Dengue virus entry and replication does not lead to productive infection in platelets

Abstract

Thrombocytopenia is a characteristic feature during the acute phase of dengue infection and has been found to associate with vascular leakage in severe dengue. Although dengue antigens have been observed in platelets, there is no strong evidence to suggest a direct infection of platelets by dengue virus as a contributing factor for thrombocytopenia. We show that dengue virus can enter platelets but replicate viral ribonucleic acid to a minimal extent and, therefore, cannot produce infectious virus. Dengue antigen was undetectable in platelets isolated from dengue patients; however, we observed an increase in CD14+CD16+ monocyte-platelet complexes, suggesting a mechanism for platelet clearance.