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Canine Oral Papillomatosis II. Immunologic Aspects of the Disease^*

Velma C. Chambers, Charles A. Evans and Russell S. Weiser

( Department of Microbiology, University of Washington, Seattle 5, Wash.)

The subcutaneous and intramuscular injection of canine oral papilloma virus preparations with adjuvants into young dogs 2–3 weeks before inoculation of virus into the oral mucosa prevented the development of papillomas.

In dogs given an initial inoculation of virus into a single site in the oral mucosa followed by subsequent inoculations at other sites, papillomas developed at sites inoculated during the first 2 weeks of the incubation period but not at sites that were inoculated 3 or more weeks after the initial inoculation. The papillomas became visible in 5–10 weeks and continued to grow for an additional 8 weeks even though the host became immune to reinfection before the tumors appeared.

All areas of the oral mucosa of young dogs were susceptible to infection with the virus. In a few instances papillomas developed in the skin around the nose and mouth and at the muco-cutaneous junction of the eyelid. Most old dogs were resistant to infection with this virus, presumably as a result of a previous natural infection. Dogs whose papillomas had regressed resisted a second challenge inoculation of virus into the oral mucosa. The virus-neutralizing antibody titer of the serum of five dogs whose tumors had regressed ranged from < 1:10 to 1:500.

Attempts to accelerate or delay the onset of regression of tumors by actively immunizing dogs to tumor extract and to living tumor cells gave no clear evidence of a significant effect. Injections of immune serum may have delayed the onset of regression of tumors in two of four dogs and in addition may have prolonged the regression period in one of the animals. Transfer of "immune" lymph node and spleen cells from dogs in which tumors had regressed to dogs with developing papillomas appeared to accelerate regression in two of eleven dogs.

^* This investigation was supported by a grant from the National Cancer Institute of the National Institutes of Health, U.S. Public Health Service.

The authors gratefully acknowledge the assistance of Kenneth S. W. Kim and Spencer W. Shaw.

Received 1/27/60.