Broad antiretroviral defence by human APOBEC3G through lethal editing of nascent reverse transcripts

摘要: Viral replication usually requires that innate intracellular lines of defence be overcome, a task accomplished by specialized viral gene products. The virion infectivity factor (Vif) protein human immunodeficiency virus (HIV) is required during the late stages production to counter antiviral activity APOBEC3G (apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like 3G; also known as CEM15), expressed notably in T lymphocytes. When produced presence APOBEC3G, vif-defective non-infectious. closely related APOBEC1, central component an RNA-editing complex deaminates cytosine residue apoB messenger RNA. APOBEC family members have potent DNA mutator through dC deamination; however, whether editing potential has any relevance HIV inhibition unknown. Here, we demonstrate it does, exerts its effect reverse transcription trigger G-to-A hypermutation nascent retroviral DNA. We find can act on broad range retroviruses addition HIV, suggesting general mechanism against this important group pathogens.