Viral gene expression within productively infected (GFP+) cells is increased in the presence of Vpr and vorinostat (VOR).

A) Top panel (cis Vpr expression): schematic of workflow with infection with Vpr revertant vs. Vpr-null virus (HIV-GFP) and lower panel (trans Vpr expression): co-infection with Vpr-mCherry lentivirus or mCherry lentivirus and HIV-GFP (created with Biorender.com). <b&g...

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Bibliografische gegevens
Hoofdauteur:	Catherine A. Lewis (22177707) (author)
Andere auteurs:	David M. Margolis (244046) (author), Edward P. Browne (8913893) (author)
Gepubliceerd in:	2025
Onderwerpen:	Cell Biology Molecular Biology Biotechnology Immunology Developmental Biology Cancer Infectious Diseases Virology vorinostat potently enhances viral factors shape viral factors interact sup >+</ sup specific viral factors div >< p critical cellular factors 1 reporter strains 1 accessory proteins 1 accessory protein reservoir formation selects preventing reservoir formation regulate latency establishment 1 latency results 1 latency establishment prevents hiv transmission cure hiv infection vpr &# 8217 latent viral reservoir 1 protein vpr whether hdacs interact cell latency model host cell factors promoting hiv expression central memory cd4 latent reservoir central memory 1 entry vpr expression new latency cell subtypes cell death latent proviruses single hiv individual hiv allow hiv vpr possesses vpr plays significant increase recently shown promoting activity primary cd4 mediated restriction induced apoptosis histone deacetylases findings suggest dramatically improved clinical prognosis binding domain antiretroviral therapy
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Viral gene expression within productively infected (GFP<sup>+</sup>) cells is increased in the presence of Vpr and vorinostat (VOR).

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