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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.
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| Copyright © 1989 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||