期刊
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
卷 41, 期 3, 页码 451-454出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.biocel.2008.07.016
关键词
HIV-1; Latency; MicroRNA; Tat; Rev; Viral reservoir; HAART
资金
- NIAID NIH HHS [R01 AI058798-04, R01 AI058798, R01 AI052732-04, R01 AI052732] Funding Source: Medline
Human immunodeficiency virus type 1 (HIV-1) latency is achieved when host cells contain integrated proviral DNA but do not produce viral particles. The virus remains in resting CD4 T-lymphocytes, evading host immune surveillance and antiviral drugs. When resting cells are activated, infectious viral particles are produced. Latency is critical for the survival of all HIV-1 strains in vivo. Recently, it has been reported that a cluster of cellular microRNAs (miRNAs) enriched specifically in resting CD4+ T-cells suppresses translation of most HIV-1-encoded proteins in the cytoplasm, sustaining HIV-1 escape from the host immune response. Complementary antisense miRNA inhibitors block the inhibitory effect of miRNAs and drive viral production from the resting T-lymphocytes without activating the cells. Therefore, inhibition of these HIV-1-specific cellular miRNAs is of great therapeutic significance for eliminating the HIV-1 reservoir in HIV-1-infected individuals receiving suppressive highly active anti retroviral therapy (HAART). (C) 2008 Elsevier Ltd. All rights reserved.
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