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KN Khan, GJ Kociba and ML Wellman
Department of Veterinary Pathobiology, College of Veterinary Medicine, Ohio
State University, Columbus.
Erythroid aplasia is induced in cats by feline leukemia virus (FeLV) of
subgroup C but not by FeLV of subgroup A. In an investigation of the role
of macrophages in FeLV-C-induced diseases, the concentrations of FeLV and
tumor necrosis factor-alpha (TNF-alpha) were compared between feline
peritoneal macrophages incubated with FeLV of subgroup A or C. FeLV of both
subgroups infected macrophages, but expression of FeLV-C was 21-fold higher
than FeLV-A in peritoneal macrophages (P = .004). The supernatants of
FeLV-C-inoculated macrophage cultures contained significantly higher levels
of TNF-alpha (70 +/- 14 U/mL) at 72 hours postincubation compared with
FeLV-A-inoculated (38 +/- 8 U/mL) and uninoculated (31 +/- 8 U/mL)
cultures. Moreover, a positive correlation was shown between
cell-associated FeLV surface glycoprotein gp70 and TNF-alpha expression in
FeLV-C-infected macrophages by immunofluorescence (r = .6; P = .001),
measured with a computer- assisted, laser-based digital imaging system. The
addition of TNF-alpha to a uniform population of FeLV-infected cells
(feline embryonic fibroblasts) caused an enhancement of viral expression (P
< .05). These results indicate that FeLV-C has tropism for macrophages,
FeLV expression is positively correlated with TNF-alpha expression in
macrophages, and TNF-alpha enhances FeLV replication in fibroblasts. We
suggest that FeLV-C infection of macrophages and secretion of TNF-alpha may
be important in hematopoietic suppression in FeLV-C-infected cats.
This article has been cited by other articles:
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| Copyright © 1993 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
