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The HIV-1 reservoir, consisting of transcriptionally silent integrated HIV-1 proviruses, is a major barrier to a cure, as it persists during effective antiretroviral therapy (ART) and is the source of viral rebound upon treatment interruption. Some of the strategies explored for HIV cure focus on the identification of compounds to either reactivate and eliminate the HIV reservoir ("shock and kill") or to prevent HIV reservoir reactivation and induce deep proviral latency ("block and lock"). Paramount in developing these HIV-1 cure strategies is determining the effect of the compounds on the size of the inducible HIV-1 reservoir in blood from people living with HIV-1 (PWH). Traditionally, viral outgrowth assays have been the primary method to determine the inducible HIV-1 reservoir in CD4+ T cells from PWH. However, these assays are labor-intensive, time-consuming, and often have low sensitivity. We have recently developed the inducible HIV-1 reservoir reduction assay (HIVRRA), a rapid, cost-effective, and sensitive method to measure the impact of compounds on the inducible replication-competent HIV-1 reservoir in total peripheral blood mononuclear cells (PBMCs) from PWH ex vivo. The HIVRRA simultaneously evaluates the effect of test conditions on the size of the inducible replication-competent HIV-1 reservoir as well as the specificity and toxicity of the test strategy. Using total PBMCs instead of purified CD4+ T cells reduces processing time and resource requirements. This makes the HIVRRA a more practical, scalable tool for evaluating potential HIV-1 cure strategies. Key features • The HIVRRA builds on the TZM-BL cell-based assay to quantify the HIV-1 reservoir by Sanyal et al.'s [1] method. • The HIVRRA uses total PBMCs from PWH to determine infectious units per million cells. • The HIVRRA requires low PBMC input compared to other reservoir analysis methods. • The HIVRRA determines the toxicity of the compounds on HIV-1-infected and uninfected cells in the same assay.
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http://dx.doi.org/10.21769/BioProtoc.5384 | DOI Listing |
J Virol Methods
September 2025
Department of Pathogenic Organism Biology, Henan University of Chinese Medicine, Zhengzhou, Henan, China. Electronic address:
Despite advances in antiretroviral therapy, HIV-1 persistence and immune dysregulation remain unresolved challenges. Here, we demonstrate that curcumin, a low-toxicity natural compound, can inhibit HIV-1 through simultaneous inhibition of the PI3K/AKT and JAK/STAT pathways, leading to downregulation of the viral co-receptor CCR5 and the immune checkpoint transcription factor FOXP3. Using CHIP and EMSA experiments, we found that curcumin disrupts the binding of FOXP3 to the CCR5 promoter, thereby reducing viral entry.
View Article and Find Full Text PDFPLoS Pathog
September 2025
INSERM UMR 1291, CNRS UMR 5051, Université de Toulouse, Toulouse Institute for Infectious and Inflammatory Diseases, Toulouse, France.
Vδ1 γδ T cells are key players in innate and adaptive immunity, particularly at mucosal interfaces such as the gut. An increase in circulating Vδ1 cells has long been observed in people with HIV-1, but remains poorly understood. We performed a comprehensive characterization of Vδ1 T cells in blood and duodenal intra-epithelial lymphocytes, obtained from endoscopic mucosal biopsies of 15 people with HIV-1 on antiretroviral therapy and 15 HIV-seronegative controls, in a substudy of the ANRS EP61 GALT study (NCT02906137).
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 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).
NPJ Drug Discov
September 2025
Department of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, CT USA.
A strategy to functionally cure AIDS by eliminating latent HIV-1 reservoirs involves non-nucleoside reverse transcriptase inhibitors (NNRTIs) that promote pyroptosis of HIV-1 infected cells. These NNRTIs stimulate dimerization of the Gag-Pol polyprotein, resulting in premature HIV-1 protease (PR) dimerization and cleavage of intracellular CARD8. A unique cell-based high-throughput screen was developed to identify potent compounds activating the CARD8 inflammasome through Gag-Pol dimerization.
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