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Retrovirus-induced feline pure red blood cell aplasia: pathogenesis and
response to suramin
JL Abkowitz
Department of Medicine, University of Washington, Seattle 98195.
Feline leukemia virus, subgroup C/Sarma (FeLV-C/Sarma) induces pure red
blood cell aplasia in cats. Although erythroid (BFU-E and CFU-E) and
granulocyte/macrophage (CFU-GM) progenitors are infected with this virus,
only erythropoiesis is impaired. Two to 3 weeks before the onset of anemia,
CFU-E become undetectable in marrow cultures while earlier erythroid
progenitors (BFU-E) persist, suggesting that FeLV-C/Sarma (presumably via
its envelope glycoprotein gp70) inhibits the differentiation of BFU-E to
CFU-E in vivo. To correlate in vitro observations with the progression of
disease, prospective studies were performed in six cats. These studies
showed that at the time that the frequencies of CFU-E decreased in marrow
cultures, BFU-E no longer responded to hematopoietic growth factor(s),
although the responses of CFU-GM were unchanged. In further studies, anemic
cats received suramin, a reverse-transcriptase inhibitor with other diverse
effects. Within 4 to 14 days, erythropoiesis improved and up to 1,616 CFU-E
were detected per 10(5) marrow mononuclear cells. However, progenitor cells
remained infected, suggesting that suramin modulated erythroid
differentiation without inhibiting progenitor infection. These observations
led to the hypothesis that the gp70 of FeLV-C/Sarma impairs BFU-E
differentiation by interference with ligand/receptor interactions or signal
transduction pathways unique to erythroid cells. Understanding this
mechanism should provide insights into the interactions controlling early
erythropoiesis.
Volume 77,
Issue 7,
pp. 1442-1451,
04/01/1991
Copyright © 1991 by The American Society of Hematology
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