Hepatitis B Virus and HLA Antigen Display in the Liver During Chronic Hepatitis B Virus Infection

✍ Scribed by Luis Montan̄to; Guido C. Miescher; Alison H. Goodall; Karl H. Wiedmann; George Janossy; Howard C. Thomas

• Publisher: John Wiley and Sons
• Year: 2007
• Tongue: English
• Weight: 651 KB
• Volume: 2
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.1840020508

✦ Synopsis

An analysis of the expression of the histocompatibility antigens in the livers of patients with chronic hepatitis B virus infection and normal subjects has demonstrated an increased expression of HLA-A,B,C antigens on the hepatocytes of patients with a low level of viral replication (HBe antibody positive) as compared with patients who exhibit a high level of viral replication (HBe antigen positive) and controls. This increase in the expression of histocompatibility antigens on the hepatocytes was associated with a decrease in the membrane expression of viral antigens by the same cells. These differences in the density of HLA and viral antigen display may influence the efficiency of T-cell cytolysis of hepatitis B virus-infected hepatocytes.

One of the most common viral infections of man is that caused by hepatitis B virus (HBV). Ninety per cent of patients infected develop an acute illness from which they recover, and 10% develop chronic infection which may lead to chronic liver disease and primary liver cell cancer (1, 2). It has been suggested that the failure of these patients to eliminate the virus is dependent, on a relative failure of cell-mediated immunity (3).

Studies in the mouse have demonstrated that the histocompatibility antigens play an important role in the initiation of the immune response to a virus (4, 5). The association of viral antigens with the Ia antigens on the surface of specialized macrophages is thought to be recognized by inducer (helper) T-lymphocytes which then assist in priming the cytotoxic T-lymphocytes and in initiating the production of sensitized B-lymphocytes (5, 6). The elimination of the virus-infected cells is then dependent on recognition by sensitized cytotoxic T-cells of the viral antigen in association with the H-2k and H-2d antigens in the cell membrane (4, 7).

Studies of the composition of the inflammatory infd-