Hepatitis B screening in HIV-infected individuals

Abstract

Viral hepatitis has become an important cause of morbidity and mortality in HIV-infected individuals since the introduction of highly active antiretroviral therapy [1,2]. Dual infection with HIV and hepatitis B virus (HBV) is common. One study of 631 HIV-infected individuals in London reported an HBV infection rate of 6% [3]. A report from France [4] demonstrated that the overall prevalence of all markers for HBV was 68 %. Current British HIV Association guidelines recommend that all HIV-infected individuals should have hepatitis B core (HBc) antibody testing within a month of diagnosis, with anti-hepatitis B surface antibody testing if previously immunized [5]. We report the case of a 40-year-old man with new-diagnosis HIV-1 infection who was subsequently started on antiretroviral therapy. The baseline serum anti-HBc test (Abbott IMx, IL, USA) was negative and the sample was not tested for hepatitis B surface antigen (HBsAg). This individual was considered to be susceptible to hepatitis B. Further tests for viral hepatitis were then sent to our laboratory after 8 weeks of antiretroviral therapy as a result of abnormal liver function tests. Neutralizable HBsAg and hepatitis B e antigen were detected. The total anti-HBc and anti-HBc IgM results were both indeterminate. The total anti-HBc assay (Diasorin Liaison, Saluggia, Italy) gave values of 0.91 and 0.98 PEI (Paul Ehrlich Institut) U/ml. The assay grey zone is between 0.9 and 1.1 PEI U/ml. The sample was also tested using the Abbott IMx total anti-HBc assay and gave a sample/cut-off value of 1.35, negative by the manufacturers’ criteria. The baseline stored serum was retested using the Diasorin Liaison total anti-HBc assay, which gave an indeterminate result (0.88 PEI U/ml) with a negative anti-HBc IgM. However, both neutralizable HBsAg and hepatitis B e antigen were detected in the sample. This demonstrates that anti-HBc testing alone is insufficient to exclude exposure to HBV in immunosuppressed individuals who may mount a suboptimal antibody response. In addition, there are a number of anti-HBc assays available commercially, but there are no reports evaluating their sensitivity and specificity. Although the manufacturers’ kit inserts state high specificity and sensitivity values, on discussing discrepant results, the view is that the few samples yielding false-negative results are within the assay performance characteristics. We have conflicting anti-HBc results with two different assays, having tested samples collected from four female hepatitis B carriers who were screened antenatally. This is critical as these assays may be used to check the pre-immunization hepatitis B status, or as part of the screening for organ transplant recipients. A false-negative result in these cases could lead to a hepatitis B carrier healthcare worker not being identified, unless an HBsAg test is also carried out, and being given an unnecessary course of hepatitis B vaccine. In addition, the transplant recipient would not be identified as being at risk of hepatitis B reactivation. It is important that further evaluation and comparison between anti-HBc assays is carried out, especially as these tests are included as part of the organ and blood donor screens. Finally, HBsAg must be included, together with anti-HBc testing, in the baseline screening tests for HIV-infected and other immunocompromised individuals.