ALTERED MEMBRANE FATTY-ACIDS OF CULTURED HUMAN RETINAL-PIGMENT EPITHELIUM PERSISTENTLY INFECTED WITH RUBELLA-VIRUS MAY AFFECT SECONDARY CELLULAR FUNCTION

Citation
Ll. Williams et al., ALTERED MEMBRANE FATTY-ACIDS OF CULTURED HUMAN RETINAL-PIGMENT EPITHELIUM PERSISTENTLY INFECTED WITH RUBELLA-VIRUS MAY AFFECT SECONDARY CELLULAR FUNCTION, Archives of virology, 134(3-4), 1994, pp. 379-392
Citations number
31
Categorie Soggetti
Virology
Journal title
ISSN journal
03048608
Volume
134
Issue
3-4
Year of publication
1994
Pages
379 - 392
Database
ISI
SICI code
0304-8608(1994)134:3-4<379:AMFOCH>2.0.ZU;2-N
Abstract
Persistent infection with rubella virus (RV) can alter secondary funct ions of host cells. Previously we had documented defective phagocytosi s of latex beads by cultured human retinal pigment epithelial cells (R PE), persistently infected with M-33 RV (RPE/RV). Here, examining poss ible mechanisms for altered function, we reported significant differen ces between the total esterified fatty acids (FA) of RPE and RPE/RV me mbranes, measured by gas liquid chromatography. RPE/RV contained an in creased proportion of saturated FA, particularly palmitic acid, with a presence of unusual chromatographic FA peaks co-eluting with odd-numb ered long-chain carbon atom FA not normally found in human cells. Apic al membrane microvilli, structures essential to phagocytic activity of RPE and RPE/RV, observed by scanning and transmission electron micros copy, were similar in number and appearance between uninfected RPE and RPE/RV cells before and after latex bead addition. However, RPE/RV mi crovilli, possibly reflecting altered membrane FA composition, engaged latex beads less effectively than uninfected RPE microvilli. In addit ion, microvilli remained abnormally distributed on RPE/RV cell surface s at 48 h after latex addition. Thus, RV persistent infection may affe ct the cellular membrane fluidity and functional activity of human cel ls with increased saturated FA proportions and altered FA components o f membrane phospholipids. These changes may participate in the defecti ve phagocytosis of RPE/RV.