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Lau JY, Bird GL, Naoumov NV, et al. Hepatic HLA antigen display in chronic hepatitis B virus infection. Relation to hepatic expression of HBV genome/gene products and liver histology. Dig Dis Sci. 1993;38(5):888-95doi: 10.1007/BF01295916.
Lau, J. Y., Bird, G. L., Naoumov, N. V., & Williams, R. (1993). Hepatic HLA antigen display in chronic hepatitis B virus infection. Relation to hepatic expression of HBV genome/gene products and liver histology. Digestive diseases and sciences, 38(5), 888-95. https://doi.org/10.1007/BF01295916
Lau, J Y, et al. "Hepatic HLA antigen display in chronic hepatitis B virus infection. Relation to hepatic expression of HBV genome/gene products and liver histology." Digestive diseases and sciences vol. 38,5 (1993): 888-95. doi: https://doi.org/10.1007/BF01295916
Lau JY, Bird GL, Naoumov NV, Williams R. Hepatic HLA antigen display in chronic hepatitis B virus infection. Relation to hepatic expression of HBV genome/gene products and liver histology. Dig Dis Sci. 1993 May;38(5):888-95. doi: 10.1007/BF01295916. PMID: 7683263.
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Dig Dis Sci. 1993 May;38(5):888-95. doi: 10.1007/BF01295916.

Hepatic HLA antigen display in chronic hepatitis B virus infection. Relation to hepatic expression of HBV genome/gene products and liver histology.

Digestive diseases and sciences

J Y Lau, G L Bird, N V Naoumov, R Williams

Affiliations

  1. Department of Medicine, University of Florida, Gainesville 32610.

PMID: 7683263 DOI: 10.1007/BF01295916

Abstract

To determine the relationship between hepatitis B virus (HBV) replication and HLA antigen display at a cellular level, the hepatic expression of HLA antigens and HBV genome (HBV-DNA)/gene products (HBsAg/HBcAg) was studied in 24 patients with chronic HBV infection using simultaneously immunohistochemistry and nonisotopic in situ hybridization. The effect of interferon-alpha and interferon-gamma on hepatocyte HLA antigen expression was also evaluated using primary hepatocyte culture in eight patients with chronic HBV infection. HLA class I antigens were detected on hepatocyte membrane in 23 patients (95.8%). Hepatocytes positive for HBcAg and HBV-DNA (cytoplasmic +/- nuclear) were either negative or only faintly positive for HLA class I antigens, while hepatocytes positive for HBsAg showed similar levels of HLA class I antigen expression compared with those hepatocytes with no HBsAg expression. In contrast, hepatocytes adjacent to inflammatory infiltrates, whether positive for HBV-DNA or HBV antigens or not, were always strongly positive for HLA class I antigens. Furthermore, active liver histology (N = 12) was associated with a higher overall level of hepatic HLA class I antigen expression as compared with inactive histology (N = 12, P = 0.003). Both interferon-alpha and interferon-gamma treatment in vitro enhanced hepatocyte HLA class I antigen expression. These data indicate that expression of HLA class I antigens is not enhanced on the membrane of hepatocytes with HBV replication, and this may be one factor that permits the development of viral persistence.

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