“…Although some CVB interact with the decay‐accelerating factor (DAF) , which is a complement regulatory protein that is expressed commonly on most cell surfaces, including human platelets , our previous studies showing that the CVB3 variant used was not blocked by soluble recombinant human DAF or by blocking antisera, as reported by others , strongly suggest that DAF was not involved. Although we observed a moderate reduction when platelet glycoproteins (GP) α IIb β 3 integrin and GPIb were blocked, the reported association of platelets with many different viruses such as Herpes, Vaccinia, Hanta, Echo, HIV or DENV, points out that platelets can bind viruses in a receptor‐independent way, as has been proven for HCV . Our data did not characterize whether CVB were inside or stuck on the surface.…”