Hepatitis B e antigen (HBeAg) plays a pivotal role in the trajectory of hepatitis B viral infection. Its appearance signals active viral replication, often concurrent with hepatitis B surface antigen (HBsAg). As the infection progresses, a decline in HBeAg with a subsequent shift to e antibody (anti-HBe) reflects a reduction in viral load and decreased infectivity, especially notable during antiviral therapy, indicating a more favorable long-term prognosis. However, in chronic hepatitis B, the absence of detectable HBeAg, coupled with the presence of anti-HBe and hepatitis B virus DNA in serum, poses challenges as it may signify ongoing viral activity despite the absence of a key antigen. Monitoring this subset of patients becomes crucial due to the potential for persistent infection. The transition from HBeAg positivity to anti-HBe serves as a critical marker in assessing the efficacy of treatment, often indicating a successful virological response in managing chronic hepatitis B infections. Understanding these antigenic dynamics is fundamental in both diagnosing the disease’s stage and guiding appropriate therapeutic interventions
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