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WOUNDING: THE PRIMARY MODE OF SEOUL VIRUS TRANSMISSION AMONG MALE NORWAY RATS

In rodent populations, males are more likely to be infected with hantaviruses and to engage in aggression than are females. To assess the relationship between aggression and Seoul virus infection, Norway rats were trapped in Baltimore, Maryland and wounding, infection status, and steroid hormone concentrations were examined. Older males and males with high-grade wounds were more likely to have IgG antibody to Seoul, to shed virus in saliva, urine, and feces, and to have viral RNA in organs than either juveniles or adult males with less severe wounds. In contrast, neither age nor wounding predicted virus shedding among females. Although viral antigen was not identified in the brain, viral protein was detected in the gonads and adrenal glands of adult males. Males with more severe wounds had higher testosterone concentrations than males with no or low-grade wounds. Because wounding, testosterone, and virus shedding are associated among males, aggression may be the primary mode of Seoul virus transmission among male, but not female, Norway rats.

Received September 16, 2003. Accepted for publication November 1, 2003.

Acknowledgments: We thank Connie Schmaljohn, Cindy Rossi, and Kristen Spik, (United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD) for providing hantavirus reagents. We also thank Jennifer Uhrlaub (Johns Hopkins School of Medicine) for assistance with developing the immunohistochemistry protocol, Ann Lawler (Johns Hopkins School of Medicine) for assistance with the radioimmunoassay, and Joshua Fine, Mike Johnson, Nikhil Joshi, Rebekah Kent, Marilyn Klein, and John Pisciotta (Johns Hopkins Bloomberg School of Public Health) for assistance with rat trapping.

Financial support: This work was supported by National Aeronautics and Space Administration grant NCC5–305 (Gregory E. Glass), National Institutes of Health (NIH) grant F32 AI–10324 (Sabra L. Klein), and in part by NIH grant P30 HD 06268.

Authors’ addresses: Ella R. Hinson, Section of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06520, E-mail: ella.hinson{at}yale.edu. Scott M. Shone, Gregory E. Glass, and Sabra L. Klein, Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, 615 North Wolfe Street, Baltimore, MD 21205, E-mails: sshone{at}jhsph.edu, ggurrigl{at}jhsph.edu, and saklein{at}jhsph.edu M. Christine Zink, Department of Comparative Medicine, Johns Hopkins School of Medicine, Baltimore, MD 21205, E-mail: mczink{at}jhmi.edu.

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