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Inferring HIV transmission networks from HIV sequences is gaining popularity in the field of HIV molecular epidemiology. However, HIV sequences are often analyzed at distance from those affected by HIV epidemics, namely without the involvement of communities most affected by HIV. These remote analyses often mean that knowledge is generated in absence of lived experiences and socio-economic realities that could inform the ethical application of network-derived information in 'real world' programmes. Procedures to engage communities are noticeably absent from the HIV molecular epidemiology literature. Here we present our team's protocol for engaging community activists living in Nairobi, Kenya in a knowledge exchange process - The CIPHR Project (Community Insights in Phylogenetic HIV Research). Drawing upon a community-based participatory approach, our team will (1) explore the possibilities and limitations of HIV molecular epidemiology for key population programmes, (2) pilot a community-based HIV molecular study, and (3) co-develop policy guidelines on conducting ethically safe HIV molecular epidemiology. Critical dialogue with activist communities will offer insight into the potential uses and abuses of using such information to sharpen HIV prevention programmes. The outcome of this process holds importance to the development of policy frameworks that will guide the next generation of the global response.
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http://dx.doi.org/10.1080/17441692.2023.2269435 | 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 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).