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• W2888974375 abstract "Despite viral suppression by antiretrovirals, HIV proteins continue to be detected in infected cells and neurologic complications remain common in infected people. Although HIV is unable to infect neurons, viral proteins, including gp120 and Tat, can enter neurons and can cause neuronal degeneration and neurocognitive impairment. Neuronal health is dependent on the functional integrity of mitochondria, and damaged mitochondria are subjected to mitochondrial control mechanisms. Multiple lines of evidence suggest that specific elimination of damaged mitochondria through mitophagy and mitochondrial dynamics play an important role in CNS diseases. Here, we show that in human primary neurons, gp120 and Tat favor the balance of mitochondrial dynamics toward enhanced fragmentation through the activation of mitochondrial translocation of DRP1 to the damaged mitochondria. However, mitophagy fails to go to completion, leading to neuronal damage. These findings support a role for altered mitophagy in HIV-associated neurological disorders and provide novel targets for potential intervention." @default.
• W2888974375 created "2018-09-07" @default.
• W2888974375 creator A5007618454 @default.
• W2888974375 creator A5017306542 @default.
• W2888974375 date "2018-11-15" @default.
• W2888974375 modified "2023-10-14" @default.
• W2888974375 title "Human Immunodeficiency Virus Type 1 gp120 and Tat Induce Mitochondrial Fragmentation and Incomplete Mitophagy in Human Neurons" @default.
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• W2888974375 doi "https://doi.org/10.1128/jvi.00993-18" @default.
• W2888974375 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6206485" @default.
• W2888974375 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30158296" @default.
• W2888974375 hasPublicationYear "2018" @default.
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