ArticleNature communications2026
A tissue-intrinsic mechanism sensitizes HIV-1 particles for TLR-triggered innate immune responses.
Article in Nature communications, 2026. 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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10 authors.
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Abstract
In vivo, HIV-1 replicates within tissues, yet the impact of three-dimensional (3D) environments on viral spread remains unclear. Our laboratory previously showed that collagen-rich 3D extracellular matrix (ECM) imposes an Environmental Restriction to cell-free Virus Infectivity (ERVI). Here, we demonstrate that ERVI is mediated by adhesive ECM components assembled into tissue-like scaffolds. Transient interactions with collagen fibers rapidly diminish virion infectivity across diverse primary strains by impairing virus fusogenicity. Notably, collagen-experienced particles also induce a distinct antiviral transcriptional program and strong pro-inflammatory cytokine secretion in monocyte-derived macrophages. Mechanistically, collagen contact induces conformational changes in the viral glycoprotein Env, enhances its interaction with toll-like receptor 2 (TLR2), and promotes trafficking into TLR8-positive endosomes, thereby amplifying innate immune sensing. Thus, ERVI functions through a dual mechanism: reducing virion fusogenicity while increasing innate immune detection. These findings identify the biophysical properties of the ECM as a tissue-intrinsic arm of antiviral innate immunity.
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