Uracil/adenine base pairs in HIV-1 DNA are attacked by the uracil base excision repair machinery in macrophages, which leads to HIV restriction and viral genome diversification by transcription-associated mutagenesis.
A comprehensive whole cell proteomic map describing expression time courses of >6,500 viral and cellular proteins during HIV infection identifies Vif-dependent antagonism of key cellular phosphatase PP2A.
Under conditions where the force of HIV infection per cell is high, partial attenuation of infection with inhibitors can increase the number of live infected cells and may paradoxically be beneficial for viral spread.
Structural and computational analyses of germline antibody/HIV-1 gp120 complexes provide both general principles relevant to the unusual evolution of potent CD4-binding site antibodies and guidelines for structure-based immunogen design.
High-resolution structures of HIV-1 RT in complex with two newly developed non-nucleoside inhibitors explain how they retain antiviral activities against drug-resistant RT mutants with considerably reduced susceptibility to rilpivirine.