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Virus Expression (virus + expression)
Selected AbstractsA new and efficient method for inhibition of RNA viruses by DNA interferenceFEBS JOURNAL, Issue 16 2009Monika Nowak We report here a new method for inhibition of RNA viruses induced by dsDNA. We demonstrated that both long dsDNA molecules and short interfering DNA with a sequence complementary to that of viral RNA inhibited tobacco mosaic virus expression and prevented virus spread. Also, the expression of the HIV-1 gp41 gene in HeLa cells was inhibited by complementary short interfering DNA. We showed that Dicer processed dsDNA, which suggests activation of the cellular machinery involved in silencing of RNA. For the silencing of viral RNA effected with dsDNA, we coined the term DNA interference technology. [source] Frequency of Epstein,Barr virus expression in various histological subtypes of Hodgkin's lymphomaHISTOPATHOLOGY, Issue 6 2008M Katebi No abstract is available for this article. [source] Upregulation of HTLV-1 and HTLV-2 expression by HIV-1 in vitroJOURNAL OF MEDICAL VIROLOGY, Issue 3 2008Upal Roy Abstract Co-infections with HIV-1 and the human T leukemia virus types 1 and 2 (HTLV-1, HTLV-2) occur frequently, particularly in large metropolitan areas where injection drug use is a shared mode of transmission. Recent evidence suggests that HIV-HTLV co-infections are associated with upregulated HTLV-1/2 virus expression and disease. An in vitro model of HIV-1 and HTLV-1/2 co-infection was utilized to determine if cell free HIV-1 virions or recombinant HIV-1 Tat protein (200,1,000 ng/ml) upregulated HTLV-1/2 expression and infectivity. Exposure to HIV-1 increased the number of HTLV-1 antigen expressing cells, from 6% at baseline to 12% at 24 hr, and 20% at 120 hr (P,<,0.05) post-exposure. A similar, although less robust response was observed in HTLV-2 infected cells. HIV-1 co-localized almost exclusively with HTLV-1/2 positive cells. Exposure to HIV-1 Tat protein (1,000 ng/ml) increased HTLV-1 p19 expression almost twofold by 48 hr, and cells co-stimulated with 10 nM phorbol myristate acetate (PMA) showed almost a fourfold increase over baseline. It is concluded that HIV-1 augments HTLV-1/2 infectivity in vitro. The findings also suggest a role for the HIV-1 Tat protein and PMA-inducible cellular factors, in HIV-1 induced HTLV-1/2 antigen expression. J. Med. Virol. 80:494,500, 2008. © 2008 Wiley-Liss, Inc. [source] Cytidine deaminase APOBEC3B interacts with heterogeneous nuclear ribonucleoprotein K and suppresses hepatitis B virus expressionCELLULAR MICROBIOLOGY, Issue 1 2008Wei Zhang Summary The cytidine deaminase apolipoprotein B mRNA editing catalytic subunit-3 (APOBEC3) proteins have been identified as potent inhibitors of diverse retroviruses, retrotransposons and hepatitis B virus (HBV). The mechanism of APOBEC3 proteins in the control of HBV infection, however, is less clear. Here we report that APOBEC3B (A3B) displays dual inhibitory effects on both HBsAg and HBeAg expression as well as HBV core-associated DNA synthesis. Heterogeneous nuclear ribonucleoprotein K (hnRNP K), a positive regulator of HBV expression, has been identified as a major interaction partner of A3B protein. A3B protein inhibited the binding of hnRNP K to the enhancer II of HBV (Enh II), and S gene transcription of HBV. Moreover, A3B directly suppressed HBV S gene promoter activity. Individual variation in A3B expression was observed in both normal primary hepatocytes and liver tissues. Interestingly, A3B was able to inhibit CMV and SV40 promoter-mediated gene expression. In conclusion, A3B suppresses HBV replication in hepatocytes by inhibiting hnRNP K-mediated transcription and expression of HBV genes as well as HBV core DNA synthesis. In addition, A3B protein may be a broad antiviral host factor. Thus, regulated A3B expression may contribute to non-cytolytic HBV clearance in vivo. [source] | ||||||||||