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Basic Sciences

Proliferative Fibromatosis in Avian Skeletal Muscle Caused by Cloned Recombinant Avian Leukosis Viruses

Nandini Kogekar, Thomas L. Spurgeon, M. Celeste Simon and Ralph E. Smith
Nandini Kogekar
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Thomas L. Spurgeon
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M. Celeste Simon
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Ralph E. Smith
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DOI:  Published April 1987
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Abstract

Two molecular recombinants (EU-8 and K-3) constructed from ringnecked pheasant virus and UR2AV, the helper virus associated with avian sarcoma virus UR2, caused a high incidence of a hitherto unreported pathological condition in chick skeletal muscle. A disease spectrum was observed in which muscle was infiltrated by proliferating fibroblasts and caused white streaks, white diffuse areas, or well-defined elongated tumors. Fibroblast proliferation was progressive, and the gross presentation depended on the rapidity and extent of proliferation. There was evidence of anaplasia but not frankly malignant disease or metastases. The disease was produced at a high frequency when 10-day-old embryos were infected. Breast muscle (pectoralis major and minor) was affected with variable severity in all birds, thigh muscles were affected occasionally, while other thoracic, external abdominal, and wing muscles were affected very rarely. Progression of proliferative muscle lesions was demonstrated by sequential necropsies and microscopic examination of muscle samples. The disease appeared before 2 weeks of age, and thin white streaks with minimal cellular proliferation were the earliest lesions observed. Elongated, spindle-shaped tumors were the most advanced form of proliferation observed. The advanced lesions showed cellular anaplasia and signs of rapid growth, and appeared most commonly at 6 weeks of age or later. Histologically, mild proliferation correlated with normal appearing fibroblasts producing collagen. Severe proliferation correlated with anaplastic, rapidly dividing cells producing little collagen and a high mitotic index.

A decrease in the virus dose resulted in less severe fibromatosis, but at least one chicken infected with a low virus dose showed severe disease. When 10- or 35-day-old hatched chicks were injected in the breast muscle with EU-8 or K-3, a low incidence of lymphoid leukosis was observed, but no fibromatosis resulted during an observation period of 27 weeks.

Infectious virus was extracted from the fibromatosis in the breast muscle, and extracted virus caused the same disease when injected in 10-day-old embryos. No transforming activity was observed on normal chick embryo fibroblast monolayers. Cell cultures were established from areas in the breast muscle affected by fibromatosis, and from discrete tumors. These cells did not show any signs of transformation in culture. Supernatants obtained from these cell cultures caused fibromatosis when injected into 10-day-old embryos, but did not transform normal chick embryo fibroblasts.

Footnotes

  • ↵1 This work was supported by USPHS Grant CA-35984.

  • ↵4 To whom requests for reprints should be addressed, at Colorado State University, College of Veterinary Medicine and Biomedical Sciences, Department of Microbiology, Fort Collins, CO 80523.

  • Received October 20, 1986.
  • Revision received January 13, 1987.
  • Accepted January 14, 1987.
  • ©1987 American Association for Cancer Research.
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April 1987
Volume 47, Issue 8
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Proliferative Fibromatosis in Avian Skeletal Muscle Caused by Cloned Recombinant Avian Leukosis Viruses
Nandini Kogekar, Thomas L. Spurgeon, M. Celeste Simon and Ralph E. Smith
Cancer Res April 15 1987 (47) (8) 2083-2091;

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Proliferative Fibromatosis in Avian Skeletal Muscle Caused by Cloned Recombinant Avian Leukosis Viruses
Nandini Kogekar, Thomas L. Spurgeon, M. Celeste Simon and Ralph E. Smith
Cancer Res April 15 1987 (47) (8) 2083-2091;
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