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- W2023397239 abstract "Astrocytes protect neurons but also evoke a proinflammatory response to injury and viral infections including HIV. We investigated the mechanism of HIV-1 infection in primary astrocytes, which showed minimal but productive viral infection independent of CXCR4. As with ectopic-CD4-expressing astrocytes, lysosomotropic agents led to increased HIV-1 infection in wild-type but not Rabs 5, 7, and 11-ablated astrocytes. Instead, HIV-1 infection was decreased in Rab-depleted astrocytes, corroborating viral entry by endocytosis. HIV-1 produced persistent infection in astrocytes (160 days); no evidence of latent infection was seen. Notably, one caveat is that endosomal modifiers enhanced wild-type HIV-1 infection (M- and T-tropic) in astrocytes, suggesting endocytic entry of the virus. Impeding endocytosis by inhibition of Rab 5, 7 or 11 will inhibit HIV infection in astrocytes. Although the contribution of such low-level infection in astrocytes to neurological complications is unclear, it may serve as an elusive viral reservoir in the central nervous system." @default.
- W2023397239 created "2016-06-24" @default.
- W2023397239 creator A5024920015 @default.
- W2023397239 creator A5033628757 @default.
- W2023397239 creator A5042129289 @default.
- W2023397239 creator A5064283570 @default.
- W2023397239 date "2014-05-01" @default.
- W2023397239 modified "2023-09-29" @default.
- W2023397239 title "Endocytosis-mediated HIV-1 entry and its significance in the elusive behavior of the virus in astrocytes" @default.
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- W2023397239 doi "https://doi.org/10.1016/j.virol.2014.03.002" @default.
- W2023397239 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4179455" @default.
- W2023397239 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24889220" @default.
- W2023397239 hasPublicationYear "2014" @default.