Eva Billerbeck
Albert Einstein College of Medicine, NY·Microbiology & Immunology
The liver is an unusual immune environment: it must tolerate a constant flow of foreign material from the gut while still fighting off viruses that target it. That balance matters clinically, because in chronic hepatitis C virus infection T cells are both the cells that can clear the virus and a source of the tissue injury that progresses to scarring (fibrosis) and liver cancer.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
Biology
- Topics
hepatitis C virus
hepacivirus
NrHV
- Grants
- 1 known grant, through May 2027
What they work on
- 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.
- Determine when CD4+ helper T cells act during hepacivirus infection and how they influence the generation of virus-specific CD8+ T cells and protective immunity on re-infection, using in vivo functional approaches in mice.
- Delineate the function of liver CD8+ T cells and NKT cells polarized toward type 2 immunity, the program linked to allergy and tissue repair, and test their impact on liver damage, virus-specific T cells and other hepatic immune cells across acute and chronic infection.
- Translate the main mouse findings to human disease by testing whether the identified type 1 and type 2 hepatic T cell and NKT cell subsets are present in patients with hepatitis C virus infection.
More about the research
Which T cell subsets protect and which do harm has been hard to determine, because human liver tissue is scarce and hepatitis C virus does not infect ordinary laboratory mice. This work addresses that gap using a mouse model the lab developed: infection with Norway rat hepacivirus, a close relative of hepatitis C that infects mice with intact immune systems and reproduces many virological and immunological features of human infection.
Why it matters
Hepatitis C still has no vaccine, and inflammatory liver disease can progress to fibrosis and liver cancer even after the virus is addressed. Distinguishing the liver T cell subsets that clear virus from those that drive or limit tissue damage could guide vaccine strategies that elicit the protective populations, and suggest immunotherapies that reduce liver injury in patients with progressive liver disease.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Ranjit Ray
Saint Louis University, MO·Microbiology & Immunology
Test whether introducing discrete point mutations into the hepatitis C virus E2 envelope protein, blocking its binding to the cell-surface receptor CD81, prevents E2 from suppressing immune cell function.
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.
Martin Joseph Richer
Indiana University-Purdue University-Indianapolis, IN·Microbiology & Immunology
Identify the extrinsic mechanisms, signals from outside T cells, through which a high-salt diet impairs CD8 T-cell responses to acute viral infection in mice.
The school
Albert Einstein College of Medicine: 21 labs on PI Pages, $361M a year on research, 36 research doctorates a year.
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