Background: It has been shown that HSA may be contaminated with parvovirus B19 (B19) DNA. However, the presence of B19 DNA does not necessarily indicate infectious virus. HSA is pasteurized at 60 degrees C for 10 hours and it remains unclear whether this procedure inactivates B19. Studies with animal parvoviruses indicate considerable heat resistance at 60 degrees C. However, due to the lack of a suitable cell culture system, the pasteurization process has not been investigated in the past.
Study design and methods: The recently described cell clone KU812Ep6 was used to establish a system for investigation of B19 inactivation during pasteurization. Virus-infected cells were detected by immunofluorescent staining of viral capsid antigen and by RT-PCR assay of virus-specific capsid mRNA.
Results: B19 was inactivated after 10 minutes at 60 degrees C for > or = 4 log. In contrast, porcine parvovirus was widely resistant at 60 degrees C. Inactivation of B19 was independent of the analyzed albumin products (5, 20, and 25% albumin from three manufacturers) and from the specific virus source used for the inactivation experiments. Degradation of B19 DNA by deoxyribonuclease I treatment after pasteurization indicated that the virus capsid is destroyed during heat treatment.
Conclusion: Heat resistance of B19 markedly differs from heat resistance of animal parvoviruses. While animal parvoviruses widely withstand pasteurization of albumin, B19 was rapidly inactivated. These results confirm the safety of pasteurized albumin and are in line with its good clinical safety record with respect to B19 infection. However, conclusions regarding the safety of other blood-derived medicinal products should not be derived from B19 inactivation in albumin, because different processes or different composition of product intermediates may significantly influence B19 stability during heat treatment.