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Colony forming T lymphocyte deficit in the development of feline retrovirus induced immunodeficiency syndrome

SL Quackenbush, JI Mullins and EA Hoover

Department of Pathology, Colorado State University, Fort Collins 80523.

The identification and molecular cloning of a feline leukemia virus (FeLV) isolate (FeLV-FAIDS) that consistently produces immunodeficiency syndrome has allowed prospective investigation of events that occur in the prodromal phase of disease. Using a T-lymphocyte colony forming assay (T-CFU-Ic) we have demonstrated that a drastic depletion of circulating T-CFU-Ic prefigures the development of clinical immunodeficiency disease in inoculated cats and correlates with the appearance and replication of the FeLV-FAIDS variant genome in serially collected bone marrow samples. During the same presymptomatic time period, no significant alterations in conventional mitogen-induced lymphocyte blastogenic responses or in circulating lymphocyte numbers were evident. Thus T-CFU-Ic assay but not conventional mitogen-driven blastogenesis identified animals destined to develop immunodeficiency syndrome. The correlation among T-CFU-Ic depletion, the replication of the lymphocytopathic FeLV-FAIDS variant genome in hematopoietic and lymphoid tissues, and the onset of clinical disease, infers that ablation of a colony-forming T lymphocyte progenitor subset is important in the early pathogenesis of feline retrovirus-induced immunodeficiency syndrome.

Volume 73, Issue 2, pp. 509-516, 02/01/1989
Copyright © 1989 by The American Society of Hematology


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J. Virol.Home page
A. S. Lauring, M. M. Anderson, and J. Overbaugh
Specificity in Receptor Usage by T-Cell-Tropic Feline Leukemia Viruses: Implications for the In Vivo Tropism of Immunodeficiency-Inducing Variants
J. Virol., October 1, 2001; 75(19): 8888 - 8898.
[Abstract] [Full Text] [PDF]



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