Immunologic dysfunction during viral oncogenesis: II. Inhibition of cellular immunity to viral antigens by malignant rabbit fibroma virus |
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Authors: | Eileen Skaletsky Patricia A. Sharp Stewart Sell David S. Strayer |
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Affiliation: | 1. Department of Pathology, University of California, San Diego, La Jolla, California 92093 USA;2. Department of Pathology and Laboratory Medicine, University of Texas Health Science Center, Houston, Texas 77025 USA;3. Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 06510 USA |
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Abstract: | The ability of two related viruses—Shope fibroma virus (SFV) and malignant rabbit fibroma virus (MV)—to induce virus-specific immune responses in lymphocytes of recipient animals was studied. SFV produces a benign local tumor which regresses in 12–14 days. Using an assay for virus-induced lymphocyte blastogenesis lymphocytes reactive to SFV were detected, both in rabbits bearing SFV-induced tumors and in rabbits whose SFV-induced tumor had regressed. These virus-reactive cells were detected in peripheral blood and spleen, and in lymph nodes draining the primary tumor. In contrast, MV produces a disseminated tumor and eventual death. MV does not induce detectable blastogenic responses in lymphocyte populations. SFV and MV are antigenically cross reactive: rabbits immune to SFV do not develop MV-induced tumors, and antisera to each virus neutralize both equally. Lymphocytes from SFV-infected rabbits proliferate in vitro in response to MV that has been inactivated by ultraviolet light (uv/MV) but not to infectious MV. In contrast, lymphocytes from rabbits infected with MV do not respond to uv-inactivated MV or to SFV. Thus, infectious MV inhibits the development of normal blastogenic responses in vivo and prevents the expression of those responses in lymphocytes from MV-resistant, SFV-immune rabbits in vitro. The relevance of this impairment to the differences in the clinical courses of SFV- and MV-induced tumors is discussed. |
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