Infection of fish cells with IHNV resulted in gradual increase in cytosolic free Ca$^$2+/ concentration ([Ca$^$2+/)] in CHSE, gradual decrease in [Ca$^$2+/] in FHM, and no significant change in RTG cells. The degree of [Ca$^$2+/] increase or decrease was dependent on the amount of infectious virus, and these [Ca$^$2+/] variations were maximal at 16 hours after virus infection (p. i.) in both cell lines. When the fish cells were infected with inactivated IHNV, evident variation in [Ca$^$2+/] was not observed. Thus, infectivity of IHNV appears to correlate with changes in [Ca$^$2+/] in virus-infected cells. These IHNV-induced [Ca$^$2+/] changes were partially blocked by cycloheximide, but not affected by cordycepin. It seems to be that virus-induced Ca$^$2+/ variations were more related with protein synthesis than RNA synthesis. Various Ca$^$2+/ related drugs were used in search for the mechanisms of the [Ca$^$2+/], changes following IHNV infection of CHSE cells. Decreasing extracellular Ca$^$2+/ concentration or blocking Ca$^$2+/ influx from extracellular media inhibited the IHNV-induced increase in [Ca$^$2+/], in CHSE cells. Similar results were obtained with intracellular Ca$^$2+/ sources are important in IHNV-induced [Ca$^$2+/] increase in CHSE cells.