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Am. J. Trop. Med. Hyg., 48(3), 1993, pp. 412-423
Copyright © 1993 by The American Society of Tropical Medicine and Hygiene

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Increased Immunogenicity and Protective Efficacy in Outbred and Inbred Mice by Strategic Carboxyl-Terminal Truncation of Japanese Encephalitis Virus Envelope Glycoprotein

Lei-Ron Jan, Czau-Siung Yang, Laraine S. Henchal, Hideo Sumiyoshi, Peter L. Summers, Doria R. Dubois AND Ching-Juh Lai
Molecular Viral Biology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland; Graduate Institute of Microbiology, Medical College, National Taiwan University, Taipei, Taiwan; National Institute of Preventive Medicine, Taipei, Taiwan; Department of Biologics, Walter Reed Army Institute of Research, Washington, DC

We constructed recombinant vaccinia viruses expressing the full-length envelope (E) glycoprotein of Japanese encephalitis virus (JEV) or a strategically truncated E glycoprotein, approximately 80% of the N-terminal sequence, and compared their antigenic structure and protective immunity in mice. The truncation site in the JEV E glycoprotein sequence corresponds to the position that had been shown to increase the immunogenicity of dengue type 4 or type 2 virus E glycoprotein. Analysis of the JEV E glycoprotein in recombinant virus-infected cells showed that C-terminally truncated E retains an antigenic structure similar to that of the full-length E glycoprotein. The full-length JEV E glycoprotein was detected predominantly intracellularly, while a small fraction (< 2%) was present on the cell surface. On the other hand, the truncated 80% E glycoprotein exhibited an alteration in the intracellular transport pathway resulting in increased accumulation (10–25%) on the cell surface and secretion (6–10%) into the medium. The C-terminally truncated E glycoprotein induced a greater antibody response and a higher level of protective immunity than did the full-length E glycoprotein in outbred CD-1 mice as well as in two strains of inbred mice that differ in their resistance to intraperitoneal (ip) JEV infection. In the case of outbred CD-1 and inbred C57/Bl mice, which possess a dominant autosomal genetic locus that controls resistance to a high dose of ip infection of JEV or the capacity to acquire resistance to intracerebral JEV infection, truncated E glycoprotein induced a higher titer of JEV neutralizing antibodies.




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Copyright © 1993 by the American Society of Tropical Medicine and Hygiene.