Journal
EXPERT REVIEW OF ANTI-INFECTIVE THERAPY
Volume 14, Issue 2, Pages 145-148Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1586/14787210.2016.1122525
Keywords
Tat inhibitor; didehydro-Cortistatin A; HIV transcription; HIV latency; deep-latency; latent reservoir; viral reactivation; antiretroviral therapy; functional cure
Funding
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI118432, R01AI097012] Funding Source: NIH RePORTER
- NIAID NIH HHS [R01 AI118432, R01 AI097012, R01 AI118432-01AI] Funding Source: Medline
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Antiretroviral therapy can effectively suppress HIV-1 infection but is ineffective against integrated proviruses. A latent viral reservoir composed of latently infected CD4(+)T cells persists under suppressive therapy, and infected individuals must remain indefinitely on antiretroviral therapy to prevent viral reactivation and propagation. Despite therapy, some degree of low-level ongoing replication is detected and transient viral reactivation may replenish the latent reservoir. An analog of the natural compound, Cortistatin A, blocks HIV-1 transcription by specifically targeting the viral transactivator, Tat. Treatment of latently infected cells with this Tat inhibitor promotes a state of deep-latency from which HIV reactivation capacity is greatly diminished. Here we discuss the use of Tat inhibitors to limit the latent reservoir to achieve a functional cure.
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