Letters to the Editor
I 13
Laboratory infection with h u m a n p a r v o v i r u s BI9 Accepted for publication 2I August I99I Sir, We read with interest the report by Shiraishi et al., 1 of two adults accidentally infected in the laboratory with h u m a n parvovirus BI 9. This adds to a larger series of probable laboratory infections with this virus reported previously. 2 Recommendations to reduce the risk of laboratory-acquired infection were made in the earlier report 2 and include inactivation of the virus by gamma irradiation. At that time, it was not possible to monitor the effect of irradiation on infectivity because a cell culture system for the virus was not available. Such a system has now been established 3 and used to study the effects of gamma irradiation on virus infectivity. We wish to report our findings with it. T w o h u m a n parvovirus B 19-positive serum samples, ' W i ,4 and ' Sig ,5 were studied. Aliquots of the samples were irradiated in a ' G a m m a c e l l ' irradiator (model 2~o, Atomic Energy of Canada Ltd) at doses ranging from o to 2"4 Mrad. T h e virus infectivity of the serum samples was titrated in h u m a n fetal erythroid progenitor cells as previously described 3 and antigenicity of the virus determined by radiommunoassay. Results are shown in Fig. I. Virus infectivity was reduced by exposure to 0"3 M r a d and showed a 4-6 log10 reduction after 0.6 Mrad. Extrapolation from these data suggests a Io log10 reduction in infectivity by I"4 Mrad, which is a radiation dose similar to that required to inactivate other viruses. 6 Antigenicity of the virus was unaffected by up to I-2 M r a d and, although reduced, remained detectable with up to 2'4 Mrad. We conclude that h u m a n parvovirus BI9-positive serum (for use as viral antigen in immunoassays) may be greatly reduced in infectivity, if not wholly inactivated, by exposure to I. 4 Mrad, while retaining its antigenicity. In contrast, methods of virus inactivation using heat, formaldehyde or beta-propiolactone destroy antigenicity of the virus (B. J. C., unpublished observations) and are therefore of no value. We recognise that a gamma source may not be available in some laboratories. Nevertheless, whether or not it is possible to irradiate the serum or plasma used as viral antigen, we recommend that potential aerosols from it should be contained within a class I cabinet and that laboratory personnel should be monitored to see whether they are immune. T h e infectiousness of h u m a n parvovirus B 19 has also been observed in other occupational settings, e.g. among hospital staff v and teachersfl Infection with the virus will remain a problem in the laboratory unless antigen is inactivated beforehand or, as a m i n i m u m precaution, aerosols are contained. T h e continuing problem of such laboratory-acquired infection highlights the need for antibody assays based on recombinant D N A - d e r i v e d or synthetic peptide antigens. Several assays of this type have been developedfl but their value is unproven and they are not yet widely used.
Virus Reference Laboratory, Central Public Health Laboratory, Colindale Avenue, London N W 9 5 H T , U.K.
B . J . Cohen K . E . Brown
References i. Shiraishi H, Sasaki T, Nakamura M, Yaegashi N, Sugamura K. Laboratory infection with human parvovirus BI9. J Infect I991 ; z2: 3o8-3Io. 2. Cohen BJ, Courouce AM, Schwarz TF, Okochi K, Kurtzman GJ. Laboratory infection with parvovirus B~9. J Clin Pathol I988; 4x: IO27-IO28. 3. Brown KE, Mori J, Cohen BJ, Field AM. In vitro propagation of parvovirus BI9 in primary foetal liver culture. J Gen Virol I99r; 72: 741-745.
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14
Letter to the Editor IO
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I 13
Laboratory infection with h u m a n p a r v o v i r u s BI9 Accepted for publication 2I August I99I Sir, We read with interest the report by Shiraishi et al., 1 of two adults accidentally infected in the laboratory with h u m a n parvovirus BI 9. This adds to a larger series of probable laboratory infections with this virus reported previously. 2 Recommendations to reduce the risk of laboratory-acquired infection were made in the earlier report 2 and include inactivation of the virus by gamma irradiation. At that time, it was not possible to monitor the effect of irradiation on infectivity because a cell culture system for the virus was not available. Such a system has now been established 3 and used to study the effects of gamma irradiation on virus infectivity. We wish to report our findings with it. T w o h u m a n parvovirus B 19-positive serum samples, ' W i ,4 and ' Sig ,5 were studied. Aliquots of the samples were irradiated in a ' G a m m a c e l l ' irradiator (model 2~o, Atomic Energy of Canada Ltd) at doses ranging from o to 2"4 Mrad. T h e virus infectivity of the serum samples was titrated in h u m a n fetal erythroid progenitor cells as previously described 3 and antigenicity of the virus determined by radiommunoassay. Results are shown in Fig. I. Virus infectivity was reduced by exposure to 0"3 M r a d and showed a 4-6 log10 reduction after 0.6 Mrad. Extrapolation from these data suggests a Io log10 reduction in infectivity by I"4 Mrad, which is a radiation dose similar to that required to inactivate other viruses. 6 Antigenicity of the virus was unaffected by up to I-2 M r a d and, although reduced, remained detectable with up to 2'4 Mrad. We conclude that h u m a n parvovirus BI9-positive serum (for use as viral antigen in immunoassays) may be greatly reduced in infectivity, if not wholly inactivated, by exposure to I. 4 Mrad, while retaining its antigenicity. In contrast, methods of virus inactivation using heat, formaldehyde or beta-propiolactone destroy antigenicity of the virus (B. J. C., unpublished observations) and are therefore of no value. We recognise that a gamma source may not be available in some laboratories. Nevertheless, whether or not it is possible to irradiate the serum or plasma used as viral antigen, we recommend that potential aerosols from it should be contained within a class I cabinet and that laboratory personnel should be monitored to see whether they are immune. T h e infectiousness of h u m a n parvovirus B 19 has also been observed in other occupational settings, e.g. among hospital staff v and teachersfl Infection with the virus will remain a problem in the laboratory unless antigen is inactivated beforehand or, as a m i n i m u m precaution, aerosols are contained. T h e continuing problem of such laboratory-acquired infection highlights the need for antibody assays based on recombinant D N A - d e r i v e d or synthetic peptide antigens. Several assays of this type have been developedfl but their value is unproven and they are not yet widely used.
Virus Reference Laboratory, Central Public Health Laboratory, Colindale Avenue, London N W 9 5 H T , U.K.
B . J . Cohen K . E . Brown
References i. Shiraishi H, Sasaki T, Nakamura M, Yaegashi N, Sugamura K. Laboratory infection with human parvovirus BI9. J Infect I991 ; z2: 3o8-3Io. 2. Cohen BJ, Courouce AM, Schwarz TF, Okochi K, Kurtzman GJ. Laboratory infection with parvovirus B~9. J Clin Pathol I988; 4x: IO27-IO28. 3. Brown KE, Mori J, Cohen BJ, Field AM. In vitro propagation of parvovirus BI9 in primary foetal liver culture. J Gen Virol I99r; 72: 741-745.
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Letter to the Editor IO
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