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Kinetic Study of Platelets and Fibrinogen in Lassa Virus-Infected Monkeys and Early Pathologic Events in Mopeia Virus-Infected Monkeys

James V. Lange^*, Sheila W. Mitchell^*, Joseph B. McCormick^*, David H. Walker^**, Bruce L. Evatt AND Rosemary R. Ramsey

^* Division of Viral Diseases, Center for Infectious Diseases, Centers for Disease Control, Public Health Service, U.S. Department of Health and Human Services, Atlanta, Georgia 30333
^** Department of Pathology, University of North Carolina, School of Medicine, Chapel Hill, North Carolina 27514
Division of Host Factors, Center for Infectious Diseases, Centers for Disease Control, Public Health Service, U.S. Department of Health and Human Services, Atlanta, Georgia 30333

The rhesus monkey, an established model of Lassa fever, was used to study hematologic and hemostatic aspects of Lassa fever and whether Mopeia (also known as Mozambique) virus induces any cellular damage in this model. Six days after subcutaneous injection of 10^3.48 plaque forming units (PFU) of Lassa virus (Josiah strain) one group of monkeys received an intravenous injection of ¹¹¹In-labeled allogeneic platelets and another group received ¹²⁵I-labeled alogeneic fibrinogen. Lassa virus-infected monkeys developed a severe clinical illness with high viremia and typical pathology. Lassa antigen was found in most tissues using a Lassa nucleocapsid-specific monoclonal antibody. Platelet counts remained within normal limits. Platelet and fibrinogen kinetics were similar in infected and control animals. Hematologic and hemostatic changes indicate that disseminated intravascular coagulation plays no role in this model of Lassa fever. Levels of plasma fibronectin were reduced in Lassa-infected monkeys. Mopeia virus-infected monkeys were normothemic, aviremic, and there was no detection of Mopeia antigen in any tissues using polyclonal or monoclonal antibodies. Mopeia virus was recovered from the spleen of one monkey. Mopeia virus was associated with hepatocellular and renal tubular damage.

Accepted for publication March 20, 1985.

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