Guangxiang Luo
Wake Forest University, NC·Microbiology & Immunology
Hepatitis B virus (HBV) infects the liver and can cause long-lasting hepatitis, scarring, cirrhosis and liver cancer. More than 250 million people carry it, and roughly a million die each year.
- Fields
Microbiology & Immunology
Biochemistry
Medicine & Clinical Research
- Topics
hepatitis B virus
apolipoprotein E
apoE
- Grants
- 2 known grants, through Apr 2029
What they work on
- 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.
- Construct mouse models in which HBV infection persists, to study long-term replication, cccDNA (the stable viral DNA that drives persistence), and pathogenesis.
- Build an immunodeficient mouse model of HBV infection and use it to determine how host immune responses control or fail to control the virus.
- Test whether apolipoprotein E is required for infection and particle production by clinical HBV isolates from patients, using apoE knockdown and knockout cells.
- Identify which apoE-binding receptors — heparan sulfate proteoglycans and LDL receptor family proteins — and which apoE–receptor contacts are needed for efficient HBV entry.
- Define the molecular mechanism by which apoE is incorporated into HBV virions and promotes morphogenesis, the assembly and release of infectious particles.
More about the research
Vaccines prevent new infections but do nothing for people already infected. The reason chronic infection is so hard to cure is a stable circular form of the viral genome inside liver-cell nuclei, called covalently closed circular DNA (cccDNA); current drugs (interferon and nucleoside analogs) suppress virus production but leave cccDNA intact. Two obstacles have slowed progress: there has been no small animal that HBV reliably infects, and the molecular steps by which HBV enters cells and assembles new particles are incompletely known. The lab's two projects attack both obstacles, and both center on one unexpected player: human apolipoprotein E (apoE), a fat-carrying blood protein.
Why it matters
Chronic hepatitis B affects roughly 250 million people and causes about a million deaths a year, and no current therapy clears the viral cccDNA that sustains it. Mouse models that support real HBV infection and replication would give researchers a way to study how the virus causes liver disease and cancer and to test candidate drugs in a living animal. Identifying apoE and its receptors as host factors the virus depends on could supply new molecular targets for antiviral drugs aimed at curing chronic infection.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
J.-H. James Ou
University of Southern California, CA·Microbiology & Immunology
Identify maternal HBV factors that support virus replication in offspring and weaken their anti-HBV immunity, using mice born to HBV transgenic mothers.
Justin Bailey
Johns Hopkins University, MD·Microbiology & Immunology
Test whether a dengue vaccine's serotype composition determines the balance, neutralizing potency, and durability of serotype-specific versus cross-reactive memory B cells and monoclonal antibodies, and whether those responses predict protection after controlled human challenge with serotype 2.
The school
Wake Forest University: 27 labs on PI Pages, $345M a year on research, 54 research doctorates a year.
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