Induction of monocyte procoagulant activity by murine hepatitis virus type 3 parallels disease susceptibility in mice

MHV-3-induction of the PCA response is also more rapid than was previously observed, with a significant increase of PCA within 1-1.5 h in vitro and with maximum activity at 12-18 h. This contrasts to the 2-3-h lag period before monocyte PCA increases in response to LPS-triggered lymphocytes. Virus growth in a fully susceptible cloned cell line (17 CL1) was not detectable until 6 h after infection, and in monocytes from BALB/c mice infectious virus was not produced until 18 h postinfection. Thus, the induction of the PCA response in PBM antedates production of infectious virus and cannot be ascribed to it per se. Furthermore, little or no viral replication occurred in monocytes from C3H/St mice, and yet a robust generation of monocyte PCA followed. Thus, these initial observations suggest that the induction of the PCA response by PBM does not depend on virus replication.