Significance of Isolated Hepatitis B Core Antibody in Blood Donors

Schifman, Ron B.; Rivers, Shirley L.; Sampliner, Richard E.; Krammes, Judith E.

doi:10.1001/archinte.1993.00410190107012

Cited by 39 publications

(16 citation statements)

References 20 publications

(1 reference statement)

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“…These samples called ''anti-HBc only" may originate either from recovered infections having lost detectable anti-HBs or from late stage chronic infections having lost detectable HBsAg. Evidence of a secondary anti-HBs response after a single dose of HBV vaccine indicated that a large proportion of anti-HBc-only donors had indeed recovered from the infection indicated by activable memory B cells [24,25]. The issue was further complicated by detecting low levels of HBV DNA not only in anti-HBc only donations but also in some units carrying low-level anti-HBs.…”

Section: Anti-hbc Testingmentioning

confidence: 99%

Transfusion-transmitted hepatitis B virus infection

Candotti

Allain

2009

Journal of Hepatology

191

158

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Hepatitis B virus (HBV) remains a major risk of transfusion-transmitted infection due to the pre-seroconversion window period (WP), infection with immunovariant viruses, and with occult carriage of HBV infection (OBI). Reduction of HBV residual risk depends upon developing more sensitive HBV surface antigen (HBsAg) tests, adopting anti-HBc screening when appropriate, and implementing HBV nucleic acid testing (NAT), either in minipools or more efficiently in individual samples. HBV NAT combines the ability to significantly reduce the window period and to detect occult HBV carriage substantiating decades of clinical observation that HBsAg-negative/anti-HBc-positive blood could transmit HBV. Clinical observations suggest limited transmission rate of occult HBV compared to WP. Low transmission rate might be related to low viral load observed in OBIs or to the presence of mutants associated with occult carriage. OBIs carrying detectable anti-HBs ( approximately 50%) are essentially not infectious by transfusion. However, recent data suggest that the neutralizing capacity of low anti-HBs may be inefficient when overcome by exposure to high viral load. Anti-HBc blood units without detectable anti-HBs appear moderately infectious except in immunocompromised recipients. Immunodeficient elderly and patients receiving immunosuppressive treatments may be susceptible to infection with lower infectious dose even in the presence of anti-HBs. The immune status of blood recipients should be taken into consideration when investigating "post-transfusion" HBV infection. Pre-transfusion testing and post-transfusion long-term follow-up of recipients, and molecular analysis of the virus infecting both donor and recipient are critical to definitively incriminate transfusion in the transmission of HBV.

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Section: Anti-hbc Testingmentioning

confidence: 99%

Transfusion-transmitted hepatitis B virus infection

Candotti

Allain

2009

Journal of Hepatology

191

158

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“…As anti-HBc is the first detectable antibody, testing for total anti-HBc allows a serological screening during the immunological window when the individual is infected with HBV but the levels of HBsAg are still undetectable. Therefore, the significance of total anti-HBc reactivity, in the absence of the surface antigen, is up to a certain point still controversial [8][9][10]. Since HBV infection can remain dormant for a long period of time, the use of highly accurate methods for viral detection, such as PCR analysis, is important [11,12].…”

Section: Introductionmentioning

confidence: 99%

Serologic and Molecular Profile of Anti-HBc-Positive Blood Bank Donors in an Area of Low Endemicity for HBV

et al. 2007

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Hepatitis B virus (HBV) infection leaves serological markers that indicate prior contact with the virus or an occult infection. The aim of this study was to determine the profile of HBV markers of individuals from a region of low HBV endemicity excluded from blood donation due to the presence of total anti-HBc antibodies but who tested negative for HBV surface antigen (HBsAg). The profile of 244 subjects exclusively anti-total hepatitis B core (anti-total HBc) reactive was determined. Markers such as anti-HBsAg, HBeAg (HBV core antigen) and anti-HBe (antibody to hepatitis Be antigen) were determined, and HB viral DNA (HBV-DNA) was identified by PCR analysis. Overall, 85.7% of the subjects had an anti-HBs (hepatitis B surface antigen antibody) titer higher than 10 IU/L; 154 samples were negative for HBeAg and 66.5% were reactive for anti-HBe. All samples were negative for HBV-DNA (n = 241). We found a significant association between the anti-HBe and anti-HBs titers (P = 0.026). Most individuals from a low endemic area for HBV have shown anti-HBs titers that confer immunity against HBV, even though they were negative for HBV-DNA. In the light of a shortage of donated blood worldwide, we suggest that special measures should be considered that would facilitate the possible use of these rejected blood units in areas of low endemicity for HBV.

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“…Detection of antibody against hepatitis B virus core antigen (anti-HBc) by enzyme immunoassay (EIA) is used solely or in combination with HBV surface antigen (HBsAg) screening for the diagnosis of hepatitis B. Anti-HBc detection is used as a screening method prior to hepatitis B vaccination in high prevalence groups [Lok et al, 1988]. The detection of anti-HBc by routine EIAs in a competitive test format is subject to frequent non-speci®c reactions causing false-positive results [Sherertz et al, 1983;Kessler et al, 1985;Schmidt et al, 1988;Caspary et al, 1989;Schifan et al, 1993]. Isolated false-positive anti-HBc reactivity (presence of anti-HBc; HBsAg and anti-HBs negative) has been attributed to cross-reactive antibodies or interfering substances in serum; this effect was also observed for anti-HBs [Sherertz et al, 1983;Kessler et al, 1985].…”

Section: Introductionmentioning

confidence: 99%

Hepatitis B virus markers in anti‐HBc only positive individuals*

Weber¹,

Melchior

Gehrke

et al. 2001

Journal of Medical Virology

136

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Isolated reactivity to hepatitis B virus (HBV) core antigen (anti-HBc) is observed relatively frequently in immunocompromised individuals, intravenous drug abusers (IVDA), and in the presence of HCV infection. The reason for the lack of HBsAg is not clear. The aim of the present study was to investigate which factors (genetic variability of S gene, low-level HBsAg, and immune complexes may be responsible for the failure of HBsAg detection with commercial HBsAg screening assays. Dilution series of two recombinant HBsAg escape mutants and dilutions of serum samples from chronic HBV carriers with multiple insertions in the a determinant and different HBsAg subtypes were tested with a highly sensitive assay that detects wild-type HBsAg (Elecsys HBsAg, Roche Diagnostics, Penzberg, Germany) and two assays that detect HBV wild-type and escape mutants (Murex HBsAg Version 3, Murex and Enzygnost HBsAg 5.0, Dade Behring, Marburg, Germany). Elecsys HBsAg showed in comparison to Murex HBsAg Version 3 and Enzygnost HBsAg 5.0 a reduced sensitivity for escape mutant detection. On the other hand, the best performance for HBsAg subtype detection was obtained with Elecsys HBsAg. In the second part of the study, a selected panel of isolated anti-HBc reactive (n = 104) serum samples (AxSYM Core) was submitted to testing by Elecsys HBsAg, Murex HBsAg Version 3, Enzygnost HBsAg 5.0, and HBsAg detection after immune complex dissociation (ICD) and anti-HBs determination with two different assays (AxSYM Ausab and Elecsys Anti-HBs). To assess the specificity of anti-HBc test results, all the samples were tested by a second anti-HBc assay (Elecsys Anti-HBc). Quantitative HBV DNA detection was undertaken with a commercially available HBV PCR assay (Amplicor HBV Monitor). HCV infection was present in 65.4% of anti-HBc only reactive individuals. Five AxSYM Core positive samples were negative by Elecsys Anti-HBc. Overall, 15 (14.4%) AxSYM Ausab negative samples gave positive results with Elecsys Anti-HBs (median value: 21 IU/ml). No low-level HBsAg carrier was detected among the isolated anti-HBc reactive individuals with Elecsys HBsAg. There was no evidence for the presence of immune complexes. Only one sample was repeatedly reactive by the Murex HBsAg, suggesting that the a mutant form of HBsAg was responsible for the isolated anti-HBc reactivity, however neutralisation assay was not interpretable and HBV DNA PCR was negative. Fifteen (14.4%) anti-HBc only positive individuals were HBV DNA carriers with concentrations ranging from 800 to more than >4,000,000 copies of viral DNA/ml. In conclusion, the most probable explanations for isolated anti-HBc reactivity in our study group are a possible interference of HBsAg synthesis by HCV infection (65.4%) and divergence of results of anti-HBs assays (14.4%). There is no evidence for the presence of low-level HBsAg carriers and immune complexes. HBsAg mutants cannot be excluded definitively by the test strategy used in the present evaluation.

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Significance of Isolated Hepatitis B Core Antibody in Blood Donors

Abstract: Isolated anti-HBc in US blood donors is usually a false-positive result, regardless of the titer.

Cited by 39 publications

References 20 publications

Transfusion-transmitted hepatitis B virus infection

Transfusion-transmitted hepatitis B virus infection

Serologic and Molecular Profile of Anti-HBc-Positive Blood Bank Donors in an Area of Low Endemicity for HBV

Hepatitis B virus markers in anti‐HBc only positive individuals*

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