ROLE OF AKATA CELL-MEMBRANE FLUIDITY IN SUSCEPTIBILITY TO EPSTEIN-BARR-VIRUS INFECTION

Infection by Epstein-Barr virus (EBV), a B lymphotropic human herpesvi rus, of its target cells is initiated by the binding of the viral enve lope glycoprotein gp350/220 to a 145-kDa cell membrane glycoprotein (C D21, CR2) which also serves as the receptor for the complement fragmen t C3d (Fingeroth et al., 1984; Nemerow at al., 1987). We used the fluo rescent probe 1-6-diphenyl-1,3,5-hexatriene (DPH), extremely sensitive to the polar environment, in order to analyse the membrane viscosity distribution in single cells of two lymphoid cell lines, pail and Akat a. Lipid analysis on both cell lines showed a slightly lower cholester ol :phospholipid molar ratio on Akata than on pail cells. Measurements of cell fluidity by DPH polarization in native cells and after choles terol enrichment indicated that the apparent Akata membrane viscosity was lower than the viscosity of pail cells. To examine the possibility that this difference could be correlated to a difference in the behav iour of Akata and Rail cells in expressing EBV early antigens, both li nes were superinfected with the EBV non-transforming P3HR1 strain. We report here evidence that lipid composition can regulate EBV entry int o cells.