Role of membrane phospholipids and glycolipids in the Vero cell surface receptor for rubella virus

Abstract

Membrane receptors for rubella virus (RV) in Vero cells were studied by means of two different approaches: (i) by enzyme treatment of the whole cell membrane and (ii) by testing the ability of isolated plasma membrane molecules to compete with cells for virus binding. The replication of RV was studied with both indirect immunofluorescence assay and molecular hybridization techniques. Phospholipases A2 and C digestion of cells greatly reduced the infectivity by the virus, pointing towards the involvement of lipid structures as receptor sites for RV. Furthermore, susceptibility of Vero cells to virus infection was also reduced after beta-N-acetyl-D-glucosaminidase, alpha-glucosidase and beta-galactosidase treatment, suggesting that carbohydrate residues may participate in a complex cellular receptor structure for RV. When the major membrane lipids were examined separately for their ability to inhibit viral infectivity, several phospholipids (phosphatidylserine, phosphatidylinositol, phosphatidylethanolamine, phosphatidylcholine, sphingomyelin) and glycolipids (gangliosides, lactosylceramide, cerebroside sulphate) showed a strong neutralizing activity, confirming the role of membrane lipid moiety in the cell surface receptor for RV.

Phosphatidylserine on HIV Envelope Is a Cofactor for Infection of Monocytic Cells

“…Anionic phospholipids, including PS, have been implicated as receptors and cofactors for several viruses, including VSV, rhabdoviruses, hepatitis B, influenza viruses, hemorrhagic septicemia, Sendai virus, rubella virus, and Sindbus virus (33)(34)(35)(36)(37)(38)(39)(40). Characterization of lipid composition of HIV-1 envelope shows that many lipids, including glycosphingolipids, cholesterol, and PS, are found in the membrane at a higher frequency than what is represented in the host membrane, suggesting a selective incorporation of these lipids (14).…”

Effects of Endocytosis Inhibitory Drugs on Rubella Virus Entry into VeroE6 Cells

“…It was previously described that purified sphingomyelin and ganglioside could competitively inhibit RV entry into Vero cells although phospholipids such as phosphatidyl serine and phosphatidyl inositol inhibited more significantly (19). It is generally believed that caveolae are formed from lipid rafts, consisting of cholesterol and sphingolipids, in the exoplasmic leaflet (31).…”

“…Concerning RV entry into cells, phospholipid and glycolipid in the cellular membrane seem to be involved in RV infection especially at the stage of viral attachment (19) and maybe form the coated pits (11), suggesting that endocytic mechanism may be operated. But the precise route of RV entry into host cells is not well understood.…”

Rubella Virus Replication and Links to Teratogenicity

“…However, RV can establish infections in a variety of cell lines (34), indicating that the host cell receptor is likely to be a ubiquitous molecule. Although the host cell receptor has not been identified, it appears that membrane phospholipids and glycolipids may be involved in viral attachment (94).…”