Absence of monocyte procoagulant activity during the immune response to influenza virus.

The ability of mononuclear phagocytes (MPh) to manifest procoagulant activity (PCA) resulting in the formation of fibrin is thought to be a key MPh effector function in tissue repair. The present study addresses the question of whether monocyte PCA is confined to tissue hypersensitivity reactions or is a general correlate of all immune responses. We show here that PCA is not the obligate outcome when the immune system is stimulated. In particular, under in vitro conditions in which a mitogen (phytohemagglutinin) or an antigen (purified protein derivative of tuberculin) elicits good PCA responses, incubation with influenza virus does not result in the generation of PCA, although other parameters of response to the virus appear to be intact. Moreover, influenza virus can cause suppression of PCA when cultures are stimulated with either phytohemagglutinin, purified protein derivative of tuberculin, or endotoxin, conditions which would otherwise result in good PCA responses. This lack of PCA persists throughout the culture period and is not caused by an effect of influenza virus on the viability of either MPh or leukocytes in general.