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Hepatitis B surface antigen (HBsAg) is frequently used as the primary marker of current hepatitis B virus (HBV) infection, and thus infectivity. However, there are reports of serologically negative patients, both with and without disease, who have HBV DNA in serum, liver, and/or mononuclear cells (1). Immune-selected HBsAg variants can persist in the presence of anti-HBsAg antibodies (anti-HBs) (2). As both variants and standard viruses can be detected using nucleic acid amplification methods such as polymerase chain reaction (PCR), HBsAg can no longer be considered the “gold standard” marker of current infection (3). Second episodes of hepatitis B, defined by the reappearance of HBsAg or HBV DNA in serum, are well described (4, 5). A history of clinical recovery from acute hepatitis B followed by HBsAg loss may not always help in classifying a second episode of hepatitis B as reinfection, because latent HBV infections occur in the absence of serological markers of active infection (6). Here, we describe two cases of HBsAg reappearance that may have been reinfection or reactivation and discuss the molecular criteria to distinguish between these two possibilities. CASE REPORTS |
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