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Journal of Virology, December 1999, p. 10079-10085, Vol. 73, No. 12
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Wild-Derived Inbred Mice Have a Novel Basis of Susceptibility to Polyomavirus-Induced Tumors

Palanivel Velupillai, Izumi Yoshizawa, Dilip C. Dey, Sharon R. Nahill, John P. Carroll, Roderick T. Bronson, and Thomas L. Benjamin*

Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115

Received 18 June 1999/Accepted 25 August 1999

Polyomavirus induces a broad array of tumors when introduced into newborn mice of certain standard inbred strains, notably those bearing the H-2k haplotype. Susceptibility in these mice is conferred by an endogenous mouse mammary tumor virus superantigen (Mtv-7 sag) that acts to delete T cells required for polyomavirus-induced tumor immunosurveillance. In the present study we show that mice of two wild-derived inbred strains, PERA/Ei (PE) and CZECH II/Ei (CZ), are highly susceptible to polyomavirus but carry no detectable Mtv sag-related sequences and show no evidence of Vbeta deletion. C57BR/cdJ (BR) mice, which are H-2k but lack the endogenous Mtv-7, are highly resistant based on an effective anti-polyomavirus tumor immune response. When crossed with BR, both PE and CZ mice transmit their susceptibility in a dominant fashion, indicating a mechanism(s) that overrides the immune response of BR. Susceptibility in PE and CZ mice is not based on interference with antigen processing or presentation since cytotoxic T cells from BR can efficiently kill F1-derived tumor cells in vitro. The expected precursors of polyomavirus-specific cytotoxic T cells are present in both the wild inbred animals and their F1 progeny. These findings indicate a novel basis of susceptibility that operates independently of endogenous superantigen and prevents the development of tumor immunity.

* Corresponding author. Mailing address: Department of Pathology, Harvard Medical School, 200 Longwood Ave., Boston, MA 02115. Phone: (617) 432-1960. Fax: (617) 277-5291. E-mail: Thomas_Benjamin{at}hms.harvard.edu.

Journal of Virology, December 1999, p. 10079-10085, Vol. 73, No. 12
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Velupillai, P., Garcea, R. L., Benjamin, T. L. (2006). Polyoma Virus-Like Particles Elicit Polarized Cytokine Responses in APCs from Tumor-Susceptible and -Resistant Mice. J. Immunol. 176: 1148-1153 [Abstract] [Full Text]  
  • Velupillai, P., Carroll, J. P., Benjamin, T. L. (2002). Susceptibility to Polyomavirus-Induced Tumors in Inbred Mice: Role of Innate Immune Responses. J. Virol. 76: 9657-9663 [Abstract] [Full Text]  
  • Li, D., Dower, K., Ma, Y., Tian, Y., Benjamin, T. L. (2001). A tumor host range selection procedure identifies p150sal2 as a target of polyoma virus large T antigen. Proc. Natl. Acad. Sci. USA 98: 14619-14624 [Abstract] [Full Text]  
  • Moser, J. M., Altman, J. D., Lukacher, A. E. (2001). Antiviral Cd8+ T Cell Responses in Neonatal Mice: Susceptibility to Polyoma Virus-Induced Tumors Is Associated with Lack of Cytotoxic Function by Viral Antigen-Specific T Cells. JEM 193: 595-606 [Abstract] [Full Text]  


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