Introduction

Viruses have long been causally linked, theoretically, with acquired idiopathic thrombocytopenia and more recently have been associated directly with megakaryocytes and platelets during retroviral infections caused by the human immunodeficiency virus and human T-cell lymphotrophic viruses. While the pathophysiology of the association of these viruses with megakaryocytes and platelets remains incompletely understood, recent investigations with molecular methods have begun to elucidate some potential mechanisms of the complex interactions between viruses and platelets. This chapter will focus on the interactions of viruses and platelets that are associated with human platelet disorders. In addition, recent technology developed to inactivate viruses in platelet concentrates prepared for transfusion is of interest. This technology appears to be an important intervention to further improve the safety of transfusion, and also may well be a significant modality for prevention of platelet transfusion associated infections due to new viruses that may enter the donor population in the future.

Substantial improvement in the safety of platelet transfusion has been achieved through addition of new tests, such as nucleic acid tests, yet residual risk persists in association with transfusion of platelet concentrates. Transfusion of platelet concentrates has been implicated in the transmission of viruses, bacteria, and protozoa. While it is commonly recognized that hepatitis B virus (HBV), hepatitis C virus (HCV), cytomegalovirus (CMV), and the retroviruses, such as human immunodeficiency virus (HIV) and the human lymphotrophic viruses (HTLV) can be transmitted through cellular components, other viruses are emerging as potentially significant transfusion transfusion associated infectious agents.