
ASJC Scopus subject areas
- Molecular Medicine
- Molecular Biology
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