Faculty Research 1990 - 1999
Wild-derived inbred mice have a novel basis of susceptibility to polyomavirus-induced tumors.
Document Type
Article
Publication Date
1999
Keywords
Animals-Wild, Antigen-Presentation, Disease-Susceptibility, Membrane-Glycoproteins, Mice, Mice-Inbred-C3H, Mice-Inbred-C57BL, Mice-Inbred-Strains, Papovaviridae-Infections, Polyomavirus, SUPPORT-U-S-GOVT-P-H-S, Tumor-Virus-Infections
First Page
10079
Last Page
10085
JAX Source
J Virol 1999 Dec; 73(12):10079-85.
Grant
R35CA44343/CA/NCI
Abstract
Polyomavirus induces a broad array of tumors when introduced into newborn mice of certain standard inbred strains, notably those bearing the H-2(k) 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-2(k) 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 F(1)-derived tumor cells in vitro. The expected precursors of polyomavirus-specific cytotoxic T cells are present in both the wild inbred animals and their F(1) progeny. These findings indicate a novel basis of susceptibility that operates independently of endogenous superantigen and prevents the development of tumor immunity.
Recommended Citation
Velupillai P,
Yoshizawa I,
Dey DC,
Nahill SR,
Carroll JP,
Bronson RT,
Benjamin TL.
Wild-derived inbred mice have a novel basis of susceptibility to polyomavirus-induced tumors. J Virol 1999 Dec; 73(12):10079-85.