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• W2127328778 endingPage "3180" @default.
• W2127328778 startingPage "3167" @default.
• W2127328778 abstract "ABSTRACT Potent drugs such as cyclosporine have provided effective probes of signal transduction pathways and, as well, of human immunodeficiency virus type 1 (HIV-1) replication mechanisms. Recently, it was reported that As 2 O 3 , a drug used to treat acute promyelocytic leukemia (PML), stimulates HIV-1 replication. We found that As 2 O 3 accelerates the kinetics of a spreading HIV-1 infection in human T cells and increases the number of cells bearing HIV-1 provirus after a single round of infection. The stimulatory effect occurred after membrane fusion and resulted in increased steady-state levels of newly synthesized viral cDNA. Stimulation was independent of HIV-1 env and most viral accessory genes, and As 2 O 3 had no detectable effects on viral expression postintegration or virion assembly. Murine leukemia virus (MLV) transduction was enhanced by As 2 O 3 to the same extent as HIV-1 transduction, but As 2 O 3 had no additional effect on Fv1 restriction. In contrast, As 2 O 3 largely overcame the specific block to N-tropic MLV reverse transcription posed by human Ref1. As 2 O 3 disrupts PML bodies, nuclear structures named for a major component, the PML protein. We observed no changes in PML bodies in response to HIV-1 infection. Experiments with PML-null target cells indicated that PML has no effect on HIV-1 infectivity and is dispensable for the stimulatory effect of As 2 O 3 . As 2 O 3 caused cell death in uninfected cells at the same concentrations which stimulate HIV-1 replication. Among four additional apoptosis-inducing agents, a boost in HIV-1 infectivity was observed only with carbonyl cyanide m -chlorophenylhydrazone, a compound which, like As 2 O 3 , disrupts the mitochondrial transmembrane potential. In summary, As 2 O 3 stimulates retroviral reverse transcription, perhaps via effects on mitochondria, and provides a useful tool for characterizing Ref1." @default.
• W2127328778 created "2016-06-24" @default.
• W2127328778 creator A5009826873 @default.
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• W2127328778 date "2003-03-01" @default.
• W2127328778 modified "2023-10-14" @default.
• W2127328778 title "As ₂ O ₃ Enhances Retroviral Reverse Transcription and Counteracts Ref1 Antiviral Activity" @default.
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• W2127328778 doi "https://doi.org/10.1128/jvi.77.5.3167-3180.2003" @default.
• W2127328778 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/149754" @default.
• W2127328778 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12584341" @default.
• W2127328778 hasPublicationYear "2003" @default.
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