Transmission of Hepatitis B by Dry Heat Treated Factor Viii and Ix Concentrates

Cj, Lush; Cs, Chapman; Ve, Mitchell; Martín, Carmen

doi:10.1111/j.1365-2141.1988.tb02385.x

Cited by 8 publications

(1 citation statement)

References 2 publications

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“…Efforts to prevent transmission by screening blood donations for HBsAg successfully decreased the incidence of post-transfusion hepatitis B in recipients of single donor products [3]; however, despite this haemophiliacs remained at risk of infection [4]. Further, certain methods of viral inactivation have failed to prevent transmission of HBV infection [5,6]. Both vaccination and natural immunity against HBV may also fail to protect against infection or re-infection with different subtypes of the virus Haemophiliacs may therefore remain at risk of HBVrelated liver disease, and transmimng the virus.…”

Section: Hepatitis B Virus (Hbv) Infection Is Recognized As a Common mentioning

confidence: 99%

Hepatitis B serology and DNA detection in multitransfused haemophiliacs and factor VIII and IX concentrates

et al. 1996

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To assess the effect of HIV infection and the introduction of virus-inactivated concentrates, we conducted a retrospective 20-year longitudinal study of hepatitis B virus (HBV) serology and look for HBV DNA in recent serum samples of 63 multiply transfused haemophiliacs. Of 63 haemophiliacs, 51 had evidence of previous HBV infection and 12 vaccinees had anti-HBs only. Of 40 HIV-negative, two had persistent HBsAg but all were HBV DNA negative. All 23 HIV-positive were HBsAg-negative. Loss of anti-HBc(46% vs. 17.5%) and anti-HBs (32% vs. 14%) was more commonly seen in HIV-infected compared with noninfected individuals. One HIV-positive individual had HBV DNA detectable by PCR. Restrospective testing demonstrated that re-emergence was associated with loss of anti-HBs and advanced HIV infection (CD4<50 × 10(6-1) L CDC II), although eight other with CDC IV disease were HBV DNA negative. Forty-three batches of concentrates produced between 1965 and 1992 from both commercial and volunteer donors and subjected to different donor screening and virus inactivation methods were negative for HBV DNA. Some of these may have been infectious for HBV and therefore being negative for HBV may not equate with noninfectivity. We conclude that both HIV-positive and -negative haemophiliacs have lost protective antibodies against HBV since 1984 and that virus replication may re-emerge at least in the HIV-positive group. These observations may have implications for the management of their chronic liver disease and the risk of infection of sexual partners and medical attendants.

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