Abstract
Infection of HEp-2 cells with HSV-1 results in an increased stability of the cell membrane in comparison to uninfected cells. This effect is characterized by a reduced release of 51Cr, by an increased resistance against the non-ionic detergent Triton-X-100 and by a protection from complement mediated immune cytolysis with anti-HSV-1 antibodies. Infection with other viruses however (Poliomyelitis type 1, Mouse Elberfeld, Coxsackie B 6, Vesicular stomatitis) leads to opposite results with an enhancement of the 51Cr-release. - Comparative experiments with 7 other cell lines (Chang liver, FL, BHK21, primary rabbit kidney, HeLa, KB, primary embryonic chick fibroblasts) confirmed the above mentioned HSV-induced stability of the cell membrane with one exception: in embryonic chick fibroblasts (ECF), HSV-1 infection leads to an enhanced release and uptake of 51Cr as well as to an increased sensitivity to Triton-X-100, and the complement mediated immune cytolysis clearly can be demonstrated (Table 1).
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