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

2005 ◽  
Vol 86 (6) ◽  
pp. 1703-1708 ◽  
Author(s):  
Annika Lundstig ◽  
Linda Eliasson ◽  
Matti Lehtinen ◽  
Kestutis Sasnauskas ◽  
Pentti Koskela ◽  
...  

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.

Author(s):  
Giuseppe Barbanti-Brodano ◽  
Silvia Sabbioni ◽  
Fernanda Martini ◽  
Massimo Negrini ◽  
Alfredo Corallini ◽  
...  

2000 ◽  
Vol 38 (1) ◽  
pp. 105-109
Author(s):  
R. S. Hamilton ◽  
M. Gravell ◽  
E. O. Major

ABSTRACT A comparison of antibody titers to JC virus (JCV) or BK virus (BKV) was made by hemagglutination inhibition (HI) and enzyme immunoassay (EIA) with 114 human plasma samples. Antibody titers to JCV or BKV determined by HI were lower than those determined by EIA. Nevertheless, as HI titers increased so did EIA titers. When antibody data were compared by the Spearman rank correlation test, highly significant correlations were found between HI and EIA titers. Results obtained by plotting EIA antibody titers for JCV against those for BKV generally showed a reciprocal relationship, i.e., samples with high antibody titers to JCV had lower antibody titers to BKV and vice versa. Some samples, however, had antibody titers to both viruses. Of the samples tested, 25.4% (25 of 114) had HI and EIA antibody titers to JCV and BKV which were identical or closely related. This is not the scenario one would expect for cross-reactive epitopes shared by the two viruses, but one suggesting that these samples were from individuals who had experienced infections by both viruses. Adsorption with concentrated JCV or BKV antigen of sera with high antibody titers to both JCV and BKV and testing by JCV and BKV EIA gave results which support this conclusion. Although 52.6% (51 of 97) of the samples from the Japanese population tested had very high antibody titers (≥40,960) to either JCV or BKV, none of the samples were found by a dot blot immunoassay to have antibodies which cross-reacted with simian virus 40. The results from this study, in agreement with those of others, suggest that humans infected by JCV or BKV produce antibodies to species-specific epitopes on their VP1 capsid protein, which is associated with hemagglutination and cellular binding.


1980 ◽  
Vol 52 (3) ◽  
pp. 367-370 ◽  
Author(s):  
Hideyuki Kosaka ◽  
Yoshinori Sano ◽  
Yasuhiko Matsukado ◽  
Takeshi Sairenji ◽  
Yorio Hinuma

✓ To probe the possible presence of papovavirus-related T antigen(s) in human brain tumors, the imprinted or cultured cells at various passage levels were examined by anticomplement immunofluorescence using antisera to T antigen of each BK virus, JC virus, and simian virus 40. No T antigen was demonstrated in any tests with cells derived from 69 patients with various brain tumors. Twenty-two tumor cell strains cultured in the presence of a tumor promoter, phorbol ester, also failed to show the T antigen.


2003 ◽  
Vol 10 (2) ◽  
pp. 278-285 ◽  
Author(s):  
Raphael P. Viscidi ◽  
Dana E. M. Rollison ◽  
Emma Viscidi ◽  
Barbara Clayman ◽  
Elizabeth Rubalcaba ◽  
...  

ABSTRACT Enzyme immunoassays (EIAs) for detection of serum antibodies to simian virus 40 (SV40), BK virus (BKV), and JC virus (JCV) were developed by using virus-like-particles (VLPs) produced in insect cells from recombinant baculoviruses expressing the VP1 protein of the respective virus. Rhesus macaque sera with neutralizing antibodies to SV40 showed a high level of reactivity in the SV40 VLP-based EIA, and these sera also showed lower levels of reactivity in the BKV and JCV VLP-based EIAs. Rhesus macaque sera negative for neutralizing antibodies to SV40 were negative in all three EIAs. Competitive binding assays showed that SV40 VLPs inhibited BKV reactivity. In rhesus macaque sera, high optical density (OD) values for antibodies to SV40 VLPs were correlated with high OD values for antibodies to BKV but not with high OD values for antibodies to JCV VLPs. Human sera with neutralizing antibodies to SV40 were more reactive to SV40 VLPs than human sera without neutralizing antibodies to SV40. The greater SV40 reactivities of human sera were correlated with greater reactivities to BKV VLPs but not JCV VLPs. These data suggest that cross-reactivity with BKV antibodies may account for part of the low-level SV40 reactivity seen in human sera. With their greater versatility and their suitability for large-scale testing, the VLP-based EIAs for SV40, BKV, and JCV are likely to contribute to a better understanding of the biology of these viruses.


2017 ◽  
Vol 45 (2) ◽  
pp. 762-770 ◽  
Author(s):  
Jianhua Hu ◽  
Siying Li ◽  
Meifang Yang ◽  
Lichen Xu ◽  
Xuan Zhang ◽  
...  

Objective The effect of polyomavirus infection in HSCT recipients is poorly understood. Methods We evaluated 38 HSCT recipients. Polyomavirus was detected by nested qualitative polymerase chain reaction (PCR) assays of urine. The risk factors for BK virus and JC virus were analysed. The kidney and liver functions of infected and uninfected patients were compared. Results BK virus, JC virus, and simian virus 40 were detected in 21%, 42%, and 0% of HSCT recipients respectively. HCMV infection was found to be an independent risk factor for JC virus infection (odds ratio (OR): 8.528), while transplants with mismatched HLA are more susceptible to BK virus infection (OR: 12.000). Liver function of JC virus-infected subjects was worse than that of uninfected subjects. Conclusion We must be vigilant for opportunistic polyomavirus infections in HSCT recipients, especially those with HCMV co-infection or a mismatched HLA transplant. When unexplained liver function deterioration is observed, JC virus infection should be considered.


2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Ugo Moens ◽  
Maria Ludvigsen ◽  
Marijke Van Ghelue

Polyomaviruses are a family of small, nonenveloped viruses with a circular double-stranded DNA genome of ∼5,000 base pairs protected by an icosahedral protein structure. So far, members of this family have been identified in birds and mammals. Until 2006, BK virus (BKV), JC virus (JCV), and simian virus 40 (SV40) were the only polyomaviruses known to circulate in the human population. Their occurrence in individuals was mainly confirmed by PCR and the presence of virus-specific antibodies. Using the same methods, lymphotropic polyomavirus, originally isolated in monkeys, was recently shown to be present in healthy individuals although with much lower incidence than BKV, JCV, and SV40. The use of advanced high-throughput sequencing and improved rolling circle amplification techniques have identified the novel human polyomaviruses KI, WU, Merkel cell polyomavirus, HPyV6, HPyV7, trichodysplasia spinulosa-associated polyomavirus, and HPyV9. The skin tropism of human polyomaviruses and their dermatopathologic potentials are the focus of this paper.


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