HIV Research and Treatment

This paper edits human T cells to mimic rodent host factors, creating resistance to HIV-1 and related lentiviruses by disrupting key viral protein interactions.

This study shows CDK8/19 inhibitors reduce HIV-1 reactivation and enhance provirus latency in T cells by impairing RNA Pol II recruitment to the HIV-1 LTR.

The paper shows HIV-1 Vpu forms stable aqueous oligomers via its transmembrane domain self-association, identified through cryoEM, EPR, and size exclusion chromatography.

This study uses a CRISPR screen to identify HIV-1 latency reversal factors, finding that CCNT1 is non-essential for T cell activation but critical for HIV reactivation from latency.

This study evaluates how stabilizing mutations in HIV-1 Env affect trimer stability, antigenicity, and glycosylation when expressed on membrane-expressed VLPs, finding some mutations reduce neutralizing antibody binding and alter glycan processing.

The paper examines HIV-1 provirus persistence in CNS tissues during ART by analyzing multiple anatomical compartments in treated individuals.

This study shows that chemical cross-linking with EDC stabilizes HIV-1 Env trimers without significant structural distortion, improving their stability, morphology, antigenicity, and immunogenicity for vaccine development.

The paper investigates the role of USF1 and USF2 in HIV-1 latency and T cell activation, finding that USF2 is critical for HIV-1 expression and combined function with USF1 is necessary for full T cell activation.

This study examines HIV-1 subtype C transmitted/founder virus LTR genetic variation and its impact on transcriptional activity and clinical outcomes.

The paper predicts transcriptional activity of HIV Tat single missense variants using a deep learning model trained on GigaAssay experiments, achieving a high correlation with experimental results.

This study identifies non-B DNA structures as genomic beacons for retroviral integration across diverse retroviruses, revealing subtype-specific preferences and shared hotspots.

This study shows TRIM24, recruited by TFII-I to the HIV-1 LTR, facilitates transcriptional elongation by enabling P-TEFb recruitment, essential for HIV-1 reactivation.

This study shows that inhibiting TRIM24's bromodomain with IACS-9571 reactivates latent HIV-1 without broadly activating T cells.

The paper introduces bayroot, a Bayesian method for estimating HIV-1 integration dates using root-to-tip regression, showing improved accuracy over conventional methods.

The paper examines HIV integration in the human brain using single nuclei transcriptomics, Hi-C, and IS-seq, finding 3D genomic reorganization and microglial activation linked to HIV infection.

This study shows morphine suppresses immune responses and alters brain myeloid gene expression in SIV-infected macaques, promoting neuropathogenesis.

This study analyzes HIV proviral diversity and compartmentalization in blood and lung during suppressive ART, finding shared sequences and limited genetic compartmentalization.

The paper identifies a novel fully-spliced transcript from EIAV that encodes a protein named Mat, which depends on Rev and the CRM1 pathway for nuclear export, suggesting a new Rev-responsive element.

The paper develops cell-based and cell-free assays to quantify HIV-1 Rev-Rev interactions using a split-luciferase complementation system and demonstrates their utility in screening inhibitors.

This study identifies six critical amino acids in NUP153 essential for HIV capsid interaction using computational and experimental methods.

Catchet-MS identifies thalidomide analogues targeting IKZF1 as novel HIV-1 latency reversal agents by reversing latency in CD4+ T-cells.

The paper quantitatively analyzes similarities and differences in the gag genome sequences of HIV and FIV using bioinformatics tools to assess sequence alignment metrics.

This study identifies 10 novel host factors involved in HIV latency using a haploid genetic screen and validates their roles through functional assays and drug testing.

The paper correlates the abundance of Nef and p-Tau217 in brain samples from HIV-infected individuals with HAND severity and lipid raft markers.

This study investigates how chronic exposure to HIV-1 viral proteins disrupts neurodevelopmental processes in the prefrontal cortex of rats, leading to synaptic and dendritic abnormalities.

This study investigates the conformational plasticity of the uncleaved HIV-1 Env trimer and its implications for antibody recognition and Env cleavage.

The paper identifies a monocyte-derived transcriptome signature linked to antibody-dependent cellular phagocytosis as a correlate of vaccine-induced protection against HIV-1 in clinical trials.

This study identifies PKC-independent signaling pathways that reactivate HIV latency by regulating P-TEFb availability in CD4+ T cells.

The paper analyzes CRF19 HIV-1 subtype sequences from Cuba to trace its origin, spread, and transmission patterns, finding early introduction and rapid progression to AIDS.