Reovirus type 3 binds to antagonist domains of the beta-adrenergic receptor

Abstract

C6 glioma, and mouse L cells. This inhibition of D-adrenergic binding was dose related. Reovirus did not interfere with dopaminergic binding or isoproterenol-induced activation of adenylate cyclase. In addition, reovirus infected Y1 cells, which bind ,-adrenergic antagonist ligands but lack agonist-induced activity. These results suggest that reovirus infection is initiated by binding to antagonist (nonfunctional) domains of the adrenergic receptor complex.

Evolution of Cell Recognition by Viruses: A Source of Biological Novelty with Medical Implications

“…Reovirus type 1 JAM (Barton et al, 2001a(Barton et al, , 2001b; carbohydrate (unknown nature) (Lerner et al, 1963;Chappell et al, 2000); EGFR (Strong et al, 1993;Tang et al, 1993) Reovirus type 3 JAM (Barton et al, 2001a(Barton et al, , 2001b; sialic acid (Gentsch and Pacitti, 1987;Paul et al, 1989;Chappell et al, 2000); type A glycophorin (Paul and Lee, 1987); -adrenergic receptor (Co et al, 1985b;Choi and Lee, 1988;Donta and Shanley, 1990) Group A human rotavirus (strain Wa)…”

A p65/p95 Neural Surface Receptor is Expressed at the S‐G2 Phase of the Cell Cycle and Defines Distinct Populations

“…Various proteins have been suggested to subserve the role of the reovirus type 3 receptor (Epstein et al, 1984;Co et al, 1985a, b;Sawutz et al, 1987;Paul et al, 1989;Choi et al, 1990;Donta and Ahanley, 1990;El Ghor et af., 1992;Shong et al, 1993;Tang et al, 1993). However, the nature of this receptor remains controversial.…”