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Eastern equine encephalitis virus (EEEV) causes severe neurologic disease in North America, but only two fatal human cases have been documented in South America. To test the hypothesis that alphavirus heterologous antibodies cross-protect, animals were vaccinated against other alphaviruses and challenged up to 3 months later with EEEV. Short-lived cross-protection was detected, even in the absence of cross-neutralizing antibodies. To assess exposure to EEEV in Peru, sera from acutely ill and healthy persons were tested for EEEV and other alphavirus antibodies, as well as for virus isolation. No EEEV was isolated from patients living in an EEEV-enzootic area, and only 2% of individuals with febrile illness had EEEV-reactive IgM. Only 3% of healthy persons from the enzootic region had EEEV-neutralizing antibodies. Our results suggest that humans are exposed but do not develop apparent infection with EEEV because of poor infectivity and/or avirulence of South American strains.
Received April 8, 2006. Accepted for publication September 30, 2006.
Acknowledgments: The authors thank Mardelle Susman for editing the manuscript. The study protocol was approved by the Naval Medical Research Center Institutional Review Board (Protocol 31535) in compliance with all U.S. federal regulations governing the protection of human study participants. The opinions expressed in this paper are those of the authors and do not reflect the official policy of the Department of the Navy, the Department of the Army, the Department of Defense, or the U.S. Government.
Financial support: This research was supported by Grant AI049725 from the National Institutes of Health through the joint National Science Foundation/National Institutes of Health program on the Ecology of Infectious Disease, and by Work UNIT NUMBER (WUN) 847705 8200 25GB B0016. IRB Protocol Number: 31535 "Surveillance and Etiology of Acute Febrile Diseases in Peru." PVA was supported by the James T. McLaughlin Fellowship Fund.
* Address correspondence to Scott C. Weaver, Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555-0609. E-mail: sweaver{at}utmb.edu
Authors’ addresses: Patricia V. Aguilar, Robert B. Tesh, Douglas M. Watts, and Scott C. Weaver, Departments of Microbiology and Immunology, Pathology, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-0609, Telephone: 409-747-0758 Fax: 409-747-2415. Rebecca M. Robich, Michael J. Turell, Monica L. O’Guinn, and Terry A. Klein, Virology Division, US Army Medical Research Institute of Infectious Diseases, 1425 Porter Street, Fort Detrick, MD. Alfredo Huaman, Carolina Guevara, Zonia Rios, and James Olson, US Naval Medical Research Center Detachment, NMRCD/Unit 3800, American Embassy, Lima, Peru.
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