Jianming Hu 胡建民 宾州大学-HBV人物介绍系列

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Jianming Hu 宾州大学

宾州大学有好几个组和PI做HBV，发过好多JV，而且大多是华人
先介绍Jianming Hu

1 简要信息
Academic title Associate Professor of Microbiology and Immunology
College College of Medicine
Campuses Penn State Milton S. Hershey Medical Center
juh13@psu.edu  

Summary
  Virus-Host Interactions; Hepatitis Viruses; Viral Replication and Pathogenesis

Educational background
M.D., Wuhan University School of Medicine, 1983
Ph.D., Penn State University College of Medicine, 1993
Post-doctoral Training, Yale University School of Medicine, 1987-1988
Post-doctoral Training, Fox Chase Cancer Center, 1993-1997

主页：
http://fred.psu.edu/ds/retrieve/fred/investigator/juh13

2 简介
老是在JV上看到他关于HBV的文章：）
具体见文章列表

3 课题
VIRUS-CELL INTERACTIONS IN HEPATITIS B VIRUS REPLICATION AND PATHOGENESIS

Hepatitis B virus (HBV) represents a significant human pathogen, with over 300 million people infected worldwide. Chronic HBV infection not only results in fatal liver diseases such as cirrhosis and liver failure but also dramatically increases the risk of liver cancer by over 100-fold. HBV infections present a fascinating system to study mechanisms of viral replication, virus-host interaction, and viral pathogenesis. HBV replicates a peculiar circular DNA genome via a reverse transcription pathway that is similar to, yet distinct from, that of retroviruses. The outcome of HBV infection ranges from transient, self-resolving acute hepatitis to life-long viral persistence with or without apparent liver pathology and its attendant sequelae. Viral clearance or persistence is clearly determined by the intricate interplay of a multitude of still largely undefined viral and host factors. We are focusing our studies on the virus-host interactions, at the molecular and cellular level, which are critical to HBV replication and pathogenesis.



On the one hand, cellular factors required for viral assembly and replication are being sought using established cell-free as well as cell culture systems. We have identified some of the host factors required during the early stages of viral assembly and reverse transcription. We are continuing these studies in order to elucidate the requirements for the different stages of the viral replication cycle. A defining feature of HBV, as a pararetrovirus, is the fact that only the mature nucleocapsids containg the double-stranded DNA genome are enveloped and secreted extracellularly as virions, whereas the immature nucleocapsids containing the viral RNA or DNA intermediates are not secreted. We have recently discovered that viral reverse transcription and nucleocapsid maturation are coupled to virion secretion through dynamic phosphorylation and dephophorylation of the nucleocapsids. We are in the process of identifying the cellular factors responsible for this process and elucidating its regulation.



On the other hand, we are seeking to identify host factors that may be involved in mediating the clearance of HBV infections, including cell intrinsic antiviral defense mechanism, which may suggest novel ways of curing HBV infections. Our recent results suggest the existence of cellular factors that can block the very early stage of viral assembly and reverse transcription and we are now pursuing the isolation of these cellular inhibitors of HBV replication. We have also obtained evidence that both the viral nucleocapsids and the episomal viral DNA genome are subject to intracellular turnover and we are in the process of elucidating these intracellular antiviral pathways.



By focusing our efforts on the critical host factors that either positively or negatively affects viral replication, persistence and pathogenesis, we hope to eventually manipulate these factors therapeutically with novel antivirals, thus helping to control HBV infection and its deadly consequences. Furthermore, we hope to gain insights into the normal functions of these cellular factors by using viruses as tools.


4 代表论文
详细在这里：
http://fred.psu.edu/ds/retrieve/ ... r/juh13/completepub

Hu J. Toft DO. Seeger C. Hepadnavirus assembly and reverse transcription require a multi-component chaperone complex which is incorporated into nucleocapsids. 1997 Jan 2. EMBO J. 16(1):59-68.
Wang X. Qian X. Guo HC. Hu J. Heat shock protein 90-independent activation of truncated hepadnavirus reverse transcriptase. 2003 Apr. J Virol. 77(8):4471-80.
National Institute of Allergy and Infectious Diseases
National Institute of Diabetes and Digestive and Kidney Diseases
Hu J. Flores D. Toft D. Wang X. Nguyen D. Requirement of heat shock protein 90 for human hepatitis B virus reverse transcriptase function. 2004 Dec. J Virol. 78(23):13122-31.
National Institute of Allergy and Infectious Diseases
Hu J. Boyer M. Hepatitis B virus reverse transcriptase and epsilon RNA sequences required for specific interaction in vitro. 2006 Mar. J Virol. 80(5):2141-50.
National Institute of Allergy and Infectious Diseases
Perlman DH. Berg EA. O'connor PB. Costello CE. Hu J. Reverse transcription-associated dephosphorylation of hepadnavirus nucleocapsids. 2005 Jun 21. Proc Natl Acad Sci U S A. 102(25):9020-5.
National Center for Research Resources
National Institute of Allergy and Infectious Diseases


楼主：bigben

bigben446

HuJianming，宾州州立大学，美国
HBV复制和cccDNA

Cui, X. and D. N. Clark, et al. (2016). "Viral DNA-Dependent Induction of Innate Immune Response to Hepatitis B Virus in Immortalized Mouse Hepatocytes." J Virol 90(1): 486-96.
Cui, X. and R. McAllister, et al. (2015). "Does Tyrosyl DNA Phosphodiesterase-2 Play a Role in Hepatitis B Virus Genome Repair?" PLoS One 10(6): e0128401.
Cui, X. and L. Luckenbaugh, et al. (2015). "Alteration of Mature Nucleocapsid and Enhancement of Covalently Closed Circular DNA Formation by Hepatitis B Virus Core Mutants Defective in Complete-Virion Formation." J Virol 89(19): 10064-72.
Clark, D. N. and J. Hu (2015). "Hepatitis B virus reverse transcriptase - Target of current antiviral therapy and future drug development." Antiviral Res 123: 132-7.
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.
Jones, S. A. and J. Hu (2013). "Protein-primed terminal transferase activity of hepatitis B virus polymerase." J Virol 87(5): 2563-76.
Jones, S. A. and E. Murakami, et al. (2013). "Noncompetitive inhibition of hepatitis B virus reverse transcriptase protein priming and DNA synthesis by the nucleoside analog clevudine." Antimicrob Agents Chemother 57(9): 4181-9.
Cui, X. and L. Ludgate, et al. (2013). "Maturation-associated destabilization of hepatitis B virus nucleocapsid." J Virol 87(21): 11494-503.
Jones, S. A. and R. Boregowda, et al. (2012). "In vitro epsilon RNA-dependent protein priming activity of human hepatitis B virus polymerase." J Virol 86(9): 5134-50.
Boregowda, R. K. and C. Adams, et al. (2012). "TP-RT domain interactions of duck hepatitis B virus reverse transcriptase in cis  and in trans during protein-primed initiation of DNA synthesis in vitro." J Virol 86(12): 6522-36.
Boregowda, R. K. and L. Lin, et al. (2011). "Cryptic protein priming sites in two different domains of duck hepatitis B virus  reverse transcriptase for initiating DNA synthesis in vitro." J Virol 85(15): 7754-65.
Ning, X. and D. Nguyen, et al. (2011). "Secretion of genome-free hepatitis B virus--single strand blocking model for virion morphogenesis of para-retrovirus." PLoS Pathog 7(9): e1002255.
Nguyen, D. H. and J. Hu (2008). "Reverse transcriptase- and RNA packaging signal-dependent incorporation of APOBEC3G into hepatitis B virus nucleocapsids." J Virol 82(14): 6852-61.
Nguyen, D. H. and L. Ludgate, et al. (2008). "Hepatitis B virus-cell interactions and pathogenesis." J Cell Physiol 216(2): 289-94.
Nguyen, D. H. and S. Gummuluru, et al. (2007). "Deamination-independent inhibition of hepatitis B virus reverse transcription by  APOBEC3G." J Virol 81(9): 4465-72.
Gao, W. and J. Hu (2007). "Formation of hepatitis B virus covalently closed circular DNA: removal of genome-linked protein." J Virol 81(12): 6164-74.
Hu, J. and D. Flores, et al. (2004). "Requirement of heat shock protein 90 for human hepatitis B virus reverse transcriptase function." J Virol 78(23): 13122-31.
Guo, J. T. and M. Pryce, et al. (2003). "Conditional replication of duck hepatitis B virus in hepatoma cells." J Virol 77(3): 1885-93.
Seeger, C. and E. H. Leber, et al. (1996). "Mutagenesis of a hepatitis B virus reverse transcriptase yields temperature-sensitive virus." Virology 222(2): 430-9.