Hantaan virus (HTNV), the prototype member of the Hantavirus genus in the family Bunyaviridae, causes
hemorrhagic fever with renal syndrome (
HFRS), which is characterized by capillary leakage,
hemorrhage, and renal injury, and is an important public health problem in China. Some kinds of immune cells, particularly CD8(+) T cells, are involved in the pathogenesis of
Hantavirus infection. The
nucleocapsid protein (NP) of the Hantavirus is the most conserved structural
protein and the most abundant
viral protein produced during
infection. It is one of the important target
antigens that induce the CD8(+) T-cell response. In this study, we examined the CD8(+) T-cell response to HTNV NP C-terminal
polypeptides. We synthesized 23 overlapping C-terminal
polypeptides and detected the
antigen-specific CD8(+) T cell response in 15 patients with
HFRS. The results demonstrated that there were NP-specific T-cell responses in bulk cultures of peripheral blood mononuclear cells (PBMCs) from 9 of 15 patients. The
peptide 51 (aa 301-315: SPSSIWVFAGAPDRC),
peptide 60 (aa 355-369: LRKKSSFYQSYLRRT), and
peptide 70 (aa 415-429: DVKVKEISNQEPLKL) induced strong CD8(+) T-cell responses. Among them,
peptide 70 induced CTL responses in donors 7, 9, and 11, and the strongest responses were seen in donor 11. Depletion of CD8(+) T cells from PBMCs completely abrogated the
peptide-specific T-cell response, while depletion of CD4(+) T cells did not diminish the number of IFN-gamma spot-forming cells. These data suggest that
infection with HTNV results in CTL responses to
immunodominant regions on the NP.