{"title":"流感病毒诱导人血小板聚集和释放反应的机制","authors":"S Hagiwara","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Mechanisms of aggregation and release reactions of human platelets induced by non-hemolytic influenza virus were studied. The influenza virus (PR/8 strain) caused aggregation of platelets with ATP release in a dose-dependent manner over the range of 640-10,240 HA titers. The aggregation was always preceded by a lag period and subsequent shape changes. The virus-induced aggregation was enhanced by exposure of the reaction mixtures to cold at 4 degrees C for 30 min and inhibited by apyrase, acetylsalicylic acid and dipyridamole. Ingestion of acetylsalicylic acid also inhibited the aggregation. Gel-filtered platelets were aggregated by influenza virus only after the reaction mixtures had been previously incubated at 4 degrees C for 30 min and then stirred at 37 degrees C. In the absence of divalent cations (Ca2+ less than or equal to 2 x 10(-5) M, Mg2+ less than or equal to 1 x 10(-5) M), gel-filtered platelets were not aggregated by influenza virus. These results suggest that influenza virus was absorbed onto the platelet surface and caused the release of ADP from platelets, which in turn, aggregated platelets.</p>","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 5","pages":"906-15"},"PeriodicalIF":0.0000,"publicationDate":"1989-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"[Mechanisms of human platelet aggregation and release reaction induced by influenza virus].\",\"authors\":\"S Hagiwara\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Mechanisms of aggregation and release reactions of human platelets induced by non-hemolytic influenza virus were studied. The influenza virus (PR/8 strain) caused aggregation of platelets with ATP release in a dose-dependent manner over the range of 640-10,240 HA titers. The aggregation was always preceded by a lag period and subsequent shape changes. The virus-induced aggregation was enhanced by exposure of the reaction mixtures to cold at 4 degrees C for 30 min and inhibited by apyrase, acetylsalicylic acid and dipyridamole. Ingestion of acetylsalicylic acid also inhibited the aggregation. Gel-filtered platelets were aggregated by influenza virus only after the reaction mixtures had been previously incubated at 4 degrees C for 30 min and then stirred at 37 degrees C. In the absence of divalent cations (Ca2+ less than or equal to 2 x 10(-5) M, Mg2+ less than or equal to 1 x 10(-5) M), gel-filtered platelets were not aggregated by influenza virus. These results suggest that influenza virus was absorbed onto the platelet surface and caused the release of ADP from platelets, which in turn, aggregated platelets.</p>\",\"PeriodicalId\":76233,\"journal\":{\"name\":\"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society\",\"volume\":\"52 5\",\"pages\":\"906-15\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1989-08-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
研究了非溶血性流感病毒诱导人血小板聚集和释放反应的机制。流感病毒(PR/8株)引起血小板聚集,并以剂量依赖的方式在640-10,240血凝素滴度范围内释放ATP。聚集之前总是有一个滞后期和随后的形状变化。将反应混合物置于4℃低温下30 min,增强了病毒诱导的聚集,并被apyrase、乙酰水杨酸和双嘧达莫抑制。摄入乙酰水杨酸也能抑制其聚集。凝胶滤过的血小板只有在反应混合物事先在4℃孵卵30分钟,然后在37℃搅拌后才会被流感病毒聚集。在没有二价阳离子(Ca2+小于或等于2 × 10(-5) M, Mg2+小于或等于1 × 10(-5) M)的情况下,凝胶滤过的血小板不会被流感病毒聚集。这些结果表明,流感病毒被吸收到血小板表面,导致血小板释放ADP,进而使血小板聚集。
[Mechanisms of human platelet aggregation and release reaction induced by influenza virus].
Mechanisms of aggregation and release reactions of human platelets induced by non-hemolytic influenza virus were studied. The influenza virus (PR/8 strain) caused aggregation of platelets with ATP release in a dose-dependent manner over the range of 640-10,240 HA titers. The aggregation was always preceded by a lag period and subsequent shape changes. The virus-induced aggregation was enhanced by exposure of the reaction mixtures to cold at 4 degrees C for 30 min and inhibited by apyrase, acetylsalicylic acid and dipyridamole. Ingestion of acetylsalicylic acid also inhibited the aggregation. Gel-filtered platelets were aggregated by influenza virus only after the reaction mixtures had been previously incubated at 4 degrees C for 30 min and then stirred at 37 degrees C. In the absence of divalent cations (Ca2+ less than or equal to 2 x 10(-5) M, Mg2+ less than or equal to 1 x 10(-5) M), gel-filtered platelets were not aggregated by influenza virus. These results suggest that influenza virus was absorbed onto the platelet surface and caused the release of ADP from platelets, which in turn, aggregated platelets.