 | WEST NILE VIRUS: DETECTION, SURVEILLANCE, AND CONTROL
Copyright © 2001 by the New York Academy of Sciences
description
Annals of the New York Academy of Sciences 951:286-297 (2001)
© 2001 New York Academy of Sciences
Antibody Prophylaxis and Therapy for Flavivirus Encephalitis Infections
JOHN T. ROEHRIGa,
LISA A. STAUDINGERa,b,
ANN R. HUNTa,
JAMES H. MATHEWSa AND
CAROL D. BLAIRb
aArbovirus Diseases Branch, Division of Vector-Borne Infectious Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, United States Public Health Service, Department of Health and Human Services, Fort Collins, Colorado 80522, USA
bDepartment of Microbiology, Colorado State University, Fort Collins, Colorado 80523, USA
Address for correspondence: John T. Roehrig, Arbovirus Diseases Branch, Division of Vector-Borne Infectious Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, U.S. Public Health Service, Department of Health and Human Services, P.O. Box 2087, Fort Collins, CO 80522. Voice: 970-221-6442; fax: 970-221-6476.
jtr1{at}cdc.gov
The outbreak of West Nile (WN) encephalitis in the United States has rekindled interest in developing direct methods for prevention and control of human flaviviral infections. Although equine WN vaccines are currently being developed, a WN vaccine for humans is years away. There is also no specific therapeutic agent for flaviviral infections. The incidence of human WN virus infection is very low, which makes it difficult to target the human populations in need of vaccination and to assess the vaccine's economic feasibility. It has been shown, however, that prophylactic application of antiflaviviral antibody can protect mice from subsequent virus challenge. This model of antibody prophylaxis using murine monoclonal antibodies (MAbs) has been used to determine the timing of antibody application and specificity of applied antibody necessary for successful prophylaxis. The major flaviviral antigen is the envelope (E) glycoprotein that binds cellular receptors, mediates cell membrane fusion, and contains an array of epitopes that elicit virus-neutralizing and nonneutralizing antibodies. The protective efficacy of an E-glycoprotein-specific MAb is directly related to its ability to neutralize virus infectivity. The window for successful application of prophylactic antibody to prevent flaviviral encephalitis closes at about 4 to 6 days postinfection concomitant with viral invasion of the brain. Using murine MAbs to modify human disease results in a human antimouse antibody (HAMA) response that eventually limits the effectiveness of subsequent murine antibody applications. To reduce the HAMA response and make these MAbs more generally useful for humans, murine MAbs can be "humanized" or human MAbs with analogous reactivities can be developed. Antiflaviviral human or humanized MAbs might be practical and cost-effective reagents for preventing or modifying flaviviral diseases.
Key Words: Passive protection • monoclonal antibodies (MAbs) • flaviviruses • cross-protection
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