HIV Research and Treatment

This study shows HIV-1 enhances cell-to-cell transmission from infected CD4+ T cells to microglia by altering surface signals and increasing phagocytosis.

This study develops Hybrid CAR-T cells that secrete broadly neutralizing antibodies, showing in vitro HIV elimination and in vivo viral suppression in humanized mice.

This study identifies the minimal MX2 region required for HIV-1 restriction and shows that MX2 binding disrupts the capsid lattice, leading to premature fragmentation and preventing viral nuclear import.

CRISPR screens with replication-competent SIVcpz identify human antiviral factors limiting efficient viral replication after zoonotic transmission.

This study identifies KLF16 as a repressive transcription factor that inhibits HIV-1 transcription by competing with Sp1 and recruiting repressive complexes.

This paper demonstrates that HLA-E-targeting diabodies can induce CD8+ T cell-mediated lysis of HIV-1-infected cells, bypassing limitations of classical MHC class I antigens.

This study shows that Fc-engineered broadly neutralizing antibodies enhance NK cell ADCC against HIV-1 across subtypes, even with limited envelope binding and CD16 downregulation.

The paper identifies frequent and genetically diverse CDRH3 topologies in the human antibody repertoire that can be targeted by vaccination to elicit broadly neutralizing antibodies.

This study shows HIV-1 gp120 triggers macropinocytosis in CD4+ T cells, which facilitates HIV-1 infection through a calcium-independent phospholipase A2-dependent pathway.

This study identifies HIV-1-induced SUMOylation of host RNA splicing factors, mediated by Vif, which regulates viral RNA splicing and infectivity.

This study identifies Bloom syndrome helicase (BLM) as a host factor that promotes HIV-1 reverse transcription and integration in macrophages through CRISPR screening and functional assays.

This study shows that conserved GGG-tracts in HIV-1 LTRs are essential for accurate RNA transcription, packaging, and reverse-transcription to prevent mutations in the LTR region.

The paper designs a bispecific CD4-CD4i fusion protein that broadly neutralizes diverse HIV-1 subtypes with potency comparable to broadly neutralizing antibodies.

The paper examines pre-HIV Th17 cell levels as predictors of early HIV disease progression, finding higher pre-infection Th17 frequencies correlate with faster CD4 decline.

AAV-delivered broadly neutralizing antibodies provide durable protection against SIV challenge in rhesus macaques, while ADCC-only antibodies do not.

This paper develops updated HIV-1 pseudovirus panels to better detect and assess B cell lineages with potential to produce broadly neutralizing antibodies against contemporary HIV-1 variants.

The paper evaluates a dual-layer serological framework using HIV-derived and host-derived peptides to improve diagnostic accuracy and reveal immune state changes in HIV-positive individuals.

This study shows that continuous ART causes senescence-like changes in alveolar macrophages, increasing inflammation and impairing immune responses to SARS-CoV-2.

This study shows HIV-1 can perform reverse transcription and partial integration without Env or infection, suggesting a retrotransposon-like mechanism.

This study shows that HIV-1 Vif's essential role in infectivity under interferon and differentiation conditions is fully explained by its antagonism of APOBEC3 proteins, not other targets.

This study identifies a new form of nonsuppressible viremia in HIV patients on ART, linked to macrophage tropism and genetic diversity, distinct from previously known CD4+ T cell-related NSV.

This study examines HIV escape from two bNAbs in vivo, identifying recurrent mutations and genetic background dependencies in viral resistance.

This paper identifies the ENL-USP7 complex as a host factor that stabilizes BRD4 to maintain HIV-1 latency and shows that disrupting this complex reactivates latent HIV.

The paper uses cfDNA/cfRNA sequencing to identify molecular correlates of bNAb development in HIV patients, finding an MHC class I activation signature and microbial changes associated with bNAb production.

This study shows that levosimendan inhibits HIV-1 infection in myeloid cells through RIOK1-dependent mechanisms.

This study shows TNFR2 binds to HIV-1 gp120, blocking its interaction with CD4 and reducing HIV-1 infection in CD4+ T cells.

This study evaluates the HIV-1 transgenic rat model for age-related neurocognitive impairments, finding significant deficits linked to neuronal dysfunction and amyloid beta accumulation.

This study examines how TB co-infection affects HIV reservoir dynamics, viral diversity, and drug resistance in ART-naive individuals.

This study shows that cannabidiol inhibits HIV-1 transmission by targeting multiple immune cells and blocking viral infection and transfer in mucosal tissues.