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Cancer Epidemiology Biomarkers & Prevention Vol. 14, 521-524, February 2005
© 2005 American Association for Cancer Research


Short Communication

Antibody Responses to Simian Virus 40 T Antigen: A Case-Control Study of Non-Hodgkin Lymphoma

Eric A. Engels1, Jinbo Chen1, Patricia Hartge1, James R. Cerhan2, Scott Davis3, Richard K. Severson4, Wendy Cozen5 and Raphael P. Viscidi6

1 Division of Cancer Epidemiology and Genetics, National Cancer Institute, Department of Health and Human Services, Rockville, Maryland; 2 Mayo Clinic College of Medicine, Rochester, Minnesota; 3 Fred Hutchinson Cancer Research Center, Seattle, Washington; 4 Karmanos Cancer Institute, Wayne State University, Detroit, Michigan; 5 University of Southern California, Los Angeles, California; and 6 Johns Hopkins University School of Medicine, Baltimore, Maryland

Requests for reprints: Eric A. Engels, Viral Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Department of Health and Human Services, 6120 Executive Boulevard, EPS 8010, Rockville, MD 20892. E-mail: engelse{at}exchange.nih.gov

A possible role for SV40, a macaque polyomavirus, in non-Hodgkin lymphoma (NHL) in humans was raised recently by the reported detection of SV40 DNA in tumor tissue. Animals with SV40-induced tumors frequently produce high-level antibodies against T antigen, the SV40 oncoprotein. In this study, we assessed whether SV40 T antibody measured in humans supported a relationship between SV40 and NHL. Subjects were sampled from a U.S. population-based case-control study of NHL, according to presence of antibodies against capsids of SV40 and BK, a related human polyomavirus (n = 85 cases, n = 95 controls). T antibody was measured by enzyme immunoassay. We also evaluated serum specimens from SV40-infected and SV40-uninfected macaques (n = 19 and n = 8, respectively), SV40-uninfected hamsters (n = 5), and hamsters with SV40-induced tumors (n = 10). Hamsters with SV40-induced tumors all produced robust SV40 T antibody [median absorbance, 0.99), whereas SV40-uninfected hamsters and macaques had much lower levels (median absorbance, 0.05 and 0.04, respectively). NHL cases, controls, and SV40-infected macaques resembled these latter two groups, generally showing only low-level T antibody (median absorbance, 0.03, 0.04, and 0.04, respectively). Overall, only five cases (6%) and five controls (5%) had T antibody responses classified as seropositive (odds ratio, 1.2; 95% confidence interval, 0.3-4.6). Interestingly, all 10 humans with T antibody responses also showed antibody responses to BK capsid. We found no association between the presence of T antibody and NHL, arguing against SV40 as a cause of NHL. Infrequent and low-level T antibody responses among humans could represent cross-reactivity to BK virus T antigen.




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D. L. Poulin and J. A. DeCaprio
Is There a Role for SV40 in Human Cancer?
J. Clin. Oncol., September 10, 2006; 24(26): 4356 - 4365.
[Abstract] [Full Text] [PDF]




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Molecular Cancer Research Cancer Prevention Research
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Copyright © 2005 by the American Association for Cancer Research.