William S. Mason, PhD, Emeritus
- 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
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.
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