Human platelets and their capacity of binding viruses: meaning and challenges?

Abstract

Blood platelets are first aimed at ensuring primary hemostasis. Beyond this role, they have been acknowledged as having functions in the maintenance of the vascular arborescence and, more recently, as being also innate immune cells, devoted notably to the detection of danger signals, of which infectious ones. Platelets express pathogen recognition receptors that can sense bacterial and viral moieties. Besides, several molecules that bind epithelial or sub-endothelial molecules and, so forth, are involved in hemostasis, happen to be able to ligate viral determinants, making platelets capable of either binding viruses or even to be infected by some of them. Further, as platelets express both Fc-receptors for Ig and complement receptors, they also bind occasionally virus-Ig or virus-Ig-complement immune complexes. Interplays of viruses with platelets are very complex and viral infections often interfere with platelet number and functions. Through a few instances of viral infections, the present review aims at presenting some of the most important interactions from pathophysiological and clinical points of view, which are observed between human viruses and platelets.

Figure 1

Platelet receptors acknowledged to bind viruses, along with their primary molecular targets. CLEC-2: C-type lectin-like type II transmembrane receptor. CR-2: Complement Receptor type 2. CCR-1, CCR-3, CCR-4: C-C chemokine Receptor type 1, 3 and 4. CXCR-1, CXCR-2, CXCR-4: C-X-C chemokine receptor type 1, 2 and 4. DC-SIGN: Dendritic Cell-Specific Intercellular adhesion molecule-3-Grabbing Non-integrin. GP-VI: Glycoprotein VI. PAR-1/PAR-4: Platelet Activating Receptor ¼.