Platelets interact with Coxsackieviruses B and have a critical role in the pathogenesis of virus-induced myocarditis

SOLEDAD, NEGROTTO*; CAROLINA JAQUENOD DE GIUSTI*; LEONARDO RIVADENEYRA; AGUSTIN E URE; HEBE A. MENA; MIRTA SCHATTNER; RICARDO M. GOMEZ

JOURNAL OF THROMBOSIS AND HAEMOSTASIS

WILEY-BLACKWELL PUBLISHING, INC

Lugar: Londres; Año: 2015

1538-7933

Background: To further understand the role of platelets in the pathogenesis of viral infections we explored platelet interaction with Coxsackievirus B (CVB) 1 and 3. CVB is a group of viruses that cause the majority of human enterovirus related viral myocarditis; their receptor (CAR) is expressed on the platelet surface and there is a well characterized CVB3-induced myocarditis murine model. Methods: Human platelets were infected with CVB1 and 3 and viruses were detected in pellets and in supernatants. C57BL/6J mice with or without platelet depletion were inoculated with CVB3 and peripheral blood and heart samples collected at different times post-infection. Results: CVB1 and 3 RNA and a capsid protein were detected in infected platelets. Despite the fact that titration assays in Vero cells showed increasing infectivity titers over time, supernatants and pellets from infected platelets showed similar levels, suggesting that platelets were not susceptible to a replicative infectivity cycle. CVB binding was CAR-independent and resulted in P-selectin and phosphatidylserine (PS) exposure.