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T. Jake Liang

Researcher at National Institutes of Health

Publications -  241
Citations -  25949

T. Jake Liang is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Hepatitis C virus & Hepatitis C. The author has an hindex of 85, co-authored 233 publications receiving 24158 citations. Previous affiliations of T. Jake Liang include Harvard University & United States Department of Health and Human Services.

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Systematic review: the effect of preventive lamivudine on hepatitis B reactivation during chemotherapy.

TL;DR: Preventing hepatitis B virus reactivation among patients with cancer who test positive for hepatitis B surface antigen (HBsAg) and are undergoing chemotherapy with lamivudine is found to reduce risk of HBV reactivation and associated death.
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Hepatitis C Virus Structural Proteins Assemble into Viruslike Particles in Insect Cells

TL;DR: A model for the production and purification of HCV-like particles in insect cells using a recombinant baculovirus containing the cDNA of the HCV structural proteins is described, suggesting that HCV core and envelope proteins without p7 were sufficient for viral particle formation.
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Hepatitis B Reactivation Associated With Immune Suppressive and Biological Modifier Therapies: Current Concepts, Management Strategies, and Future Directions.

TL;DR: This review provides a comprehensive update on the current concepts, risk factors, molecular mechanisms, prevention, and management of hepatitis B reactivation and provides recommendations for future research in this area.
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Progression of fibrosis in chronic hepatitis C

TL;DR: The best predictors of fibrosis progression in CHC are the extent of serum aminotransferase elevations and the degree of hepatocellular necrosis and inflammation on liver biopsy.
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Exploring the biological basis of hepatitis B e antigen in hepatitis B virus infection

TL;DR: Clinical and experimental data suggest that serum HBeAg may serve an immunoregulatory role in natural infection and its ability to activate or tolerize T cells show the complexity of the interactions between the H beAg and the host during HBV infection.