Hepatitis B e antibody (anti-HBe) emerges early in acute hepatitis B but fades after ALT peaks. Its persistence beyond three months post-illness onset suggests a potential shift to chronic infection. In chronic cases, a positive HBeAg indicates high viral replication and infectivity during the immune tolerant and early clearance phases. The critical transition, HBeAg seroconversion, marks the shift from HBeAg to anti-HBe. Following this change, most patients enter an inactive HBsAg carrier state, showing low HBV DNA, normal ALT, and limited liver inflammation. However, persistent liver disease and detectable HBV DNA can persist due to wild-type virus or mutations hindering HBeAg secretion, like precore or basal core promoter mutations.
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