Role of miRNA in HIV-1 latency. (May 2008)

• Record Type: Journal Article
• Authors: Zhang, Hui
• Is Part Of: Future HIV therapy. Volume 2:Number 3(2008)
• Page Start: 281
• Page End: 290
• Publication Date: 2008-05
• Subjects: CD4+ T lymphocytes -- HAART -- HIV-1 -- latency -- miRNA -- Rev -- Tat -- viral reservoir; HIV (Viruses) -- Treatment -- Periodicals; HIV (Viruses) -- Research -- Periodicals; 616.979206
• DOI: 10.2217/17469600.2.3.281
• Languages: English
• ISSNs: 1746-9600

Abstract

Postintegration latency of HIV-1 is achieved when host cells contain integrated provirus but viral particles are not being produced. When the cells are activated, infectious viruses can be produced from the cells. Latent infection is one of the important characteristics for all HIV-1 strains to survive in vivo . To avoid exposing itself to immune recognition, HIV-1 has evolved various strategies to prevent the expression of viral antigens. The resting CD4 + T lymphocytes infected with HIV-1 in a state of latency are the major reservoir for viral relapse after termination of highly active antiretroviral therapy. It has been demonstrated that the latency could be due to the transcriptional inefficiency and post-transcriptional suppression. Recent studies have also found that the cellular miRNAs inhibit HIV-1 expression in primary resting CD4 + T cells by interactions with the 3´´-termini of HIV-1 RNA, and therefore contribute to viral latency. It is known that almost all spliced or unspliced HIV-1 mRNAs share the same 3´´-terminus as their 3´´-untranslated region during translation. The cellular miRNAs, which bind to the 3´´-end of HIV-1 RNA, can inhibit the translation of almost all HIV-1 encoded proteins, including Tat and Rev, which play a key role in the transcription and translocation of viral RNA. Inefficient Tat and Rev protein synthesis could further enforce the viral latency. Therefore, manipulation of cellular miRNAs could become a novel strategy to activate HIV-1 latency for therapeutic purposes.