Herpes virus infection alters electrical parameters of heart cell aggregates.
The spontaneous beat of embryonic heart cell aggregates in culture grew gradually weaker and stopped about 18 h after inoculation with herpes simplex virus 1 (HSV-1). Before electrical activity ceased, maximal action potential upstroke velocity fell to about 20% of control values, whereas overshoot and plateau duration declined about 50%. Maximal diastolic potential was reduced by only about 10%. Eighteen hours after viral inoculation, specific membrane resistance and intercellular coupling were measured in quiescent aggregates with injected current pulses passed between two widely spaced intracellular electrodes. These parameters were unaltered as compared with control aggregates. However, pairs of infected aggregates brought into contact required 8 h to synchronize their beats; mock-inoculated aggregates coupled in less than 1 h. It is concluded that the cell surface alterations caused by HSV-1 infection specifically reduce both fast and slow inward currents and interfere with the formation of new nexal junctions.
D000200:Action Potentials; D000818:Animals; D002642:Chick Embryo; D005071:Evoked Potentials; D006321:Heart / Q000196:embryology / Q000503:physiopathology*; D006339:Heart Rate; D006566:Herpesviridae Infections / Q000503:physiopathology*; D008564:Membrane Potentials; D013997:Time Factors