Copertina

A tissue-intrinsic mechanism sensitizes HIV-1 particles for TLR-triggered innate immune responses

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 demo...

Descrizione completa

Salvato in:
Dettagli Bibliografici
Autori principali: Sid Ahmed, Samy (Autore) , Zimmermann, Liv (Autore) , Imle, Andrea (Autore) , Wuebben, Katrin (Autore) , Tibroni, Nadine (Autore) , Rauch-Wirth, Lena (Autore) , Münch, Jan (Autore) , Chlanda, Petr (Autore) , Graw, Frederik (Autore) , Fackler, Oliver Till (Autore)
Natura: Article (Journal)
Lingua:inglese
Pubblicazione: 09 May 2026
In: Nature Communications
Year: 2026, Volume: 17, Pages: 1-23
ISSN:2041-1723
DOI:10.1038/s41467-026-72586-3
Accesso online:Verlag, kostenfrei, Volltext: https://doi.org/10.1038/s41467-026-72586-3
Verlag, kostenfrei, Volltext: https://www.nature.com/articles/s41467-026-72586-3
Testo
Note sull'autore:Samy Sid Ahmed, Liv Zimmermann, Andrea Imle, Katrin Wuebben, Nadine Tibroni, Lena Rauch-Wirth, Jan Münch, Petr Chlanda, Frederik Graw & Oliver T. Fackler
Descrizione
Riassunto: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.
Descrizione del documento:Online veröffentlicht: 09. Mai 2026
Gesehen am 07.08.2026
Descrizione fisica:Online Resource
ISSN:2041-1723
DOI:10.1038/s41467-026-72586-3

Documenti analoghi