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Identification and analysis for cross-reactivity among hantaviruses of H-2^b-restricted cytotoxic T-lymphocyte epitopes in Sin Nombre virus nucleocapsid protein

Ken Maeda

Tomoko Toyosaki-Maeda

Center for Infectious Disease and Vaccine Research, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA

Correspondence
Masanori Terajima
Masanori.Terajima{at}umassmed.edu

Sin Nombre virus (SNV) causes hantavirus pulmonary syndrome (HPS), with a high rate of mortality in humans who are infected by the transmission of virus from the natural rodent host. In humans, cytotoxic T lymphocytes (CTL) specific for SNV appear to play an important role in the pathogenicity of HPS. There is a correlation between the frequencies of SNV-specific CTLs and the severity of HPS disease. In order to create a mouse model to study the role of SNV-specific T cells in vivo, T cell responses to SNV nucleocapsid (N) protein in B6.PL Thy1^a/Cy mice (H-2^b) immunized with plasmid DNA or recombinant vaccinia virus expressing SNV N protein were examined. Four peptides, NC94–101, NC175–189, NC217–231 and NC331–345, were recognized by CD8⁺ T cells in CTL and ELISPOT assays in SNV N-immunized mice. Interestingly, two of these epitopes are located in the central region of the SNV N protein, where several human CD8⁺ T-cell epitopes have been defined in Puumala virus and SNV. CTL lines specific for these four epitopes were cross-reactive to corresponding Puumala virus peptides, but only one of them was cross-reactive to Hantaan virus peptides. These results will enable the analysis of the roles of CTL in immunopathology of HPS in experimental mouse models of HPS.

Present address: Department of Veterinary Microbiology, Faculty of Agriculture, Yamaguchi University, 1677-1 Yoshida, Yamaguchi 753-8515, Japan.

Present address: Medical Biology 2, Discovery Research Laboratories, Shionogi & Co. Ltd, 2-5-1, Mishima, Settsu-shi, Osaka 566-0022, Japan.

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