Prevalence and stability of human serum antibodies to simian virus 40 VP1 virus-like particles

1 Department of Medical Microbiology, Malmö University Hospital, Entrance 78, 20502 Malmö, Sweden 2 Department of Infectious Disease Epidemiology, National Public Health Institute, Mannerheimintie 166, FIN-00300 Helsinki, Finland 3 Institute of Biotechnology, Graiciuno 8, LT-02241 Vilnius, Lithuania...

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Veröffentlicht in:Journal of general virology 2005-06, Vol.86 (6), p.1703-1708
Hauptverfasser: Lundstig, Annika, Eliasson, Linda, Lehtinen, Matti, Sasnauskas, Kestutis, Koskela, Pentti, Dillner, Joakim
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Sprache:eng
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Zusammenfassung:1 Department of Medical Microbiology, Malmö University Hospital, Entrance 78, 20502 Malmö, Sweden 2 Department of Infectious Disease Epidemiology, National Public Health Institute, Mannerheimintie 166, FIN-00300 Helsinki, Finland 3 Institute of Biotechnology, Graiciuno 8, LT-02241 Vilnius, Lithuania 4 Department of Microbiology, National Public Health Institute, PO Box 310 (Aapistie 1), FIN-90101 Oulu, Finland Correspondence Joakim Dillner joakim.dillner{at}mikrobiol.mas.lu.se Possible human infection with simian virus 40 (SV40) has been of great concern ever since SV40 was discovered in polio vaccines. Human populations are SV40-seropositive, but because of serological cross-reactivity between SV40 and the human polyomaviruses BK virus (BKV) and JC virus (JCV), it is debatable whether these antibodies are specific. An SV40-specific serological assay was established, based on purified virus-like particles (VLPs), where the SV40 VLPs were blocked with hyperimmune sera to BKV and JCV. Competition with SV40 hyperimmune sera was used as a confirmatory test. Among 288 Swedish children of between 1 and 13 years of age, 7·6 % had SV40-specific antibodies. SV40 seroprevalence reached a peak of 14 % at 7–9 years of age. Among 100 control patients with benign tumours, 9 % were SV40-seropositive. However, SV40 DNA was not detectable in corresponding buffy-coat samples. In serial samples taken up to 5 years apart from 141 Finnish women participating in the population-based serological screening for congenital infections, only two of 141 women were SV40-seropositive in both samples. Six women seroconverted and eight women had a loss of antibodies over time. None of the SV40-seropositive samples contained detectable SV40 DNA. In conclusion, there is a low prevalence of SV40-specific antibodies in the Nordic population. The SV40 antibodies appear to have a low stability over time and their origin is not clear.
ISSN:0022-1317
1465-2099
1465-2099
DOI:10.1099/vir.0.80783-0