Genetic studies on hepatitis B virus(HBV) carriers.

Watanabe, Fumitoki; Zeniya, Mikio; Aizawa, Yoshifusa; Andoh, Hideki; Ohkoshi, Hirofumi; Miyazaki, Hiroshi; Kameda, Haruo; Andoh, Asako; Inoko, Hidetoshi; Tsuji, Kimiyoshi

doi:10.2957/kanzo.30.614

Cited by 3 publications

(2 citation statements)

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“…3 Most studies to date of HBV and HCV have employed this method of study, but difficulties involved in designing such studies include an inappropriate control group (detailed later) or a small number of study participants. [14][15][16][17][18][19][20][21] The control group in most of the viral hepatitis studies is from the general population [22][23][24][25][26][27][28] or from blood or bone marrow donors, [29][30][31] which can lead to a misclassification bias because some of these individuals may not have been exposed to the virus. In such cases, true associations may be missed because unexposed subjects capable of becoming infected are included as controls.…”

Section: Thio Thomas and Carringtonmentioning

confidence: 99%

“…All of these studies examined associations with persistence of HBV and a few studies additionally examined disease progression. 14,15,[22][23][24][28][29][30][36][37][38][39] Seven of the twelve studies used controls who had cleared the infection, 14,15,28,29,36,37,39 and the remainder used controls from the general population. None of the seven identified associations between class I alleles and viral persistence, but only one used molecular typing.…”

Section: Hepatitis B Virusmentioning

confidence: 99%

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Chronic viral hepatitis and the human genome

Thio¹,

Thomas²,

Carrington

2000

Hepatology

109

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Section: Thio Thomas and Carringtonmentioning

confidence: 99%

Section: Hepatitis B Virusmentioning

confidence: 99%

Chronic viral hepatitis and the human genome

Thio¹,

Thomas²,

Carrington

2000

Hepatology

109

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Analysis of HLA alleles in Japanese patients with cirrhosis due to chronic hepatitis C

Higashi

Kamikawaji

Suko

et al. 1996

J of Gastro and Hepatol

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Hepatitis C virus (HCV) leads to chronic liver disease in at least 50-60% of infected people and approximately 40-50% of these patients will go on to develop cirrhosis due to chronic hepatitis C (HCV-C). The pathogenic mechanisms that result in HCV-C are unknown. Sixty Japanese patients with HCV-C were examined for HLA-A, B, C and DR alleles by serologic typing and for HLA-DQB1 alleles by DNA typing using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. As the control population, 293 healthy un-related Japanese were used. The frequencies of HLA-B61, C(omega)3, DR4, DQB1*0401 and DQB1*0402 were increased, while those of HLA-DR9, DQB1*0301 and DQB1*0303 were decreased in the patients. The co-ordinate increase in the frequency of HLA-DR4, DQB1*0401 or 0402 and decrease in the frequency of DR9 or DQB1*0303 were suggestive of a strong linkage disequilibrium between HLA-DR4 and DQB1*0401 or 0402 and between HLA-DR9 and DQB1*0303, respectively. From the odds ratio (OR) analysis, the combinations of HLA-C(omega)3+ DR4-DQB1*0401 or 0402, or HLA-B61 + DR4 - DQB1*0401 or 0402 increased the risk for developing HCV-C when compared to each HLA allele alone. This suggested an additive effect for these classes I and II HLA allele combinations in HCV-C. In contrast, HLA-DR9-DQB1*0303 and DQB1*0301 may confer resistance to this disease. These results suggest the existence of HLA-linked susceptibility genes to HCV-C.

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The Effects of Recombinant Interleukin 2 on HBe Antigen Positive Chronic Hepatitis B.

et al. 1991

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Recombinant interleukin (IL-2) was administered to 16 patients with HBeantigen-positive chronic active hepatitis in which the diagnosis was ascertained histologically. In 7 of the 16 patients, a decrement of the serum HBe antigen value was observed (Group A). In group A, the findings showed an increment of peripheral Leu ll-positive cells and NKand LAKcell activity, an acute exacerbation during and after IL-2 administration, disappearance of HBe antigen observed in liver biopsy histology, and decrement of serum DNA-pactivity. However,seroconversion of HBsantigen was not observed and no case showedthe elimination status of continuous HBvirus infection. On the other hand, in the other 9 patients (Group B), these changes were not observed and the existence of a HLAtype difference between Group A and B was shown by HLAanalysis. These results indicated that the immuneresponses mediated by IL-2 may play an important role in the development of chronic hepatitis B, and these results maybe regulated genetically.

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Genetic studies on hepatitis B virus(HBV) carriers.

Cited by 3 publications

References 0 publications

Chronic viral hepatitis and the human genome

Chronic viral hepatitis and the human genome

Analysis of HLA alleles in Japanese patients with cirrhosis due to chronic hepatitis C

The Effects of Recombinant Interleukin 2 on HBe Antigen Positive Chronic Hepatitis B.

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