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Am. J. Trop. Med. Hyg., 77(5), 2007, pp. 919-924
Copyright © 2007 by The American Society of Tropical Medicine and Hygiene

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Yellow Fever 17-D Vaccine Is Neurotropic and Produces Encephalitis in Immunosuppressed Hamsters

Rosa I. Mateo, Shu-Yuan Xiao, Amelia P. A. Travassos da Rosa, Hao Lei, Hilda Guzman, Liang Lu, AND Robert B. Tesh*
Departments of Pathology and Internal Medicine and Center for Biodefense and Emerging Infectious Diseases, University of Texas Medical Branch, Galveston, Texas

Immunosuppressed (cyclophosphamide) adult golden hamsters inoculated intraperitoneally (IP) with wild-type Asibi yellow fever virus (YFV) developed a rapidly fatal illness. Histopathologic and immunohistochemical studies of tissues from these animals showed typical hepatic changes of severe yellow fever (inflammation, hepatocyte necrosis, and steatosis) without brain involvement. In contrast, 50% of immunosuppressed hamsters receiving the YFV-17D–attenuated vaccine developed a slowly progressive encephalitic-type illness. Brain tissue from these latter animals revealed focal neuronal changes, inflammation, and YFV antigen–positive neurons; however, the liver and spleen appeared normal. YFV was isolated from brain cultures of many of these animals. Immunocompetent (non-immunosuppressed) hamsters inoculated with both viruses developed a subclinical infection. Results of this study indicate that wild-type YFV is hepatotropic in immunosuppressed hamsters, whereas the attenuated YFV-17 is primarily neurotropic. These findings support current recommendations against yellow fever vaccination of immunosuppressed/ immunocompromised people and suggest that this hamster model might be useful for monitoring the safety of other live-attenuated YFV vaccines.

Received November 3, 2006. Accepted for publication July 19, 2007.

Acknowledgments: The authors thank Dora Salinas for help in preparing the manuscript and Patrick Newman for preparing the histological sections.

Financial support: This work was supported by National Institutes of Health Contracts NO1-AI25489 and NO1-AI 30027. RIM was supported by the James W. McLaughlin Fellowship Fund.

* Address correspondence to Robert B. Tesh, Department of Pathology, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555–0609. E-mail: rtesh{at}utmb.edu

Authors’ addresses: Rosa Mateo, Shu-Yuan Xiao, Amelia P.A. Travassos da Rosa, Hao Lei, Hilda Guzman, Liang Lu, and Robert B. Tesh, Department of Pathology, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555–0609, Telephone: 409–747–2431, Fax: 409–747–2429, E-mail: rtesh{at}utmb.edu.

Reprint requests: Robert B. Tesh, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555–0609, E-mail: rtesh{at}utmb.edu.






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