Effect of Viruses on Platelet Aggregation and Platelet Survival in Rabbits

Abstract

Thrombocytopenia may occur in association with some viral infections. The objective of the present study was to examine the mechanisms by which myxoviruses may induce thrombocytopenia via a direct effect on platelets. Newcastle disease virus (NDV) caused platelet aggregation and loss of granule and cytoplasmic constituents from washed rabbit platelet suspensions. This effect of NDV was abolished by heating the virus at 56°C. In contrast, influenza virus did not cause these platelet reactions. Pretreatment of platelets with NDV abolished their ability to respond to NDV and reduced their response to ADP and thrombin, but treatment of platelets with heated NDV or with influenza virus did not have a major effect on their function in vitro. NDV and influenza virus, which contain neuraminidase activity, removed platelet sialic acid. When platelets pretreated with these viruses were injected into normal rabbits, they were rapidly removed from the circulation. Since platelets pretreated with purified neuraminidase are also rapidly cleared after injection, it seems likely that the loss of platelet sialic acid caused by these viruses is responsible for the removal of the platelets from the circulation. In contrast, platelets treated with inactivated NDV, inactivated influenza virus, or chikungunya virus (which does not have neuraminidase activity) survived normally. Thus there may be at least two mechanisms directly involved in virus-induced thrombocytopenia: (1) paramyxoviruses such as NDV may cause intravascular platelet aggregation, and (2) platelets exposed to viruses with neuraminidase activity may lose surface sialic acid and be rapidly cleared from the circulation.