Structural and biophysical studies help to follow the disassembly of the HIV-1 capsid in vitro, and reveal the role of a small molecule called IP6 in regulating capsid stability.

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.

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.

An early start to long-term antiretroviral therapy limits the size of the HIV-1 reservoir more effectively than treatment that starts later.

Disassembly of the HIV-1 capsid is a catastrophic process, whereby initiation and propagation can be controlled independently by molecules that bind to different features of the capsid lattice.

Whole genome deep sequencing of many longitudinally sampled HIV-1 populations reveals that reversions towards ancestral HIV-1 genome sequences occur throughout the course of infection.

Human proteins that add or remove the methyladenosine modification of cellular RNA, or recognize methylated RNA significantly affect HIV-1 infection or viral protein synthesis in cells, suggesting an important role for HIV-1 RNA methylation in regulating viral replication.

Combined tissue clearing, 3D-immunofluorescence, and electron tomography spatially revealed the dynamics of early HIV-1 spread within lymphoid tissues of humanized mice at the resolution of single cells and individual virions.

By inhibiting the activation of NF-κB, HIV-1 Vpu exerts much broader immunosuppressive effects than previously anticipated and may be an important determinant of chronic inflammation in HIV-1 infected individuals.