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Selective effect of feline leukaemia virus on early erythroid precursors

Abstract

Feline leukaemia virus (FeLV), a horizontally transmitted retro-virus, is the aetiological agent of feline lymphosarcoma and leukaemia1–3. In addition, the establishment of persistent FeLV viraemia in cats has been associated with the induction of a wide range of non-neoplastic conditions including immunosuppression, reproductive disorders and anaemias4,5. FeLV isolates from cats may be divided into three subgroups, A, B and C, based on their interference patterns6,7. In natural isolates, FeLV-C is always found in association with subgroups A or AB but the subgroup C component may be separated as a non-defective virus capable of establishing a persistent viraemia in neonatal cats. Pure red cell hypoplasia (PRCH) is one of three primary forms of FeLV-associated anaemia recognized in cats8,9 and we report here that three new biologically cloned FeLV-C isolates will reproduce this disease. We have demonstrated that infection of cats with FeLV-C/Sarma results in rapid depletion of early erythroid precursors (burst-forming units–erythroid; BFU-E) while the proportion of the myeloid precursor (granulocyte-macrophage colony-forming cells; GM-CFC) in the bone marrow remains normal.

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Onions, D., Jarrett, O., Testa, N. et al. Selective effect of feline leukaemia virus on early erythroid precursors. Nature 296, 156–158 (1982). https://doi.org/10.1038/296156a0

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