Replication of HIV-1 inside host cells is dependent on both viral and host factors. MicroRNAs are small noncoding RNAs that regulate protein synthesis. MicroRNAs may control viral replication either by directly targeting the viral genome or indirectly through cellular proteins that are required during the viral lifecycle. HIV infection may, in turn, regulate host microRNA expression to facilitate its propagation inside cells. miR-150 has been reported to be an essential factor involved in T-cell activation and may serve as a biomarker for HIV disease progression. The current study provides valuable insights into the role of miR-150 in HIV infection. We quantified miR-150 expression in HIV-infected Jurkat cells and observed a time-dependent increase in the expression of miR-150. In addition, HIV infection led to an enhanced influx of glucose inside the infected cells, which further increased on overexpression of miR-150. The increased uptake of glucose was due to miR-150-mediated increase in expression of glucose transporter-1 (GLUT1). In an attempt to decipher the mechanism, we identified that HIV Tat protein enhanced the expression of miR-150 which then upregulated GLUT1 in HIV-infected cells. In summary, this study sheds light on the role of miR-150 in HIV infection and paves the way for miR-150 as a novel therapeutic target against HIV-1.
Keywords: GLUT1; HIV; glucose; microRNA.
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