The AUTOBIO hepatitis B e antigen (HBeAg) chemiluminescence immunoassay (CLIA) is intended for the quantitative determination of HBeAg concentration in human serum and plasma.
Hepatitits B is a disease caused by viral infection. The route of infection can be improper needle puncture, blood transfusion or even by taking contaminated food or water. Hepatitis B is an immune disease. Invasion of the human body by Hepatitis B virus induces autoimmune reactions, which damage the liver.
The Hepatitis e antigen (HBeAg) is a peptide and normally detectable in the bloodstream when the hepatitis B virus is actively reproducing, this in turn leads to the person being much more infectious and at a greater risk of progression to liver disease. The exact function of this non structural protein is unknown, however it is thought that HBeAg may be influential in suppressing the immune systems response to HBV infection. HBeAg is generally detectable at the same time as HBsAg and disappears before HBsAg disappears. The presence of HBeAg in chronic infection is generally taken to indicate that HBV is actively reproducing and there is a higher probability of liver damage. In acute infection HBeAg is generally only transiently present. However mutant strains of HBV exist that replicate without producing HBeAg.
The present studies suggest that quantitation of HBeAg in serum may be a useful adjunct to serum HBV DNA assays to fully evaluate the response to antiviral therapy in patients treated with peginterferon. Among patients who ultimately achieved HBeAg seroconversion, levels of HBeAg decreased consistently and remained at the lowest levels during the follow-up period. In contrast, a rebound was observed in patients who failed to achieve seroconversion after treatment was discontinued. In addition, analysis of HBeAg levels after 24 weeks of treatment provided a better indicator of nonresponse to peginterferon alfa-2a than did a similar analysis of HBV DNA levels. Quantifying HBeAg during therapy also allowed demarcation of late responders from nonresponders, a subgroup of patients who were not differentiated by changes in HBV DNA levels. Among late HBeAg responders, HBV DNA levels were lower than for non-HBeAg responders. The analysis we conducted in this study suggests that quantification of HBeAg may be a useful clinical tool for predicting the absence of response to peginterferon alfa-2a in an individual patient. Our results suggest that a critical level of reduction of HBeAg may be definable which, if not achieved by patients undergoing treatment, may indicate that a discontinuation of peginterferon monotherapy should be considered.
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