Detection of hepatitis B virus DNA in the serum of Canadian hepatitis B surface antigen negative, anti‐HBc positive individuals, using the polymerase chain reaction

Abstract

Continuing hepatitis B virus (HBV) infection is normally associated with the presence of hepatitis B surface antigen (HBsAg) in the serum. In spite of sensitive screening assays for HBsAg, rare cases of post-transfusion HBV infection are still observed. Antibody to hepatitis B core antigen (anti-HBc) often indicates remote HBV infection but DNA hybridisation and more sensitive polymerase chain reaction (PCR) assays have demonstrated that some HBsAg negative individuals, positive for anti-HBc, have continuing HBV replication. To determine the incidence of ongoing HBV infection in a Canadian HBsAg negative, anti-HBc positive population we studied three groups with this combination of HBV markers: Group A, 36 patients referred for investigation of raised serum aminotransferases; Group B, 21 Canadian Red Cross blood donors; Group C, seven vaccinees in an Ottawa Health Care Student hepatitis B vaccination programme. The PCR was carried out using a nested PCR reaction with primers specific for the pre-core region of HBV. Seven of 36 (19%) patients in Group A had detectable HBV DNA whereas none of Group B or C were positive. This data indicates that in some HBsAg negative patients with ongoing hepatic inflammation, continuing HBV replication may persist. This was not observed in any healthy blood donors or health care students investigated. Larger studies are required, but this data would suggest that, in Canada, the addition of anti-HBc testing for all blood donors for detection of low level HBV replication would not be indicated.

Retrospective analysis of non‐A–E hepatitis: Possible role of hepatitis B and C virus infection

“…HBV DNA was detected in the sera, PBMC and liver tissue of the patients who lack serological markers of hepatitis viruses A-E [Scully et al, 1994;Uchida et al, 1994;Alter and Bradley, 1995;Fan et al, 1996;Zhuang et al, 2000]. In this study, very sensitive nPCR and RT-nPCR methods were also used to determine the roles of HBV and HCV infection in non-A-E hepatitis.…”

“…Therefore, GBV-C virus and TT virus may also contribute to some cases of occult hepatitis that lack infection markers of hepatitis viruses A-E. In addition, HBV DNA was detected by more sensitive assays in patients with chronic hepatitis that lack serological markers of HBV infection [Scully et al, 1994;Uchida et al, 1994;Alter and Bradley, 1995;Fan et al, 1996;Zhuang et al, 2000]. Failure of serological methods to detect HBV infection is probably caused by mutations in the HBV genome, which might result in escape of immune epitopes from detection by conventional serological methods.…”

Occult hepatitis B virus infection: A hidden menace?

“…Thus, occult HBV infection is most commonly reported in high endemic areas where 70% to 90% of the population have been exposed to HBV and infrequently reported in low endemic areas where 5% to 20% of the population had prior infection with HBV. [10][11][12] The prevalence of occult HBV infection also depends on the population studied, being more common in patients with chronic liver disease and less common among healthy blood or organ donors. Patients with fulminant hepatitis B may be misdiagnosed as occult HBV infection because of rapid virus clearance with undetectable HBsAg at the time of presentation.…”

Prevalence of antibodies to hepatitis B core antigen in blood donors in the middle west region of Brazil

“…In low prevalence areas for HBV, the occurrence of isolated anti-HBc practically exempts the possibility of PTH (Scully et al 1994, Mosley et al 1995. In contrast, in high endemicity areas, anti-HBc as the sole HBV marker has been associated with the presence of HBV-DNA detected using the polymerase chain reaction (PCR) (Luo et al 1991, Wang et al 1991, Nandi & Banerjee 1992, Chung et al 1993, Sánchez-Quijano et al 1993.…”