Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatitis B virus (HBV) infection is one of the major causes of chronic liver diseases. The current therapeutics show limited efficacy. In the HBV life cycle, virus core antigen (HBcAg) plays important multiple roles. Blocking the pleiotropic functions of HBcAg may thus represent a promising strategy for anti-HBV replication. In this study, monoclonal antibody (MAb) against core antigen of human HBV was coupled with TAT protein transduction domain (TAT PTD) to form transbody, and the effect on virus replication was evaluated in vitro. The HBV transbody, HBcMAb-TAT PTD conjugate, recognized HBcAg and retained cell-penetrating activity in living cells. In HBV-transfected liver cell line HepG2.2.15, HBV transbody suppressed not only the extracellular HBsAg, HBeAg and HBV DNA, but also the intracellular HBsAg, HBeAg, HBcAg and HBV DNA in a dose-dependent manner. These results indicate that the transbody prepared possesses readily cell-penetrating ability and potent antiviral activity, providing a novel approach, a cell-permeable antibody against HBcAg, for the treatment of HBV infection.
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PMID:Transbody against hepatitis B virus core protein inhibits hepatitis B virus replication in vitro. 2567 32

In Hepatitis B virus (HBV) infection, the virus generates numerous viral mRNAs/proteins and viral loads, which plays a major role in driving T cell tolerance, viral persistence, and hepatocellular carcinoma. However, currently available anti-HBV agents have no direct effect on viral mRNA transcription and protein expression. In this study, we designed a recombinant fusion of p53 protein with the cell-penetrating peptide PTD (protein transduction domain of trans-activator of transcription), which mediated p53 internalization into hepatocytes. PTD-p53 effectively suppressed HBV transcription and antigen expression by interaction with viral enhancers. We further provide evidence that PTD-p53 counteracts the viral transcription feedback loop and effectively suppressed HBV production of viral mRNAs, as well as HBsAg, HBeAg, and HBcAg, both in vitro and in vivo. Our results thereby provide a basis for developing a new therapeutic approach against HBV infection.
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PMID:PTD-fused p53 as a potential antiviral agent directly suppresses HBV transcription and expression. 2678 93

In hepatitis B virus (HBV) infection, the virus produces redundant hepatitis B surface antigen (HBsAg) that plays a key role in driving T-cell tolerance and viral persistence. However, currently available anti-HBV agents have no direct effect on HBsAg transcription and protein expression. In this study, we designed a heat shock protein gp96 inhibitor p37 with the cell penetrating peptide PTD (protein transduction domain of trans-activator of transcription), which mediated p37 internalization into hepatocytes. PTD-p37 effectively suppressed HBsAg expression and viral replication both in vitro and in vivo. We further provide evidence that PTD-p37 suppressed HBV enhancer/promoter activity via p53 upregulation. Moreover, PTD-p37 had antiviral activity against a lamivudine-resistant HBV strain. Considering that suppression of HBsAg expression is a major goal for treatment of HBV infection, our results provide a basis for developing a new therapeutic approaches targeting host factors against viral expression.
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PMID:A peptide-based inhibitor of gp96 suppresses HBsAg expression and HBV replication by upregulation of p53. 3120 72