ArticleFrontiers in immunology2025
Inflammatory and redox reprogramming of macrophages by HIV cell-to-cell transmission inhibits bone resorption capacity.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: People with HIV experience bone loss, but how viral spread perturbs osteoclastogenesis remains unclear. We asked whether cell-to-cell transmission of HIV from infected CD4 Methods: We co-cultured Jurkat cells infected with R5- or X4-tropic HIV with human monocyte-derived macrophages (M0/M1/M2) and quantified infection (p24/GFP), inflammasome activation and death (IL-1β, AnnexinV/7-AAD, z-YVAD), adhesion molecules/tetraspanins (ICAM-1, LFA-1, CD9/CD63/CD81), mROS (MitoSOX, NAC), polarization markers/cytokines, and osteoclastogenesis (TRAP, actin ring, CD51/61, adhesion, bone resorption). Results: R5 HIV infected M0>M2>M1 macrophages via contact, sustaining p24 release across differentiation and reducing TRAP Discussion: The effects scaled with the proportion of infected T cells. HIV cell-to-cell spread induces inflammatory and redox reprogramming in macrophage precursors that blocks osteoclast differentiation and function, offering testable targets (inflammasome, adhesion, ROS) to protect bone in HIV.
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