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Am. J. Trop. Med. Hyg., 79(2), 2008, pp. 275-282
Copyright © 2008 by The American Society of Tropical Medicine and Hygiene

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Pathogenesis of XJ and Romero Strains of Junin Virus in Two Strains of Guinea Pigs

Nadezhda E. Yun, Nathaniel S. Linde, Natallia Dziuba, Michele A. Zacks, Jeanon N. Smith, Jennifer K. Smith, Judy F. Aronson, Olga V. Chumakova, Heather M. Lander, Clarence J. Peters, AND Slobodan Paessler*
Center for Biodefense and Emerging Infectious Diseases, Institute for Human Infections and Immunity, Department of Pathology, University of Texas Medical Branch, Galveston, Texas

Argentine hemorrhagic fever (AHF), a systemic infectious disease caused by infection with Junin virus, affects several organs, and patients can show hematologic, cardiovascular, renal, or neurologic symptoms. We compared the virulence of two Junin virus strains in inbred and outbred guinea pigs with the aim of characterizing this animal model better for future vaccine/antiviral efficacy studies. Our data indicate that this passage of the XJ strain is attenuated in guinea pigs. In contrast, the Romero strain is highly virulent in Strain 13 as well as in Hartley guinea pigs, resulting in systemic infection, thrombocytopenia, elevated apartate aminotransferase levels, and ultimately, uniformly lethal disease. We detected viral antigen in formalin-fixed, paraffin-embedded tissues. Thus, both guinea pig strains are useful animal models for lethal Junin virus (Romero strain) infection and potentially can be used for preclinical trials in vaccine or antiviral drug development.


Received January 22, 2008. Accepted for publication May 5, 2008.

Acknowledgments: We thank Dr. Robert Tesh (UTMB) for providing the Junin XJ strain and anti-XJ mouse ascitic fluid; Dr. Tom Ksiazek (Centers for Disease Control and Prevention, Atlanta, GA) for providing the Junin Romero strain; Drs. Dennis Hruby, Tove’ Bolken, Sean Amberg (SIGA Technologies, Inc., Corvallis, OR), and Dr. Mary C. Guttieri (United States Army Medical Research Institute for Infectious Disease, Fort Detrick, MD) for helpful scientific and technical advice; Melinda J. Kelley for helpful technical assistance; and Jenna Linde and Nicolette Ward for assistance with preparation of the manuscript.

Financial support: The study was supported by National Institutes of Health (NIH) contract no. 5R44A1056525, NIH K08 award no. AI059491-01, and faculty start-up funding provided by the Institute for Human Infections and Immunity at UTMB.

* Address correspondence to Slobodan Paessler, Department of Pathology, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-1019. E-mail: slpaessl{at}utmb.edu

Authors’ address: Nadezhda E. Yun, Nathaniel S. Linde, Natallia Dziuba, Michele A. Zacks, Jeanon N. Smith, Jennifer K. Smith, Judy F. Aronson, Olga V. Chumakova, Heather M. Lander, Clarence J. Peters, and Slobodan Paessler, Center for Biodefense and Emerging Infectious Diseases, Institute for Human Infections and Immunity, Department of Pathology, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-1019.

Reprint requests: Slobodan Paessler, Department of Pathology, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-1019, E-mail: slpaessl{at}utmb.edu.







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