Abstract

SIR-Silva et al. [1] suggested that in the population they have studied, isolated antibodies to hepatitis B core antigen (anti-HBc) are false-positive results. Their arguments are based on the facts that only five persons among the 133 investigated had hepatitis B virus (HBV) DNA detected in their serum and that most had a primary to HBV vaccination. However, as many as 47 persons (35%) in their study had antibodies to hepatitis B surface antigen (anti-HBs) as well, detectable by radioimmunoassay (groups C and D). The presence of this marker can be considered further evidence of previous contact with HBV. Among these 47 persons, only 19 (40%) had a response to HBV vaccine, as defined by the authors, indicating that a booster is not sensitive enough to predict a previous contact with the virus. This is confirmed by the fact that, among five persons with HBV DNA detectable by use of PCR, only three had vaccine responses of the booster type. Actually, at least 49 persons (37%) in the study of Silva et al. can be considered as having previous contact with HBV, rather than <20% as measured by vaccine type. Other investigators have demonstrated the inadequacy of HBV vaccination for predicting previous HBV infection in individuals with isolated anti-HBc [2]. A more effective strategy might be proposed to determine whether individuals have had a previous contact with the virus. I suggest screening for other HBV markers, such as antibodies to HBs antigen and antibodies to hepatitis B e antigen (HBe Ag). Determination of alanine aminotransferase activity, HBe Ag, and HBV DNA would also help to detect possible occult HBV carriers. The search for an associated hepatitis C infection could possibly identify patients with low levels of HBV replication [3]. The presence of occult HBV infection has been demonstrated in patients with isolated anti-HBc as well as in patients without any markers of HBV infection, and also after serological recovery from HBV infection [3-5]. In all these studies it has been demonstrated that the infection was still active. Several groups have reported the selection of surface (S) gene escape mutants of HBV in infants of HBV carrier mothers, probably due to the administration of hepatitis B immunoglobulins and vaccination [6, 7]. Transmissibility of these mutants and their maintenance as a dominant and stable viral population have been demonstrated [8, 9]. Thus, it is possible that HBV vaccination of patients with occult HBV infection leads to the selection of escape S mutants, thereby increasing circulation of these mutants in the population. Vaccination of individuals with previous contact with HBV could represent a risk for the community, because hepatitis B immunoglobulins and vaccine will probably be ineffective in preventing infections with escape S mutants and because such mutants can escape detection by conventional HBs antigen detection assays [7].

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