Inactivation of hepatitis A virus by heat and high hydrostatic pressure: variation among laboratory strains.

BACKGROUND AND OBJECTIVES: Hepatitis A virus (HAV) transmission via contaminated blood products has been reported. Cell-adapted HAV strains are generally used to confirm virus inactivation in manufacturing blood products, but the strains may differ in their sensitivity to inactivation treatment. To select an appropriate cell-adapted HAV strain for virus validation, we compared the inactivation efficiency among four strains under two different physical inactivation treatments: heat and high hydrostatic pressure. MATERIALS AND METHODS: The cell-adapted HAV strains used here were KRM238, KRM003 (subgenotype IIIB), KRM031 (IA), and TKM005 (IB). The strains were treated at 60 degrees C for up to 10 h or under high hydrostatic pressure (up to 420 MPa). The reduction in HAV infectivity was measured by an immunofocus-staining method. RESULTS: The heat treatment at 60 degrees C for 10 h reduced HAV infectivity in the range of 3 to 5 log(10) among the strains; KRM238 and TKM005 were harder to inactivate than the other two. The high hydrostatic pressure treatment at 420 MPa also reduced infectivity in the range of 3 to 5 log(10) among the strains, and KRM031 was easier to inactivate than the other strains. CONCLUSION: Heat treatment and high hydrostatic pressure treatment revealed differences in inactivation efficiencies among cell-adapted HAV strains, and each strain reacted differently depending on the treatment. KRM238 may be the best candidate for virus validation to ensure the safety of blood products against viral contamination, as it is harder to inactivate and it replicates better in cell culture than the other strains.

Presence of interferon and antibodies to BK virus in amniotic fluid of normal pregnant women.

Paired samples of maternal sera, umbilical cord sera and amniotic fluids were tested for antibodies to BK virus (BKV) and for interferon content. It was found that two out of 14 pregnant women were antibody negative, the latter were estimated to be susceptible to BKV primary infection. In contrast, there was no foetal case among those which were at risk of foetal infection with BKV as judged from the presence of BKV antibody in maternal sera and interferon in the placentas. It might be hypothesized that BKV may be transmitted to the foetus only in the case of BKV primary infection of antibody-negative pregnant women with undetectable amount of interferon (IFN) in the placenta.

Prevalence rate and age of acquisition of antibodies against JC virus and BK virus in human sera.

A total of 480 serum samples from donors including 384 children up to 10 years of age were examined by the hemagglutination-inhibition (HI) test for the rates of prevalence and age of acquisition of HI antibodies against JC virus and BK virus. Among 136 serum samples from various age groups, there were five (4%) with no detectable antibodies against BK or JC virus, 75 (55%) with antibodies against both viruses, 41 (30.1%) with antibodies against only BK virus and 26 (19%) with antibodies against only JC virus. The prevalence of antibodies against JC and BK viruses was 70.5% and 80.8%, respectively, and the mean HI titers (4 x 2n,n greater than or equal to 1) were 4.90 and 4.30. About 50% of the children had acquired antibodies against BK virus by 3 years of age and against JC virus by 6 years of age. These results indicate that dual latent infections with both viruses are common, although independent infections with either virus are predominant in the human population.