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William S. Mason, PhD, Emeritus

About

Professor Emeritus

Research Program

Focus of virus free hepatocytes in a woodchuck liver chronically infected with WHV
Clonal expansion of hepatocytes in a chimpanzee chronically infected with HBV

 

Education, Training & Credentials

Educational Background

  • Postdoctoral Fellow, University of Southern California, Los Angeles, CA, 1971-1973
  • PhD, Biophysics, University of Chicago, Chicago, IL, 1971
  • BS, Mathematics, Stevens Institute of Technology, Hoboken, NJ, 1965
Research Profile

Research Program

Research Interests

Hepatitis B virus (HBV) chronically infects hepatocytes, the major parenchymal cell of the liver. Hepatocytes represent a long-lived, self-replenishing population in the healthy liver. If the immune system fails to clear the infection within a few months, individuals usually remain infected for life. Chronic infections lead to chronic liver injury, cirrhosis and hepatocellular carcinoma (HCC). The primary cause of these diseases is the injury caused by the antiviral immune response to infected hepatocytes, as infection per se does not appear to be cytotoxic. The goal of ongoing research is to test the hypothesis that chronic immune killing of infected hepatocytes selects for clonal expansion of hepatocytes that have lost the ability to support HBV replication. Clonal hepatocyte repopulation of the liver is an HCC risk factor.

Publications

Selected Publications

Seeger C, Zoulim F, Mason WS. Hepadnaviruses. In: Fields Virology (Knipe D, Howley P, eds), 6th Edition, Chapter 69, pp. 2185-2221. Lippincott, Williams, and Wilkins, 2013.

Seeger C, Mason WS. Sodium-dependent taurocholic cotransporting polypeptide: a candidate receptor for human hepatitis B virus. Gut. 2013:62:1093-95. PubMed

Cai D, Mills C, Yu W, Yan R, Aldrich CE, Saputelli JR, Mason WS, Xu X, Guo JT, Block TM, Cuconati A, Guo H. Identification of the disubstituted sulfonamide compounds as specific inhibitors of hepatitis B virus covalently closed circular DNA formation. Antimicrob Agents Chemother. 2012;56:4277-78. PubMed

Zoulim F, Mason WS. Reasons to consider earlier treatment of chronic HBV infections. Gut. 2012;61:333-6. PubMed

Mason WS, Low HC, Xu C, Aldrich CE, Scougall CA, Grosse A, Clouston A, Chavez D, Litwin S, Peri S, Jilbert AR, Lanford RE. Detection of clonally expanded hepatocytes in chimpanzees with chronic hepatitis B virus infection. J Virol. 2009 Sep;83(17):8396-408.PubMed

Reaiche GY, Le Mire MF, Mason WS, and Jilbert AJ. The persistence in the liver of residual duck hepatitis B virus covalently closed circular DNA is not dependent upon new viral DNA synthesis. Virology. 2010 Oct 25;406(2):286-92. Epub 2010 Aug 12. PubMed

Mason WS, Liu C, Aldrich CE, Litwin S, and Yeh MM. Clonal expansion of normal appearing hepatocytes during chronic HBV infection. J Virol. 2010;84:8308-15. PubMed

Seeger C, Lai MMC, and Mason WS. Molecular Biology of Hepatitis Viruses. In "The liver, biology and pathobiology", 5th edition. Lipincott, Williams & Wilkins, NY.

Mason WS, Low HC, Xu C, Aldrich CE, Scougall CA, Grosse A, Clouston A, Chavez D, Litwin S, Peri S, Jilbert AR, Lanford RE. Detection of clonally expanded hepatocytes in chimpanzees with chronic hepatitis B virus infection. J Virol. 2009;83:8396-408. PubMed

Mason WS, Xu C, Low HC, Saputelli J, Aldrich CE, Scougall C, Grosse A, Colonno R, Litwin S, Jilbert AR. The amount of hepatocyte turnover that occurred during resolution of transient hepadnavirus infections was lower when virus replication was inhibited with entecavir. J Virol. 2009 Feb;83(4):1778-89. PubMed