The course of HIV infection is arrested by antiretroviral therapy (ART). However, life-long ART is undesirable. To eradicate infection, strategies are needed to deplete the rare population of proviral genomes that persist and reemerge if ART is interrupted. Proviral HIV persists due to the simultaneous deficiency of factors required to allow proviral expression and virion production, and a predominance of factors that obstruct proviral expression. Combining ART with global inducers of T-cell activation has so far failed to eradicate HIV infection. One approach to the selective removal of obstacles to proviral expression, inhibition of the chromatin remodeling enzyme histone deacetylase, has entered clinical testing. Additional approaches may be needed. Ultimately, therapies that eliminate rare cells that persistently express HIV and interrupt low levels of viremia that persist in some patients may be required to render depletion of proviral HIV infection clinically relevant, and lead to the clearance of HIV infection.
Confronting proviral HIV infection. Publishing Authors By Initials
Confronting proviral HIV infection. Journal Published:
PUBLICATION TYPE: Review
Journal: Current HIV/AIDS reports
VOLUME: 4
Page Numbers: 60-4
Journal Abbreviation:
ISSN: 1548-3568
DAY: 3
MONTH: May
YEAR: 2007
Confronting proviral HIV infection. Information
Number of References: 47
LANGUAGE: eng
NlmUniqueID: 101235661
Confronting proviral HIV infection. Keywords Mesh Terms:
KEYWORDS: T-Lymphocytes
MESH TERMS: drug effects
Chemical & Substance for Abstract: Confronting proviral HIV infection. Information
Substance Name: Histone Deacetylases
Registry Number: EC 3.5.1.-
Grant and Affiliation Information for Confronting proviral HIV infection.
AFFILIATION: Department of Medicine, 3302 Michael Hooker Research Building, CB#7435, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7435, USA. dmargo@med.unc.edu
Country: United States
AGENCY: United States NCRR
GRANT: RR00046
ACRONYM: RR
MEDLINETA: Curr HIV/AIDS Rep
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