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• W2810401535 endingPage "1375" @default.
• W2810401535 startingPage "1359" @default.
• W2810401535 abstract "Although antiretroviral therapy is highly effective in suppressing human immunodeficiency virus type-1 (HIV) replication, treatment has failed to eliminate viral reservoirs and discontinuation of treatment results in viral reactivation. Here, we demonstrate that peptides Tat-vFLIP-α2 and Tat-Beclin 1/BECN1 which have been shown to induce a Na+/K+-ATPase- and a macroautophagy/autophagy-dependent form of cell death, autosis, can preferentially kill HIV-infected macrophages while preventing virological rebound. To improve bioavailability and drug delivery, Tat-vFLIP-α2 was encapsulated into biodegradable PLGA (poly lactic-co-glycolic acid)-lipid-PEG (polyethylene glycol) nanoparticles for long-lasting intracellular delivery. After a single dose of NP-vFLIP-α2, HIV-infected macrophages were preferentially killed in a dose-dependent manner compared to uninfected or untreated HIV-infected cells with complete inhibition of HIV infection at 10 μM of peptide. HIV-infected macrophages treated with NP-vFLIP-α2 exhibited increased markers of autophagy including LC3B lipidation, SQSTM1/p62 degradation and Na+/K+-ATPase expression compared to untreated uninfected or infected cells. Moreover, the increased cell death observed in HIV-infected cells was not altered by treatment with bafilomycin A1 (BAF) or the caspase inhibitor Z-VAD-FMK, but could be reversed following treatment with the Na+/K+-ATPase inhibitor, digoxin, or knockdown of ATG5 or ATG7. NP-vFLIP-α2 induced preferential killing was also detected in HIV-infected macrophages under antiretroviral suppression without inducing viral reactivation. Additionally, we found that Na+/K+-ATPase was upregulated in HIV-infected cells, which enhanced NP-vFLIP-α2 induced cell death. These findings provide a novel strategy to eradicate HIV-infected macrophages by selectively killing infected cells through the induction of Na+/K+-ATPase dependent autophagy, while preventing reactivation of virus and new infection of uninfected bystander cells." @default.
• W2810401535 created "2018-07-10" @default.
• W2810401535 creator A5000549201 @default.
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• W2810401535 creator A5083005519 @default.
• W2810401535 date "2018-07-23" @default.
• W2810401535 modified "2023-10-14" @default.
• W2810401535 title "Induction of a Na⁺/K⁺-ATPase-dependent form of autophagy triggers preferential cell death of human immunodeficiency virus type-1-infected macrophages" @default.
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• W2810401535 doi "https://doi.org/10.1080/15548627.2018.1476014" @default.
• W2810401535 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6103741" @default.
• W2810401535 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29962265" @default.
• W2810401535 hasPublicationYear "2018" @default.
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