Abstract
PROFOUND modifications in the macromolecular structure of cell membranes and membrane-related functions have been demonstrated on infection with various viruses1,2. For example, shortly after infection with certain herpesviruses, synthesis and insertion of host proteins into plasma membranes cease and new virus-specified proteins begin to appear3,4. These viral proteins differ from the cell membrane proteins in size, electrophoretic mobility, extent of glycosylation and sulphate incorporation3–5. The changes in membrane structure are reflected in altered morphology, antigenic characteristics and contact interactions of herpesvirus-infected cells4,6. They also appear to affect the ion-dependent electrical properties of the cells as shown by alterations in the transmembrane potential of cells infected by herpesviruses in vitro and in vivo7,9. To elucidate further alterations in membrane-related cell functions, as well as virus–cell interactions associated with herpesvirus infection, we are studying the effects of herpes simplex viruses (HSV) type 1 and 2 on chick embryo heart cells, which provide a useful system, particularly when aggregated into spontaneously beating spheroidal clusters10–13. We found that these viruses stopped the spontaneous beating of the cells before cell ‘death’.
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