Lassa Virus Hepatitis: a Study of Fatal Lassa Fever in Humans

Joseph B. McCormickDivision of Viral Diseases, Center for Infectious Diseases, Centers for Disease Control, Atlanta, Georgia 30333

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David H. WalkerDepartment of Pathology, University of North Carolina, Chapel Hill, North Carolina 27514

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Isabel J. King5 Beverley Gardens, Barrow Lane, Cheshunt, Hertfordshire EN7 5LX, England

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Patricia A. WebbDivision of Vector-Borne Viral Diseases, Centers for Disease Control, P.O. Box 2087, Fort Collins, Colorado 80522

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Luanne H. ElliottDivision of Viral Diseases, Center for Infectious Diseases, Centers for Disease Control, Atlanta, Georgia 30333

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Sylvia G. WhitfieldDivision of Viral Diseases, Center for Infectious Diseases, Centers for Disease Control, Atlanta, Georgia 30333

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Karl M. JohnsonDivision of Viral Diseases, Center for Infectious Diseases, Centers for Disease Control, Atlanta, Georgia 30333

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In order to explore the significance of a previous observation that the most important pathologic changes in fatal Lassa fever are hepatic, we have studied postmortem liver biopsies from 19 patients with fatal Lassa fever. We observed a vigorous macrophage response to cellular damage, but we found no evidence of lymphocyte infiltration in infected hepatic tissues. Using semi-quantitative estimates of liver cell damage, we found a wide range in the severity and progression of Lassa virus hepatitis in our fatal cases. We have classified for descriptive purposes three general nosopoeitic phases: active hepatocellular injury (<20% necrosis), continued damage and early recovery, and mitotic activity representing hepatic recovery. We conclude that the liver goes through cellular injury, necrosis and regeneration and any or all may be present at death. In no instance was the degree of hepatic damage sufficient to implicate hepatic failure, and all three phases were represented among our cases. We conclude that the hepatitis of Lassa fever in humans is not the primary cause of death.

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