Likely role of APOBEC3G-mediated G-to-A mutations in HIV-1 evolution and drug resistance.

ABSTRACT: The role of APOBEC3 (A3) protein family members in inhibiting retrovirus infection and mobile element retrotransposition is well established. However, the evolutionary effects these restriction factors may have had on active retroviruses such as HIV-1 are less well understood. An HIV-1 variant that has been highly G-to-A mutated is unlikely to be transmitted due to accumulation of deleterious mutations. However, G-to-A mutated hA3G target sequences within which the mutations are the least deleterious are more likely to survive selection pressure. Thus, among hA3G targets in HIV-1, the ratio of nonsynonymous to synonymous changes will increase with virus generations, leaving a footprint of past activity. To study such footprints in HIV-1 evolution, we developed an in silico model based on c

SUBMITTER: Jern P 

PROVIDER: S-EPMC2659435 | biostudies-literature | 2009 Apr

REPOSITORIES: biostudies-literature