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.
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.
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.
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.
Intravital imaging with HIV-1 viral-like particle in mouse model reveals a mechanism for HIV-1 uptake by subcapsular sinus macrophages that facilitates HIV-1 spreading tofollicular dendritic and B cells.
Large-volume light microscopy combined with higher-resolution electron tomography revealed the spatial distribution of virus-producing cells and highlighted mechanisms of HIV-1 dissemination in bone marrow from a small animal model.