期刊
ANNUAL REVIEW OF PHARMACOLOGY AND TOXICOLOGY, VOL 51, 2011
卷 51, 期 -, 页码 397-418出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-pharmtox-010510-100237
关键词
antiretroviral therapy; ART; viral reservoir; eradication
资金
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U19AI082608, R21AI081613] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH085597] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [R01DA030156] Funding Source: NIH RePORTER
- NIAID NIH HHS [R21-AI081613, AI082608, R21 AI081613, U19 AI082608] Funding Source: Medline
- NIDA NIH HHS [R01 DA030156, DA030156] Funding Source: Medline
- NIMH NIH HHS [R01 MH085597, MH085597] Funding Source: Medline
HIV-1 infection persists even after years of antiretroviral therapy (ART). Although ART can halt viral replication and thereby reduce viremia to clinically undetectable levels, proviral latency established within the host genome remains largely unaffected by ART and can replenish systemic infection following interruption of therapy. Pharmacologic strategies, which not only target viral replication but also deplete proviral infection, are required for successful clearance of HIV-1 infection. This review highlights the current understanding of molecular mechanisms that establish and maintain HIV-1 latency in its major reservoir, the resting memory CD4(+) T cell. We also identify the molecular targets that might be exploited to induce HIV-1 expression, remove epigenetic restrictions, or enhance effective transcription. Finally, we discuss the potential pharmacologic approaches toward targeting viral persistence in different cellular and anatomical reservoirs to achieve a cure of HIV-1 infection.
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