J.-H. James Ou
University of Southern California, CA·Microbiology & Immunology
Hepatitis B virus (HBV) chronically infects hundreds of millions of people. It can cause liver scarring (cirrhosis) and liver cancer, and it leads to about a million deaths each year.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
Pharmacology
- Topics
hepatitis B virus
chronic hepatitis B
mother-to-child transmission
- Grants
- 3 known grants, through Mar 2030
What they work on
- Identify maternal HBV factors that support virus replication in offspring and weaken their anti-HBV immunity, using mice born to HBV transgenic mothers.
- Determine how HBV antigens cross the placenta and genetically reprogram fetal Kupffer cells, the liver's resident macrophages, into an anti-inflammatory state.
- Define how HBV e antigen (HBeAg) shifts macrophage metabolism toward oxidative phosphorylation, and test whether toll-like receptor 4 (TLR4) acts as its receptor.
- Test whether HBeAg alone is enough to promote HBV persistence and to train Kupffer cells in the womb.
- Test whether IL-1β and the diabetes drug repaglinide suppress HBV gene expression and clear infection, in human hepatocytes and in transgenic, persistent-infection and humanized FRG mice, alone and with entecavir.
More about the research
Most lifelong carriers caught the virus from their mothers early in life, while adults infected by other people usually clear it. These projects ask why the virus persists, especially after mother-to-child transmission, and how to turn its genes off. HBV infects very few species. To study it, the lab built a mouse model in which pups born to HBV-carrying mothers cannot clear the virus.
Why it matters
Current HBV drugs block viral copying but do not silence the viral genome, so most patients never reach a lasting response. Two of these projects explain why infections passed from mother to child become chronic, which could point to new treatment targets. The third could yield new therapies by testing whether IL-1β or the repurposed diabetes drug repaglinide can shut down viral gene expression and move patients toward a "functional cure."
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Guangxiang Luo
Wake Forest University, NC·Microbiology & Immunology
Develop an immunocompetent mouse model of hepatitis B virus infection and replication by co-expressing the entry receptor NTCP with human apolipoprotein E3 and LDLR in mice lacking PCSK9, a protein that degrades LDLR.
Zhongde Wang
Utah State University, UT·Microbiology & Immunology
Create a humanized-NTCP Syrian hamster using CRISPR gene editing to change the two codons in the hamster NTCP entry receptor that encode the amino acid residues required for hepatitis B virus infection.
Eva Billerbeck
Albert Einstein College of Medicine, NY·Microbiology & Immunology
Define the functional roles of distinct virus-specific effector and memory CD8+ killer T cell subsets in the liver during Norway rat hepacivirus infection, using high-dimensional flow cytometry and transcriptome analysis.
The school
University of Southern California: 47 labs on PI Pages, $1.3B a year on research, 882 research doctorates a year.
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