HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by McCormick, J. B. Articles by Johnson, K. M. Search for Related Content PubMed PubMed Citation Articles by McCormick, J. B. Articles by Johnson, K. M.

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

Joseph B. McCormick^*, David H. Walker^**, Isabel J. King, Patricia A. Webb, Luanne H. Elliott^*, Sylvia G. Whitfield^* AND Karl M. Johnson^*

^* Division of Viral Diseases, Center for Infectious Diseases, Centers for Disease Control, Atlanta, Georgia 30333
^** Department of Pathology, University of North Carolina, Chapel Hill, North Carolina 27514
5 Beverley Gardens, Barrow Lane, Cheshunt, Hertfordshire EN7 5LX, England
Division of Vector-Borne Viral Diseases, Centers for Disease Control, P.O. Box 2087, Fort Collins, Colorado 80522

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.

Accepted for publication October 30, 1985.

This article has been cited by other articles:

				M. M. Djavani, O. R. Crasta, J. C. Zapata, Z. Fei, O. Folkerts, B. Sobral, M. Swindells, J. Bryant, H. Davis, C. D. Pauza, et al. Early Blood Profiles of Virus Infection in a Monkey Model for Lassa Fever J. Virol., August 1, 2007; 81(15): 7960 - 7973. [Abstract] [Full Text] [PDF]

				R. Carrion Jr., K. Brasky, K. Mansfield, C. Johnson, M. Gonzales, A. Ticer, I. Lukashevich, S. Tardif, and J. Patterson Lassa Virus Infection in Experimentally Infected Marmosets: Liver Pathology and Immunophenotypic Alterations in Target Tissues J. Virol., June 15, 2007; 81(12): 6482 - 6490. [Abstract] [Full Text] [PDF]

				S. Muller, R. Geffers, and S. Gunther Analysis of gene expression in Lassa virus-infected HuH-7 cells J. Gen. Virol., May 1, 2007; 88(5): 1568 - 1575. [Abstract] [Full Text] [PDF]

				E. SBRANA, R. I. MATEO, S.-Y. XIAO, V. L. POPOV, P. C. NEWMAN, and R. B. TESH CLINICAL LABORATORY, VIROLOGIC, AND PATHOLOGIC CHANGES IN HAMSTERS EXPERIMENTALLY INFECTED WITH PIRITAL VIRUS (ARENAVIRIDAE): A RODENT MODEL OF LASSA FEVER Am J Trop Med Hyg, June 1, 2006; 74(6): 1096 - 1102. [Abstract] [Full Text] [PDF]