Effects of ecotropic murine retroviruses on the dual-function cell surface receptor/basic amino acid transporter.

Cell surface receptor for ecotropic host-range mouse retroviruses: a cationic amino acid transporter

“…These results and other more detailed studies [23], strongly imply that interference to ecoMuL V superinfection can be accomplished without complete removal of ecoR from cell surfaces. One possibility is that interference involves competitive blockade of ecoR due to adsorption of endogenously synthesized viral env glycoprotein onto the cell surface receptors.…”

“…We also found that purified ecoMuLV env glycoprotein (gp70) acts as a specific weak impermeant inhibitor of mouse y+ when it is adsorbed onto mammalian cells at 37°C [23]. The amino acid uptake cycle of mouse y+ is slowed but not blocked by gp70 attachment.…”

“…We have detected several effects of ecoMuLV that are specific to mouse y+ and not to the homologuous mink y+ transporter [23]. When mouse fibroblasts or mink fibroblasts that express recombinant ecoR are persistently infected with ecoMuLVs, they become completely resistant to superinfection.…”

“…In the cases of HIV and an avian reticuloendotheliosis retrovirus, infection down-modulates receptor expression on cell surfaces. This involves an intracellular interaction of the newly-synthesized receptors and viral glycoproteins that prevents their processing to cell surfaces [21,23]. Presumably, severe ecoR downmodulation in chronically infected tissues could cause starvation for essential basic amino acids, with attendant abnormalities in cellular functions.…”

A Putative Cell Surface Receptor for Anemia-Inducing Feline Leukemia Virus Subgroup C Is a Member of a Transporter Superfamily

“…These findings suggest that the aplastic anemia may result from FeLV-C binding to its receptor, either on erythroblasts or on other cells that control the bone marrow microenvironment (1,27,28). By analogy to other retroviruses (4,19,22,52), the FeLV-C envelope glycoprotein might perturb the normal function of its receptor, resulting in cell killing or in changes in cytokine production. The observation that FeLV-C can infect other hematopoietic cells, including myeloid and lymphoid cells (7), implies that erythroblasts may be either exceptionally sensitive to secondary sequelae of infection or critically dependent on the normal function of the FeLV-C receptor.…”