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[Association between hepatitis B surface antigenemia and HLA histocompatibility phenotypes]
To test whether HLA histocompatibility phenotypes might be associated with circulating hepatitis B surface antigen (HBsAg), we performed chi-square test with Yate's correction and Fisher's exact test on findings in 315 normal healthy hospital staffs with known HLA types and HBsAg status. A significant relation between locus A of HLA types and HBs antigenemia was demonstrated, with negative association suggested between A1, AW23, A26, A29, +AW30 +AW31 and AW32 types and HBs antigenemia. Another significant relation between locus B of HLA types and HBs antigenemia was shown, with negative association suggested between B7, B8, BW21, BW44 and BW49 and HBs antigenemia. There was no significant relation between locus C of HLA type and HBs antigenemia, but type CW4 was revealed to have a relative risk of 2.11. Therefore, previous suggestion that both susceptability and resistance to hepatitis B virus infection may be in part genetically determined and previous observation of population differences in HBsAg prevalences could be interpreted by these findings.
To test whether HLA histocompatibility phenotypes might be associated with circulating hepatitis B surface antigen (HBsAg), we performed chi-square test with Yate's correction and Fisher's exact test on findings in 315 normal healthy hospital staffs with known HLA types and HBsAg status. A significant relation between locus A of HLA types and HBs antigenemia was demonstrated, with negative association suggested between A1, AW23, A26, A29, +AW30 +AW31 and AW32 types and HBs antigenemia. Another significant relation between locus B of HLA types and HBs antigenemia was shown, with negative association suggested between B7, B8, BW21, BW44 and BW49 and HBs antigenemia. There was no significant relation between locus C of HLA type and HBs antigenemia, but type CW4 was revealed to have a relative risk of 2.11. Therefore, previous suggestion that both susceptability and resistance to hepatitis B virus infection may be in part genetically determined and previous observation of population differences in HBsAg prevalences could be interpreted by these findings.