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

A Ono, H Tatsumi, K Yamamoto, Y Katayama
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Abstract

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.

人B淋巴细胞对eb病毒的反应是细胞内Ca2+浓度的增加。
用fura-2荧光法测定钙离子浓度,检测eb病毒感染人B淋巴细胞的早期事件。B淋巴细胞胞内钙离子浓度([Ca2+]i)在EBV作用下升高。观察到三种类型的[Ca2+]i升高:(1)早期瞬态[Ca2+]i升高;(3)缓慢的[Ca2+]i增加,没有早期的瞬态[Ca2+]i增加。在零Ca2+条件下观察到早期的短暂性增加,但当细胞在暴露于病毒之前用ryanodine预处理时,它被抑制。在无Ca(2+)的细胞外条件下,没有观察到缓慢持续的[Ca2+]i增加。这些结果表明,早期短暂的[Ca2+]i增加是由细胞内钙储存位点的Ca2+释放介导的,而缓慢持续的[Ca2+]i增加是由Ca2+通过质膜内流介导的。用荧光标记物罗丹明对B淋巴细胞表面的病毒受体进行染色,并在共聚焦显微镜下观察EBV应用后的盖帽过程。应用EBV后,观察了病毒封顶过程和病毒受体的定位。封顶过程的时间过程似乎与缓慢,持续的[Ca2+]i增加相似。
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