Macrophage Tropism of Feline Leukemia Virus (FeLV) of Subgroup-C and Increased Production of Tumor Necrosis Factor-α by FeLV-Infected Macrophages

Abstract

AbstractErythroid 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-α (TNF-α) 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-α (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-α 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-α 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-α expression in macrophages, and TNF-α enhances FeLV replication in fibroblasts. We suggest that FeLV-C infection of macrophages and secretion of TNF-α may be important in hematopoietic suppression in FeLV-C–infected cats.