John E. Tavis，密苏里——HBV相关实验室及人物介绍系列

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John E. Tavis，密苏里——HBV相关实验室及人物介绍系列

John E. Tavis，Saint Louis University School of Medicine, Saint Louis, Missouri

Lu, G. and E. Lomonosova, et al. (2015). "Hydroxylated tropolones inhibit hepatitis B virus replication by blocking viral ribonuclease H activity." Antimicrob Agents Chemother 59(2): 1070-9.
Tavis, J. E. and E. Lomonosova (2015). "The hepatitis B virus ribonuclease H as a drug target." Antiviral Res 118: 132-8.
Jones, S. A. and D. N. Clark, et al. (2014). "Comparative analysis of hepatitis B virus polymerase sequences required for viral RNA binding, RNA packaging, and protein priming." J Virol 88(3): 1564-72.
Cai, C. W. and E. Lomonosova, et al. (2014). "Hepatitis B virus replication is blocked by a 2-hydroxyisoquinoline-1,3(2H,4H)-dione (HID) inhibitor of the viral ribonuclease  H activity." Antiviral Res 108: 48-55.
Gehring, A. and A. Bertoletti, et al. (2014). "Host factor-targeted hepatitis B virus therapies." Intervirology 57(3-4): 158-62.
Cao, F. and S. Jones, et al. (2014). "Sequences in the terminal protein and reverse transcriptase domains of the hepatitis B virus polymerase contribute to RNA binding and encapsidation." J Viral Hepat 21(12): 882-93.
Hu, Y. and X. Cheng, et al. (2013). "beta-Thujaplicinol inhibits hepatitis B virus replication by blocking the viral ribonuclease H activity." Antiviral Res 99(3): 221-9.
Schvoerer, E. and R. Moenne-Loccoz, et al. (2013). "Hepatitis C virus envelope glycoprotein signatures are associated with treatment  failure and modulation of viral entry and neutralization." J Infect Dis 207(8): 1306-15.
Terrault, N. A. and J. L. Dodge, et al. (2013). "Sexual transmission of hepatitis C virus among monogamous heterosexual couples: the HCV partners study." Hepatology 57(3): 881-9.
Tavis, J. E. and X. Cheng, et al. (2013). "The hepatitis B virus ribonuclease h is sensitive to inhibitors of the human immunodeficiency virus ribonuclease h and integrase enzymes." PLoS Pathog 9(1): e1003125.
Lara, J. and J. E. Tavis, et al. (2011). "Coordinated evolution among hepatitis C virus genomic sites is coupled to host factors and resistance to interferon." In Silico Biol 11(5-6): 213-24.
Tavis, J. E. and M. J. Donlin, et al. (2011). "Prospects for personalizing antiviral therapy for hepatitis C virus with pharmacogenetics." Genome Med 3(2): 8.
Cao, F. and J. E. Tavis (2011). "RNA elements directing translation of the duck hepatitis B Virus polymerase via ribosomal shunting." J Virol 85(13): 6343-52.
Wagoner, J. and A. Negash, et al. (2010). "Multiple effects of silymarin on the hepatitis C virus lifecycle." Hepatology 51(6): 1912-21.
Cannon, N. A. and M. J. Donlin, et al. (2009). "Evidence for action of ribavirin through the hepatitis C virus RNA polymerase." J Viral Hepat 16(8): 595-604.
Aurora, R. and M. J. Donlin, et al. (2009). "Genome-wide hepatitis C virus amino acid covariance networks can predict response to antiviral therapy in humans." J Clin Invest 119(1): 225-36.
Cao, F. and C. A. Scougall, et al. (2009). "Pre-P is a secreted glycoprotein encoded as an N-terminal extension of the duck hepatitis B virus polymerase gene." J Virol 83(3): 1368-78.
Cannon, N. A. and M. J. Donlin, et al. (2008). "Hepatitis C virus diversity and evolution in the full open-reading frame during antiviral therapy." PLoS One 3(5): e2123.
Brodsky, L. I. and A. S. Wahed, et al. (2007). "A novel unsupervised method to identify genes important in the anti-viral response: application to interferon/ribavirin in hepatitis C patients." PLoS One 2(7): e584.
Taylor, M. W. and T. Tsukahara, et al. (2007). "Changes in gene expression during pegylated interferon and ribavirin therapy of chronic hepatitis C virus distinguish responders from nonresponders to antiviral  therapy." J Virol 81(7): 3391-401.
Donlin, M. J. and N. A. Cannon, et al. (2007). "Pretreatment sequence diversity differences in the full-length hepatitis C virus  open reading frame correlate with early response to therapy." J Virol 81(15): 8211-24.
Zhou, D. and X. Fan, et al. (2007). "Separation of near full-length hepatitis C virus quasispecies variants from a complex population." J Virol Methods 141(2): 220-4.
Cao, F. and J. E. Tavis (2006). "Suppression of mRNA accumulation by the duck hepatitis B virus reverse transcriptase." Virology 350(2): 475-83.
Zhang, Z. and J. E. Tavis (2006). "The duck hepatitis B virus reverse transcriptase functions as a full-length monomer." J Biol Chem 281(47): 35794-801.
Cao, F. and M. P. Badtke, et al. (2005). "Identification of an essential molecular contact point on the duck hepatitis B virus reverse transcriptase." J Virol 79(16): 10164-70.
Tester, I. and S. Smyk-Pearson, et al. (2005). "Immune evasion versus recovery after acute hepatitis C virus infection from a shared source." J Exp Med 201(11): 1725-31.
Cao, F. and J. E. Tavis (2004). "Detection and characterization of cytoplasmic hepatitis B virus reverse transcriptase." J Gen Virol 85(Pt 11): 3353-60.
Yao, E. and J. E. Tavis (2004). "Localization of duck hepatitis B virus polymerase within cells." Methods Mol Med 95: 281-93.
Sen, N. and F. Cao, et al. (2004). "Translation of duck hepatitis B virus reverse transcriptase by ribosomal shunting." J Virol 78(21): 11751-7.
Yao, E. and J. E. Tavis (2003). "Kinetics of synthesis and turnover of the duck hepatitis B virus reverse transcriptase." J Biol Chem 278(2): 1201-5.
Yao, E. and H. Schaller, et al. (2003). "The duck hepatitis B virus polymerase and core proteins accumulate in different patterns from their common mRNA." Virology 311(1): 81-8.
Gong, Y. and E. Yao, et al. (2001). "Evidence that the RNAseH activity of the duck hepatitis B virus is unable to act  on exogenous substrates." BMC Microbiol 1: 12.
Gong, Y. and E. Yao, et al. (2000). "Evidence that the first strand-transfer reaction of duck hepatitis B virus reverse transcription requires the polymerase and that strand transfer is not needed for the switch of the polymerase to the elongation mode of DNA synthesis." J Gen Virol 81(Pt 8): 2059-65.
Yao, E. and Y. Gong, et al. (2000). "The majority of duck hepatitis B virus reverse transcriptase in cells is nonencapsidated and is bound to a cytoplasmic structure." J Virol 74(18): 8648-57.
Tavis, J. E. and B. Massey, et al. (1998). "The duck hepatitis B virus polymerase is activated by its RNA packaging signal, epsilon." J Virol 72(7): 5789-96.
Tavis, J. E. and D. Ganem (1996). "Evidence for activation of the hepatitis B virus polymerase by binding of its RNA template." J Virol 70(9): 5741-50.
Gerelsaikhan, T. and J. E. Tavis, et al. (1996). "Hepatitis B virus nucleocapsid envelopment does not occur without genomic DNA synthesis." J Virol 70(7): 4269-74.
Wei, Y. and J. E. Tavis, et al. (1996). "Relationship between viral DNA synthesis and virion envelopment in hepatitis B viruses." J Virol 70(9): 6455-8.
Tavis, J. E. and D. Ganem (1995). "RNA sequences controlling the initiation and transfer of duck hepatitis B virus minus-strand DNA." J Virol 69(7): 4283-91.
Tavis, J. E. and D. Ganem (1993). "Expression of functional hepatitis B virus polymerase in yeast reveals it to be the sole viral protein required for correct initiation of reverse transcription." Proc Natl Acad Sci U S A 90(9): 4107-11.