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CD4 T cell depletion is central to HIV pathogenesis and disease progression. Different subsets of CD4 T cells cooperate to combat an infection. Therefore, the immune balance among Th17, Th1, and Treg cells may be critical in HIV immunopathogenesis which is not adequately defined yet. The impact of HIV-1 infection on the interplay of Th17/Th1/Treg cells in HIV-1 infected Indian individuals was examined in the present study and report that HIV-1 Gag specific peripheral blood Th17 cells were significantly depleted in late infected subjects, compared to early infected subjects and slow progressors. Although, the gradual loss of Th1 cells was also reported during HIV-1 disease progression but relative to Th17 cells, Th1 cells were found to be more resistant to HIV-1 infection. Additionally, a significant and progressive gain in Treg cellular frequency was observed as disease progress from early to late stage of HIV-1 infection. This study also indicate that slow progressors might have an intrinsic capacity to develop strong HIV-1 specific Th17 and Th1 cell responses contrasted with a faint Treg cellular performance signifies the importance of these cellular subsets in progressive versus nonprogressive HIV-1 infection. A significant gradual loss of Th17/Treg ratio was found to be associated with disease state, plasma viral load and immune activation.
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http://dx.doi.org/10.1002/jmv.23810 | DOI Listing |
Sci Signal
September 2025
Department of Pathology, Microbiology and Immunology, New York Medical College, Valhalla, NY, USA.
Replication of HIV-1 requires the coordinated action of host and viral transcription factors, most critically the viral transactivator Tat and the host nuclear factor κB (NF-κB). This activity is disrupted in infected cells that are cultured with extracellular vesicles (EVs) present in human semen, suggesting that they contain factors that could inform the development of new therapeutics. Here, we explored the contents of semen-derived EVs (SEVs) from uninfected donors and individuals with HIV-1 and identified host proteins that interacted with HIV Tat and the NF-κB subunit p65.
View Article and Find Full Text PDFPLoS Biol
September 2025
Department of Virology, Immunology & Microbiology, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, United States of America.
Despite the success of antiretroviral therapy in suppressing plasma viremia in people living with human immunodeficiency virus type-1 (HIV-1), persistent viral RNA expression in tissue reservoirs is observed and can contribute to HIV-1-induced immunopathology and comorbidities. Infection of long-lived innate immune cells, such as tissue-resident macrophages and microglia may contribute to persistent viral RNA production and chronic inflammation. We recently reported that de novo cytoplasmic expression of HIV-1 intron-containing RNA (icRNA) in macrophages and microglia leads to MDA5 and MAVS-dependent innate immune sensing and induction of type I IFN responses, demonstrating that HIV icRNA is a pathogen-associated molecular pattern (PAMP).
View Article and Find Full Text PDFAIDS Res Hum Retroviruses
September 2025
Clinical Laboratory, The People's Hospital of Baoding, Baoding, China.
The emergence of CRF80_0107 resulted from recombination between co-circulating CRF01_AE and CRF07_BC genotypes. To date, no secondary recombinants involving CRF80_0107 as a parental strain have been documented in public sequence databases. Here, we report the identification and characterization of a novel HIV-1 CRF80_0107/B recombinant form isolated from a treatment-naïve men who have sex with men (MSM) individual in Baoding City, Hebei Province, China.
View Article and Find Full Text PDFmBio
September 2025
Centre de Recherche du CHUM, Montreal, Québec, Canada.
HIV-1-mediated CD4 downregulation is a well-known mechanism that protects infected cells from antibody-dependent cellular cytotoxicity (ADCC). While CD4 downregulation by HIV-1 Nef and Vpu proteins has been extensively studied, the contribution of the HIV-1 envelope glycoprotein (Env) in this mechanism is less understood. While Env is known to retain CD4 in the endoplasmic reticulum (ER) through its CD4-binding site (CD4bs), little is known about the mechanisms underlying this process.
View Article and Find Full Text PDFFront Microbiol
August 2025
Institute of Infectious Diseases, Guangzhou Eighth People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
Introduction: Low-level viremia (LLV) in HIV infection, defined as detectable but low plasma viral load, is associated with an increased risk of virological failure (VF); however, the mechanisms underlying LLV remain unclear. Monocytes, as potential viral reservoirs, can migrate into tissues and differentiate into tissue-resident macrophage reservoirs, playing a critical role in viral dissemination and potentially driving persistent viremia.
Methods: This study aimed to analyze and compare the molecular characteristics of near-full-length HIV-1 proviral DNA quasispecies from monocytes in three distinct virological response groups: VF, LLV, and virological suppression (VS).