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Reversal of HIV-1 latency with anti-microRNA inhibitors Zhang HInt J Biochem Cell Biol 2009[Mar]; 41 (3): 451-4Human 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 antiretroviral therapy (HAART).|Antiretroviral Therapy, Highly Active/trends[MESH]|CD4-Positive T-Lymphocytes/physiology/*virology[MESH]|Gene Expression Regulation, Viral[MESH]|Gene Silencing[MESH]|HIV Infections/enzymology/*genetics/prevention & control[MESH]|HIV-1/*physiology[MESH]|Humans[MESH]|Immunologic Memory[MESH]|Lymphocyte Activation[MESH]|MicroRNAs/*genetics[MESH]|T-Lymphocyte Subsets/physiology/*virology[MESH]|Virus Latency[MESH]|Virus Replication/genetics[MESH]|p300-CBP Transcription Factors/antagonists & inhibitors/biosynthesis[MESH] |
