原创力文档significant impact of sequence variations in the nucleoprotein on cd8 t cell-mediated cross-protection against influenza a virus infections显著影响核蛋白质序列变化的cd8 t细胞介导教训对甲型流感病毒感染.pdfVIP
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significant impact of sequence variations in the nucleoprotein on cd8 t cell-mediated cross-protection against influenza a virus infections显著影响核蛋白质序列变化的cd8 t细胞介导教训对甲型流感病毒感染
Significant Impact of Sequence Variations in the
Nucleoprotein on CD8 T Cell-Mediated Cross-Protection
against Influenza A Virus Infections
1 1 1 1 1 2
Weimin Zhong *, Feng Liu , Libo Dong , Xiuhua Lu , Kathy Hancock , Ellis L. Reinherz , Jacqueline M.
Katz1, Suryaprakash Sambhara1
1 Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, United States of America,
2 Department of Medical Oncology, Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, Massachusetts, United States of America
Abstract
Background: Memory CD8 T cells to influenza A viruses are widely detectable in healthy human subjects and broadly cross-
reactive for serologically distinct influenza A virus subtypes. However, it is not clear to what extent such pre-existing cellular
immunity can provide cross-subtype protection against novel emerging influenza A viruses.
Methodology/Principal Findings: We show in the mouse model that naturally occurring sequence variations of the
conserved nucleoprotein of the virus significantly impact cross-protection against lethal disease in vivo. When priming and
challenge viruses shared identical sequences of the immunodominant, protective NP366/Db epitope, strong cross-subtype
protection was observed. However, when they did not share complete sequence identity in this epitope, cross-protection
was considerably reduced. Contributions of virus-specific antibodies appeared to be minimal under these circumstances.
Detailed analysis revealed that the magnitude of the memory CD8 T cell response triggered by the NP366/Db variants was
significantly lower than those triggered by the homologous NP366/Db ligand. It appears
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