MicroRNAs control herpesviral dormancy

Tumor Virology Program, Greehey Children's Cancer Research Institute, Department of Pediatrics, Microbiology and Immunology, Medicine, and Molecular Medicine, and Cancer Therapy and Research Center, University of Texas Health Science Center at San Antonio, San Antonio, TX USA.
Cell cycle (Georgetown, Tex.) (Impact Factor: 5.01). 04/2010; 9(7):1225-6. DOI: 10.4161/cc.9.7.11387
Source: PubMed


Available from: Shou-Jiang Gao, May 28, 2015
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    ABSTRACT: Human retrovirus HTLV-1 replication and spread are controlled by different viral and cellular factors. Although several anti-HIV cellular microRNAs have been described, such regulation for HTLV-1 has not been reported. In this study, we found that miR-28-3p inhibits HTLV-1 virus expression and its replication by targeting a specific site within the genomic gag/pol viral mRNA. Since miR-28-3p is highly expressed in resting T cells, which are resistant to HTLV-1 infection, we investigate a potential protective role of miR-28-3p against de novo HTLV-1 infection. To this end, we develop a new sensitive and quantitative assay based on the detection of products of reverse transcription. We demonstrate that miR-28-3p does not prevent virus receptor interaction or virus entry but instead induces a post-entry block at the reverse transcription level. In addition, we found that HTLV-1 subtype 1A isolates, corresponding to the Japanese strain ATK-1, present a natural single nucleotide polymorphism within the miR-28-3p target site. As a result of this polymorphism, the ATK-1 virus sequence was not inhibited by miR-28. Interestingly, genetic studies on transmission of virus had shown that the ATK-1 strain, which carries a T-to-C transition mutation, was efficiently transmitted between spouses, suggesting that miR-28 may play an important role in HTLV-1 transmission. Copyright © 2015, The American Society for Biochemistry and Molecular Biology.
    Journal of Biological Chemistry 01/2015; 290(9). DOI:10.1074/jbc.M114.626325 · 4.60 Impact Factor