Raymond Chung, MD
Director of Hepatology and Liver Center. Vice Chief Gastrointestinal Division. Kevin and Polly Maroni Research Scholar. Massachusetts General Hospital
Contact: email@example.com (617) 724-7562
Dr. Chung’s group focuses on the medical complications of drug use, including acute and chronic hepatitis C virus infection, cirrhosis, and HIV infection. His group helped define the genetic determinants of spontaneous clearance of HCV, and has been instrumental in defining mechanisms of accelerated liver disease progression in persons with HCV-HIV co-infection. His group is interested in understanding how the medical complications of drug use, coupled with the effects of drug use itself, contribute to hepatic fibrosis. Dr. Chung currently mentors eight post-doctoral fellows and four pre-doctoral trainees.
Mechanisms of immune failure in chronic infection: Hepatitis C as a key paradigm
NIAID U19 AI082630 2014-19
The overall objective is to define the mechanisms by which hepatitis C virus (HCV) can establish a chronic infection in the face of adaptive host immune responses. The Center is comprised of four research projects, an administration Core (Core A), a Pilots Project Core (Core B), and three scientific cores: a Tissue & Clinical Core (Core C) a Virology Core (Core D) and a Antibody and Fusion Protein Core (Core E).
Patient-oriented research on hepatitis in special populations
NIDDK K24 DK078772 2007-18
Mid-Career Investigator Award in Patient-Oriented Research to allow PI to mentor fellows and junior faculty in initiation of patient-oriented research careers in the study of HCV-related disease in special populations, predominantly in (a) HCV and HIV coinfection and (b) the relationship between HCV and insulin resistance and initiate innovative pilot clinical trials in difficult to treat HCV-related liver disease based on key observations from our mechanistic work.
HIV-hepatitis C virus cooperative interactions and liver disease progression
NIDDK R01 DK098079 2013-18
The goals of the current proposal are to (1) extend our studies to evaluate the specific contributions of HCV and HIV to fibrosis progression for the first time in in vivo models; (2) evaluate the contribution of microbial translocation to fibrogenesis; and (3) evaluate the effect of antiretroviral therapy on cooperative HCV-HIV fibropathogenesis.
Harvard hepatitis B consortium
NIDDK U01 DK082919 2008-20
As part of the NIDDK Hepatitis B Clinical Trials Network, the Harvard Hepatitis B Consortium seeks to promote translational research on hepatitis B focusing upon elucidating the pathogenesis and natural history and developing means of treatment and control.
HIV-associated macrophage alterations and liver disease
NIDDK R01 DK108370 2015-20
This proposal will explore the hypothesis that HIV accelerates liver disease progression through its alteration of the hepatic macrophage phenotype to a more pro-fibrotic state and antiretroviral therapy partially but does not completely reverse this state
HIV, HCV, YAP-TAZ and liver disease progression
NIAID R01 AI36715 2017-22
The specific aims of this project are to: 1) define the contribution of YAP/TAZ pathway activation to hepatic fibrogenesis in the context of HCV and other liver diseases; 2) determine the mechanism(s) by which HIV induces YAP/TAZ activation with/without HCV; and 3) define the contribution of the extracellular matrix to HIV-mediated YAP/TAZ activation
Hepatic fibrosis project
Boehringer Ingelheim International. 2016- 19
The major goals of this project are to identify, 1) small molecules that can revert primary human HSC myifibroblasts into non-fibrotic quiescent HSCs and 2) genes whose products are required to maintain the HSC myofibroblast state
Janssen liver biopsy consortium
Janssen Pharmaceutical, Inc. 2017- 23
The goals of the liver biopsy collaboration is to: 1) develop a liver sampling methodology applicable for multisite studies allowing systematic analysis of immunological profiles in chronic HBV patients, 2) identify the critical cellular and molecular drivers for evolution to permanent immune control in the liver of chronic HBV patients