Reduction of immunity in HIV-infected individuals: Can fibrosis induce hypoplasia in palatine and lingual tonsils of individuals with HIV infection?

Beghini, Marcela; Montes, Jean M.C.; Rodrigues, Denise Bertulucci Rocha; Teixeira, Vicente P. A.; Pereira, Sanívia Aparecida de Lima

doi:10.1016/j.prp.2014.06.032

Cited by 1 publication

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“…The copyright holder for this this version posted September 27, 2021. ; https://doi.org/10.1101/2021.09.27.461933 doi: bioRxiv preprint impairing the immune function of secondary lymphoid organs (Beghini et al, 2015;Estes, 2009;Schacker et al, 2002;Zeng et al, 2011). We now provide evidence that (i) HIV-1 infection of T lymphocytes increases collagen secretion/production, possibly through a Tat-dependent mechanism that has been reported in other cell types (McArthur et al, 2001;Taylor et al, 1992;Tuyama et al, 2010); (ii) virally induced collagen confers a specific organized architecture on surface-bound HIV-1 colonies, creating threads that connect virions with one another and thus forming a 2D and 3D meshwork; (iii) the collagen scaffolding enables collective transmission of part of the viral progeny and increases HIV-1 infectivity.…”

Section: Discussionmentioning

confidence: 99%

HIV-1 hijacks the cell extracellular matrix to spread collectively and efficiently between T lymphocytes

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et al. 2021

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Collective transmission via structures containing several virions has recently emerged as a highly efficient mode of viral spread. Here, we demonstrate that HIV-1 spreads between T lymphocytes in the form of viral particles colonies that are concentrated and sheltered in an extracellular matrix (ECM) lattice enabling their collective transmission upon cell contacts. Intrinsically, ECM-clustered viruses infect T lymphocytes more efficiently than individual viral particles. They preserve HIV-1 transmission from antiretroviral treatment (ArT) and potent broadly neutralizing antibodies. We also show that collagen induced by HIV-1 infection controls the clustering of virions and their collective spread, thereby enhancing infectivity. CD4+ T cells from HIV-1-infected patients produce and transmit ECM-virus clusters, supporting that they could be involved in vivo. This study provides new insights into modes of HIV-1 transmission and identifies a novel fundamental role for collagen in this process. HIV-1 spread via ECM-virus clusters may have important implications for viral dissemination and persistence, including during therapy.

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