期刊
JOURNAL OF VIROLOGY
卷 80, 期 12, 页码 5854-5861出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.02671-05
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资金
- Intramural NIH HHS Funding Source: Medline
- NIAID NIH HHS [R01 AI054952, R21 AI054952, AI-054952] Funding Source: Medline
The cytotoxic T-lymphocyte (CTL) response is important for the control of viral replication during respiratory syncytial virus (RSV) infection. The attachment glycoprotein (G) of RSV does not encode major histocompatibility complex class I-restricted epitopes in BALB/c mice (H-2(d)). Furthermore, studies to date have described an absence of significant CTL activity directed against this protein in humans. Therefore, G previously was not considered necessary for the generation of RSV-specific CTL responses. In this study, we demonstrate that, despite lacking H-2(d)-restricted epitopes, G enhances the generation of an effective CTL response against RSV. Furthermore, we show that this stimulatory effect is independent of virus titers and RSV-induced inflammation; that it is associated primarily with the secreted form of G; and that the effect depends on the cysteine-rich region of G (GCRR), a segment conserved in wild-type isolates worldwide. These findings reveal a novel function for the GCRR with potential implications for the generation of protective cellular responses and vaccine development.
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