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Host restriction factors that block cross-species transmission also play a role in limiting the replication of highly-adapted HIV-1 in IFN-stimulated cells.

Sarcoidosis, a granulomatous disease characterized by macrophage and T-cell activation, is found to be associated with increased HIF-1α transcriptional activity, and modulation of HIF-1α regulates inflammatory immune responses.

Structure-function analysis of the super elongation complex formed when HIV replicates inside cells reveals that the HIV-1 Tat protein binds to a cleft between P-TEFb, an enzyme that is involved in normal transcription, and AFF4, a protein that is used to build the super elongation complex

The presence of certain HLA alleles drives the emergence or maintenance of otherwise deleterious drug-resistant mutations in patients living with HIV, even when the patient is antiretroviral treatment naïve.

Glycans are remodeled by HIV and are determinants of CD4+ T cell susceptibility to HIV infection.

Inflamasomme inhibition prevents immune activation, HIV-1 pathogenesis and the splenic content of HIV-1 total DNA in humanized mice when administrated early after HIV-1 infection.

HIV-specific antibodies that mediate antibody-dependent cellular cytotoxicity vary in their paths to achieve function but commonly rely on mutations in multiple regions, including framework regions, to reach full potency.

An in-depth view of the in vivo blood and tissue HIV reservoir is presented highlighting shared phenotypic features between individuals, thus enabling marked ex vivo enrichment of replication-competent latent cells.

Folding and unfolding of a 6-helix bundle controls HIV assembly and maturation.

The nuclear export receptor Crm1 cooperatively binds its HIV Rev-RRE cargo as a dimer using a species-specific interface that supports viral replication by enhancing nuclear export of HIV RNA.