Jianming Hu

ORCID: 0000-0002-3967-2133
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Hepatitis B Virus Studies
  • Hepatitis C virus research
  • Viral gastroenteritis research and epidemiology
  • Liver Disease Diagnosis and Treatment
  • Hepatitis Viruses Studies and Epidemiology
  • HIV Research and Treatment
  • Bacteriophages and microbial interactions
  • Animal Virus Infections Studies
  • RNA Interference and Gene Delivery
  • Viral Infections and Outbreaks Research
  • Immunotherapy and Immune Responses
  • HIV/AIDS drug development and treatment
  • Heat shock proteins research
  • Virus-based gene therapy research
  • Herpesvirus Infections and Treatments
  • Viral Infections and Vectors
  • Lung Cancer Treatments and Mutations
  • Pancreatic function and diabetes
  • Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
  • Glycosylation and Glycoproteins Research
  • Pulmonary Hypertension Research and Treatments
  • Endoplasmic Reticulum Stress and Disease
  • Bioactive Compounds and Antitumor Agents
  • CNS Lymphoma Diagnosis and Treatment
  • Phenothiazines and Benzothiazines Synthesis and Activities

Penn State Milton S. Hershey Medical Center
2009-2025

Pennsylvania State University
2015-2024

Jiangxi Provincial People's Hospital
2009-2018

University of Pennsylvania
2017

National Institutes of Health Clinical Center
2017

Soochow University
2009-2013

First Affiliated Hospital of Soochow University
2009-2013

Lanzhou University
2011-2013

First Hospital of Lanzhou University
2011-2013

Gilead Sciences (United States)
2013

The heat shock protein Hsp90 is known as an essential component of several signal transduction pathways and has now been identified host factor for hepatitis B virus replication. interacts with the viral reverse transcriptase to facilitate formation a ribonucleoprotein (RNP) complex between polymerase RNA ligand. This RNP required early in replication assembly initiation DNA synthesis through protein-priming mechanism. These results thus invoke role pathway RNP.

10.1073/pnas.93.3.1060 article EN Proceedings of the National Academy of Sciences 1996-02-06

ABSTRACT Hepatitis B virus (HBV) contains a small, partially double-stranded, relaxed circular (RC) DNA genome. RC needs to be converted covalently closed (CCC) DNA, which serves as the template for all viral RNA transcription. As first step toward understanding how CCC is formed, we analyzed and host factors that may involved in formation, using transient stable transfections of HBV related avian hepadnavirus, duck hepatitis (DHBV). Our results show formed hepatoma cells was derived...

10.1128/jvi.02721-06 article EN Journal of Virology 2007-04-05

As a para-retrovirus, hepatitis B virus (HBV) is an enveloped with double-stranded (DS) DNA genome that replicated by reverse transcription of RNA intermediate, the pregenomic or pgRNA. HBV assembly begins formation "immature" nucleocapsid (NC) incorporating pgRNA, which converted via within maturing NC to DS genome. Only mature, DNA-containing NCs are and secreted as virions whereas immature containing single-stranded (SS) not enveloped. The current model for selective virion morphogenesis...

10.1371/journal.ppat.1002255 article EN cc-by PLoS Pathogens 2011-09-22

The initiation of reverse transcription and nucleocapsid assembly in hepatitis B virus (HBV) depends on the specific recognition an RNA signal (the packaging signal, epsilon) pregenomic (pgRNA) by viral transcriptase (RT). RT-epsilon interaction duck (DHBV) was recently shown to require molecular chaperone complex, heat shock protein 90 (Hsp90). However, requirement for human HBV has remained unknown due inability obtain a purified RT active epsilon binding. We now report that Hsp90 is also...

10.1128/jvi.78.23.13122-13131.2004 article EN Journal of Virology 2004-11-12

The APOBEC3 family of mammalian cytidine deaminases, including APOBEC3G (A3G), has been shown to function as innate antiviral factors against retroviruses and can also suppress the replication hepatitis B virus (HBV). mechanism by which A3G inhibits HBV remains be elucidated. In this study, we show that inhibitory effect proteins on was mainly at DNA level, with only a minor viral RNA packaging. anti-HBV independent DNA-editing function, mode inhibition not due degradation....

10.1128/jvi.02510-06 article EN Journal of Virology 2007-02-22

Hepatitis B viruses are pararetroviruses that contain a partially dsDNA genome and replicate this DNA through an RNA intermediate (the pregenomic RNA, pgRNA) by reverse transcription. Viral assembly begins with the packaging of pgRNA into nucleocapsids (NCs), subsequent transcription within NCs converting characteristic genome. Only containing so-called “mature” NCs) enveloped viral envelope proteins secreted as virions; “immature” NCs, i.e., those or immature intermediates, excluded from...

10.1073/pnas.0502138102 article EN Proceedings of the National Academy of Sciences 2005-06-10

The mature nucleocapsid (NC) of hepatitis B virus containing the relaxed circular (RC) DNA genome can be secreted extracellularly as virions after envelopment with viral surface proteins or, alternatively, disassembled to release RC (i.e., uncoating) into host cell nucleus form covalently closed (CCC) DNA, which sustains replication and persistence. In contrast, immature NCs single-stranded or pregenomic RNA are incompetent for either uncoating. Little is currently known about how NCs, not...

10.1128/jvi.01912-13 article EN Journal of Virology 2013-08-22

Potential conflict of interest: Dr. Block owns stock, holds intellectual property rights, and received grants from Arbutus. He is employed by stock in Contravir. director has equity Glycotest. Chisari consults for Gilead. H. Guo Assembly. Alios. J. Lok Bristol‐Myers Squibb Kowdley consults, advises, on the speakers' bureau Glenn by, Riboscience. Eiger. Feld AbbVie, Gilead, Janssen, Merck. Abbott. Hu Gilead Roche. Sanofi El‐Serag Wako, Mason Revill Chang advises Arbutus Alnylam. Locarnini...

10.1002/hep.29509 article EN cc-by-nc Hepatology 2017-09-06

10.1007/978-3-030-03502-0_9 article EN Cancer treatment and research 2018-12-06

ABSTRACT Multiple subunits of the hepatitis B virus (HBV) core protein (HBc) assemble into an icosahedral capsid that packages viral pregenomic RNA (pgRNA). The N-terminal domain (NTD) HBc is sufficient for assembly, in absence pgRNA or any other host factors, under conditions high and/or salt concentrations. C-terminal (CTD) deemed dispensable assembly although it essential packaging. We report here expressed a mammalian cell lysate, rabbit reticulocyte lysate (RRL), was able to capsids...

10.1128/jvi.00394-16 article EN Journal of Virology 2016-04-14

ABSTRACT Hepatitis B virus (HBV) replicates its DNA genome through reverse transcription of a pregenomic RNA (pgRNA) by using multifunctional polymerase (HP). A critical function HP is specific recognition viral signal termed ε (Hε) located on pgRNA, which required for packaging pgRNA into nucleocapsids and initiation transcription. initiates itself as protein primer (protein priming) Hε the obligatory template. We have purified from human cells that retained binding activity in vitro ....

10.1128/jvi.07137-11 article EN Journal of Virology 2012-03-01

Complete virions of hepatitis B virus (HBV) contain a DNA genome that is enclosed in capsid composed the HBV core antigen (HBcAg), which turn surrounded by lipid envelope studded with viral surface antigens (HBsAg). In addition, HBV-infected cells release subviral particles HBsAg only (HBsAg 'spheres' and 'filaments') or enveloping HBcAg but devoid ('empty virions'). The e (HBeAg), soluble related to HBcAg, also secreted some patients. goals this study were explore levels empty patients...

10.1111/jvh.12361 article EN Journal of Viral Hepatitis 2014-11-14

Hepatitis B virus (HBV) replication and persistence are sustained by a nuclear episome, the covalently closed circular (CCC) DNA, which serves as transcriptional template for all viral RNAs. CCC DNA is converted from relaxed (RC) in virion early during infection well RC intracellular progeny nucleocapsids via an amplification pathway. Current antiviral therapies suppress but cannot eliminate DNA. Thus, of remains obstacle toward curing chronic HBV infection. Unfortunately, very little known...

10.1371/journal.pone.0128401 article EN cc-by PLoS ONE 2015-06-16

ABSTRACT During the morphogenesis of hepatitis B virus (HBV), an enveloped virus, two types virions are secreted: (i) a minor population complete containing mature nucleocapsid with characteristic, partially double-stranded, relaxed circular DNA genome and (ii) major empty capsid no or RNA (empty virions). Secretion both requires interactions between HBV core protein (HBc) viral surface envelope proteins. We have studied requirements from HBc proteins for virion secretion in comparison those...

10.1128/jvi.00272-18 article EN Journal of Virology 2018-05-10

Hepatitis B virus (HBV) covalently closed circular (CCC) DNA functions as the only viral template capable of coding for all RNA species and is thus essential to initiate sustain replication. CCC converted, in a multistep ill-understood process, from relaxed (RC) DNA, which neither two strands closed. To detect putative intermediates during RC conversion, 3' exonucleases, exonuclease I (Exo I) Exo III, were used combination degrade with free end, would nevertheless preserve either...

10.1128/jvi.00539-17 article EN Journal of Virology 2017-06-22

ABSTRACT Hepatitis B virus (HBV) core protein consists of an N-terminal assembly domain and a C-terminal (CTD) with seven conserved serines or threonines that are dynamically phosphorylated/dephosphorylated during the viral replication cycle. Sulfamoylbenzamide derivatives small molecular allosteric modulators (CpAMs) bind to heteroaryldihydropyrimidine (HAP) pocket between dimer-dimer interfaces. CpAM binding alters kinetics pathway capsid can result in formation morphologically “normal”...

10.1128/jvi.02139-17 article EN Journal of Virology 2018-04-17
Coming Soon ...