HIV Research and Treatment

This paper demonstrates that combining HIV-specific CAR T cells with rapamycin and latency reversing agents can reduce immune exhaustion and effectively target HIV-infected cells.

This study shows that BCL11B/CTIP2 regulates the TLR3-mediated cellular response to viral infections by inhibiting NEAT1 expression and dampening interferon production, thereby reinforcing HIV-1 latency.

This study identifies microbiome-derived metabolites, particularly p-cresol sulfate, that alter CD4 T-cell metabolism and promote immune aging in HIV-1 infection.

The paper introduces HIV SMRTcap, a method for characterizing HIV-1 reservoirs by identifying integration sites and proviral integrity using long-read sequencing, and validates its performance across subtypes and tissue samples.

This study identifies a hybrid Gag lattice as an intermediate in HIV-1 maturation, showing it is stabilized by IP6 and essential for infectivity.

This paper develops a dual-reporter HTS assay to identify HIV-1 latency-modulating agents, finding 27 candidate LPAs and LRA compounds from a chemical library.

This study reveals conformational differences in HIV-1 Env glycoprotein on virions compared to soluble forms, highlighting the role of the viral membrane in maintaining native structure.

The paper shows that residual HIV production in lymph nodes of ART-suppressed individuals drives pyroptosis and is counter-regulated by GLP-1 upregulation in the ileum.

This study visualizes chromatin structure and HIV-1 nuclear trafficking in situ, showing HIV-1 cores preferentially associate with open chromatin and are excluded from compact regions.

This study shows daily HIV PrEP with TDF/FTC increases monocyte activation, enhances pro-inflammatory responses, and reprograms immune cell metabolism in HIV-negative individuals.

This study investigates how HIV forms CPSF6 puncta and their fusion with nuclear speckles, identifying key domains and factors involved in this process and its role in viral persistence.

This study shows that reprogramming CD4 T cells can eliminate HIV DNA reservoirs, offering a potential functional cure by restoring intracellular antiviral immunity.

This paper designs a rigid divalent immunogen that selectively binds VRC01-class antibodies with higher avidity than non-target antibodies, supporting its use in vaccine development.

The paper identifies IL-17A, STAT1, CEBPB, and cGAS-STING as key drivers of HIV-associated neuroinflammation using HIV-infected cerebral organoids and validates findings in a primate model.

This study shows HIV Nef induces a soft phenotype in infected CD4+ T cells, reducing their susceptibility to cytotoxic T lymphocyte killing through cytoskeletal remodeling and intrinsic heterogeneity.

This study identifies Arf1 and Arf6 as essential for HIV-1 Gag trafficking, assembly, and release, independent of BST-2 antagonism.

This study identifies how HIV-1 Nef recruits Serinc3 by binding its N-terminal tail, revealing a conserved pocket important for antiviral resistance and drug target discovery.

This study shows that SIV infection in rhesus macaques leads to increased p16 and decreased SIRT1, associated with neurodegeneration and aging markers in multiple brain regions.

This study identifies a noncanonical PRDM1+ Tfh subset selectively depleted in HIV viremia but recoverable under ART, highlighting its susceptibility to infection and implications for HIV reservoirs.

This study shows that early HIV-1 maturation steps, specifically partial Gag cleavage, promote Env clustering and fusion competence by reorganizing the membrane-proximal lattice.

This paper shows HIV-1CRF01_AE Env frequently adopts an open conformation (State 2A) that is susceptible to ADCC, unlike clade A/B Envs which require anti-cluster A antibodies to reach this state.

This study shows PD-1 blockade enhances HIV-1 vaccine-induced CD8+ T-cell responses in early ART-treated PWH, improving proliferation, IFN-gamma production, and activation.

This study shows dietary indoles restore gut barrier function in SIV-infected macaques by reactivating the AhR-IL-22 pathway, reducing intestinal epithelial barrier disruption markers.

This study identifies female-predominant anti-CD4 IgG autoantibodies in HIV-infected patients on ART, linked to lower progesterone, microbial translocation, and poor immune recovery.

This study examines how antiretroviral therapy (ART) affects macrophage movement in and out of the CNS in SIV-infected macaques, showing ART reduces perivascular macrophage accumulation but not meningeal or choroid plexus macrophages.

This study shows Lenacapavir causes HIV-1 capsid damage, exposing genomic DNA in nuclear speckles and altering capsid structure.

This study shows that the CD4 mimetic CJF-III-288 enables anti-CoRBS antibodies to mediate ADCC by stabilizing an asymmetric open Env conformation.

This study identifies extracellular condensates (ECs) from macaques as endogenous factors that modulate HIV transcription and latency reactivation, with THC treatment altering their anti-inflammatory properties.

This study identifies Rad18 as a suppressor of late HIV-1 replication by inhibiting viral post-transcription and virion production through interactions with HIV-1 IN, Tat, and Vif proteins.