Human B lymphocytes respond to Epstein-Barr virus with an increase in intracellular Ca2+ concentration.

Early events in the infection of human B lymphocytes by Epstein-Barr virus (EBV) were examined by measuring calcium ion concentration from fluorescence with fura-2. Intracellular Ca ion concentration ([Ca2+]i) of B lymphocytes increased in response to EBV application. Three types of [Ca2+]i-increase were observed: (1) an early transient [Ca2+]i-increase; and (3) a slow [Ca2+]i-increase without the early transient [Ca2+]i-increase. The early transient increase was observed in the zero Ca2+ condition, but it was suppressed when cells were pretreated with ryanodine before exposure to the virus. The slow sustained [Ca2+]i increase was not observed in Ca(2+)-free extracellular conditions. These results suggest that the early transient [Ca2+]i increase is mediated by Ca2+ release from intracellular Ca storage sites, and the slow sustained [Ca2+]i increase is mediated by the Ca2+ influx through the plasma membrane. Virus receptors on the surface of B lymphocytes were stained with a fluorescence marker, rhodamine, and the capping process after EBV application was observed under a confocal microscope. The capping process and the localization of virus receptors were observed after EBV application. The time course of the capping process seems similar to that of the slow, sustained [Ca2+]i increase.