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There have been great strides in understanding the virology and immune response of HBV infection, but the molecular mechanisms whereby the host fails to clear the virus and develops chronic infection remain largely unknown. In addition, the adaptive evolution of virus under host immune pressure remains to be elucidated. Finally, the pathogenesis of various extra-hepatic manifestations associated with HBV infection is poorly understood. Further research in these areas is crucial not only in better understanding the natural history and disease progression but also in improving treatment for chronic hepatitis B.
What is the genetic basis of the diverse clinical manifestations and disease outcomes of HBV infection? With the recent advances in genetic and genomic medicine, there are increasing opportunities to elucidate the genetic basis for variations in expression and susceptibility to HBV-associated diseases.
Genome-wide association studies and other genomic technological advances would provide crucial information to identify useful genetic markers for disease outcome, clinical manifestations, and treatment response of HBV-associated disease. Potential conflict of interest: Nothing to report.
National Center for Biotechnology Information , U. Author manuscript; available in PMC Jan Jake Liang. Author information Copyright and License information Disclaimer.
Copyright notice. The publisher's final edited version of this article is available at Hepatology. See other articles in PMC that cite the published article. Abstract Hepatitis B virus HBV infects more than million people worldwide and is a common cause of liver disease and liver cancer.
Open in a separate window. Diagnosis and Serology HBV infection leads to a wide spectrum of liver disease ranging from acute hepatitis including fulminant hepatic failure to chronic hepatitis, cirrhosis, and hepatocellular carcinoma HCC. The clinical course and serologic profiles of A acute and B chronic hepatitis B.
Acute Hepatitis B About two-thirds of patients with acute HBV infection have a mild, asymptomatic and subclinical illness that usually goes undetected. Chronic Hepatitis B Chronic hepatitis B has a variable and dynamic course. Important Questions and Needs for Future Research How does HBV establish productive infection in vivo and what is the host response early during the infection?
Footnotes Potential conflict of interest: Nothing to report. References 1. Ganem D, Schneider RJ. Hepadnaviridae and their replication. Fields Virology. Hepatitis B virus. Structure of hepatitis B surface antigen: characterization of the lipid components and their association with the viral proteins. J Biol Chem. Gerlich W, Robinson WS. J Virol. Milich D, Liang TJ. Exploring the biological basis of hepatitis B e antigen in hepatitis B virus infection.
X-deficient woodchuck hepatitis virus mutants behave like attenuated viruses and induce protective immunity in vivo. J Clin Invest. Altered proteolysis and global gene expression in hepatitis B virus X transgenic mouse liver. The enigmatic X gene of hepatitis B virus. Genetic and biochemical evidence for the hepatitis B virus replication strategy. Yee J. A liver-specific enhancer in the core promoter region of human hepatitis B virus.
Hepatitis B virus DNA contains a glucocortcoid response element. Huang J, Liang TJ. Mol Cell Biol. Klingmuller U, Schaller H. Hepadnavirus infection requires interaction between the viral pre-S domain and a specific hepatocellular receptor. Carboxypeptidase D gp , a Golgi-resident protein, functions in the attachment and entry of avian hepatitis B viruses. Phosphorylation of hepatitis B virus Cp at Ser87 facilitates core assembly.
Biochem J. Kock J, Schilicht H-J. Analysis of the earliest steps of hepadnavirus replication genome repair after infectious entry into hepatocytes does not depend on viral polymerase activity. Internal entry of ribosomes and ribosomal scanning involved in hepatitis B virus P gene expression.
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