Prevention of transfusion-transmitted hepatitis

Sacher, Ronald A.; Schreiber, George B.; Kleinman, Steven

doi:10.1016/s0140-6736(99)00391-8

Cited by 13 publications

(14 citation statements)

References 11 publications

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“…The role of HBV DNA screening in pools has been considered to be complex and potentially of low value because HBV seems to be present in low titres during the window period when compared with HCV [9]. In addition, the availability of highly sensitive HBsAg assays further reduces the perceived benefits of HBV DNA screening.…”

Section: Discussionmentioning

confidence: 99%

Superiority of minipool nucleic acid amplification technology for hepatitis B virus over chemiluminescence immunoassay for hepatitis B surface antigen screening

Minegishi¹,

Yoshikawa²,

Kishimoto³

et al. 2003

Vox Sanguinis

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Section: Discussionmentioning

confidence: 99%

Superiority of minipool nucleic acid amplification technology for hepatitis B virus over chemiluminescence immunoassay for hepatitis B surface antigen screening

Minegishi¹,

Yoshikawa²,

Kishimoto³

et al. 2003

Vox Sanguinis

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“…Individuals positive for either are disqualified because of ongoing or past infections. The strategy of combined HBsAg and anti-HBc screening virtually eliminates blood-transmitted HBV, with the rare exception of donations in the window-period when serological markers are still negative [1,14,17,18]. To further reduce the risk of transfusion-related infections in the window period, NAT is used to directly detect viral genomes and has already been implemented in Germany and Japan [19][20][21][22][23][24][25][26].…”

Section: Introductionmentioning

confidence: 99%

Transmission of occult hepatitis B virus by transfusion to adult and pediatric recipients in Taiwan

Liu

Kao

et al. 2006

Journal of Hepatology

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“…The value of HBV NAT has been a matter of debate. [26][27][28][29] However, it seems to be less useful because the nucleic acid load is often markedly lower than it is in HCV infection, so that an adequate HBV NAT can only be performed on a single (not pooled) blood donation.…”

Section: Introductionmentioning

confidence: 99%

Frequency and load of hepatitis B virus DNA in first-time blood donors with antibodies to hepatitis B core antigen

Hennig

Puchta

Luhm

et al. 2002

Blood

113

104

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IntroductionThe risk of transfusion-transmitted hepatitis B virus (HBV) infection has been reduced by screening all blood donations for HBV surface antigen (HBsAg) since 1970. It was generally accepted that the disappearance of HBsAg indicates the clearance of HBV. Meanwhile, many reports on positive findings for HBV DNA in the liver and blood of HBsAg-negative individuals positive for antibodies against HBV core antigen (anti-HBc) and/or HBsAg (anti-HBs) have been published. 1-8 Blum et al described, in a patient with HBsAg-negative chronic hepatitis who was positive for anti-HBc, anti-HBs, and antibodies against HBe antigen (anti-HBe), a latent HBV infection in hepatocytes with extrachromosomal presence of a full-length viral genome. 9 Michalak et al demonstrated the long-term persistence of HBV DNA in serum and peripheral blood mononuclear cells of patients up to 70 months after complete clinical, biochemical, and serologic recovery from acute viral hepatitis. 10 Rehermann et al showed that traces of HBV were often detectable in the blood for many years after clinical recovery from acute hepatitis, despite the presence of serum antibodies and HBV-specific cytotoxic T lymphocytes (CTLs). 11 These findings suggest that sterilizing immunity to HBV frequently fails to occur and that traces of virus can maintain the CTL response for decades, apparently creating a negative feedback loop that keeps the virus under control, perhaps for life. This was supported by Pasquetto et al, who showed that cytoplasmic HBV nucleocapsids and their cargo of replicative DNA intermediates survive CTL-induced apoptosis of hepatocytes in vitro, 12 and by other groups that demonstrated ongoing viral replication in the liver tissue of patients and healthy individuals after loss of HBsAg. [13][14][15] Furthermore, reactivation of apparently cured HBV infection has been described under chemotherapy or immunomodulating therapy after renal and bone marrow transplantation, and in some of these cases a reverse seroconversion from anti-HBs to HBsAg has been observed. [16][17][18][19] The residual risk of posttransfusion HBV infection has been calculated by several groups in the United States and Germany on the basis of HBV incidence data and the duration of the early window period until HBsAg becomes detectable to be 1:63 000 and less than 1:100 000 blood donations, respectively. 20,21 It has been shown that blood donations of HBsAg-and anti-HBs-negative but anti-HBc-positive HBV carriers can cause posttransfusion hepatitis B. 22;23 Thus, Mosley et al suggested that anti-HBc screening of blood donations might prevent HBV transmission from HBsAgnegative blood donors and that donors positive for anti-HBs as well should be considered noninfectious for HBV. 24 The feasibility of routine polymerase chain reaction (PCR) screening of blood donations in a blood bank setting has been shown by Roth et al. 25 In Germany, the Paul Ehrlich Institute (PEI, Langen, Germany), the institute that defines German Drug Law and is responsible for specific regulati...

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Prevention of transfusion-transmitted hepatitis

Cited by 13 publications

References 11 publications

Superiority of minipool nucleic acid amplification technology for hepatitis B virus over chemiluminescence immunoassay for hepatitis B surface antigen screening

Superiority of minipool nucleic acid amplification technology for hepatitis B virus over chemiluminescence immunoassay for hepatitis B surface antigen screening

Transmission of occult hepatitis B virus by transfusion to adult and pediatric recipients in Taiwan

Frequency and load of hepatitis B virus DNA in first-time blood donors with antibodies to hepatitis B core antigen

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