Activation of the immune coagulation system by murine hepatitis virus strain 3.
Viral infections result in alterations in hemostasis and coagulation. It has previously been shown that susceptibility to murine hepatitis virus strain 3 (MHV-3), a coronavirus, correlates directly with the spontaneous, T lymphocyte-instructed expression of a procoagulant monokine that exhibits prothrombin-cleaving activity (procoagulant activity [PCA]). A biologic role for PCA in the pathogenesis of MHV-3 infection is suggested by results of in vivo microscopic observations made during acute MHV-3 infection. Recently, it has been demonstrated that prostaglandin E2 abrogates the induction of PCA by MHV-3 both in vivo and in vitro and prevents hepatic necrosis and the associated microcirculatory changes. These data suggest that MHV-3 induces cellular injury through the activation of the coagulation cascade and provide further evidence for a role for PCA in the pathogenesis of MHV-3 infection.
Levy
G
G
University of Toronto, Ontario, Canada.
Abecassis
M
M
D000818:Animals; D001777:Blood Coagulation; D001779:Blood Coagulation Factors / Q000096:biosynthesis; D006524:Hepatitis, Viral, Animal / Q000097:blood* / Q000276:immunology; D006801:Humans; D008099:Liver / Q000098:blood supply / Q000473:pathology; D008833:Microcirculation; D006517:Murine hepatitis virus / Q000276:immunology; D011453:Prostaglandins / Q000378:metabolism
D001779:Blood Coagulation Factors; D011453:Prostaglandins; C045071:leukocyte procoagulant activity; C045072:macrophage procoagulant activity