Francis V. Chisari

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Francis "Frank" Vincent Chisari (born 5 April 1942 in New York City)[1] is a physician, experimental pathologist, virologist, and immunologist, known for his research on virus-host interactions of hepatitis B and hepatitis C.[2]

Education and career[]

Chisari graduated in 1963 with a bachelor's degree in biology from Fordham University and in 1968 with an M.D. from Cornell University's Weill Medical College. He was in 1970 and 1971 a fellow in anatomic pathology at the Mayo Clinic and in 1972 a staff associate in immunopathology at the NIH's Laboratory of Pathology. In 1973 he completed his residency in internal medicine at Dartmouth Medical School. At Scripps Research he became a research fellow, then an assistant professor from 1975 to 1981, an associate professor from 1981 to 1988, and a full professor from 1988 to 2015, retiring as professor emeritus in 2015. At Scripps Research he headed the Division of Experimental Pathology from 1988 to 2008 and the Laboratory of Experimental Virology from 2008 to 2015. From 1983 to 1984 he was a Fogarty Scholar in molecular biology at the Institut Pasteur.[3] He is now a scientific advisor for Ionis Pharmaceuticals and for Vir Biotechnology.[4][5]

Chisari studies the immunological basis for viral clearance and disease pathogenesis during persistent viral infections, especially HBV and HCV, the signaling pathways and effector molecules that mediate these antiviral effects, and the viral evasion strategies that subvert them. He is most well known for demonstrating that chronic immune-mediated injury and inflammation can cause liver cancer and for discovering that antiviral T cells can purge viruses from infected cells noncytolytically by secreting antiviral cytokines that inhibit viral replication, thus controlling the infection while preserving the vital functions of the infected tissue.

Chisari’s group has made vast contributions to our understanding of the immunobiology and pathogenesis of hepatitis-B and hepatitis-C virus (HBV and HCV) infections, acute and chronic viral hepatitis and hepatocarcinogenesis ... In the 1980s, they produced a transgenic mouse model that overexpressed the large envelope protein of the hepatitis B surface antigen (HBsAg) and discovered that it induced severe, prolonged hepatocellular injury, an inflammatory response and regenerative hyperplasia of the remaining liver cells, resulting in the development of HCC ... This was the first transgenic mouse model in which the development of HCC was triggered by the function of a single viral protein.[6]

Chisari's laboratory developed cell-based models and animal models of HBV and HCV infection and performed foundational studies elucidating the T-cell response to these viruses in infected humans, subhuman primates, and transgenic mice. His group discovered that cytotoxic T lymphocytes (CTL) secrete antiviral cytokiness that inhibit viral replication in the liver cell without killing the cell, thus controlling the infection while preserving the life-saving function of the liver, a new paradigm in hepatitis B virus immunobiology. His research has informed novel immunotherapeutic approaches for the treatment of (chronic) hepatitis, via vaccination that triggers the production of antiviral cytokine-producing T cells and via the activation of dendritic cells.[7]

Chisari's laboratory first demonstrated that HCV RNA an be transmitted via exosomes from infected hepatocytes to uninfected hepatocytes while masked from detection by anti-HCV antibodies, identifying a unique mechanism for viral spread by escaping recognition by the immune response while in transit. They also demonstrated that exosomes released by infected cells can deliver HCV RNA to (nonpermissive) plasmacytoid dendritic cells, triggering an innate host response that was shown by many groups to exert a profound antiviral impact on viral spread, illustrating the existence of an elegant balance between virus and host mediated by HCV RNA-containing exosomes, a new paradigm in hepatitis C virus immunobiology.

Chisari has served on the editorial boards of many scientific journals, including the American Journal of Pathology, Hematology, the Journal of Clinical Investigation, the Journal of Immunology, the Journal of Virology, PLoS Pathogens, Virology, and Current Opinion in Virology.[3] He is the inventor or co-inventor for many patents on various peptides for treating or preventing viral infections caused by hepatitis-B or hepatitis-C.[8]

Awards and honors[]

Selected publications[]

References[]

  1. ^ biographical information from American Men and Women of Science, Thomson Gale 2004.
  2. ^ Jump up to: a b "Francis V. Chisari". National Academy of Sciences (nasonline.org).
  3. ^ Jump up to: a b "Frank Chisari, MD". Department of Immunology and Microbiology, Scripps Research.
  4. ^ "Francis V. Chisari, M.D." Vir Biotechnology (vir.bio).
  5. ^ "Vir Biotechnology".
  6. ^ Ohkoshi, S.; Hirono, K; Watanabe, K.; Hasegawa, K.; Yano, M. (2015). "Contributions of transgenic mouse studies on the research of hepatitis B virus and hepatitis C virus-induced hepatocarcinogenesis". World Journal of Hepatology. 7 (28): 2834–2840. doi:10.4254/wjh.v7.i28.2834. ISSN 1948-5182. PMC 4670955. PMID 26668695.
  7. ^ "Rous-Whipple Award - 1999, Francis V. Chisari" (PDF). American Society for Investigative Pathology.
  8. ^ "Patents by Inventor Francis V. Chisari". Justia Patents (patents.justia.com).
  9. ^ "Historic Fellows Listing". American Association for the Advancement of Science.
  10. ^ Chisari, Francis V. (2000). "Viruses, Immunity, and Cancer: Lessons from Hepatitis B". The American Journal of Pathology. 156 (4): 1117–1132. doi:10.1016/S0002-9440(10)64980-2. ISSN 0002-9440. PMC 1876872. PMID 10751335.
  11. ^ "Distinguished Achievement Award Recipients". American Association for the Study of Liver Diseases (aasld.org).
  12. ^ "Chisari, Francis V., Member Directory". National Academy of Medicine.
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