H1N1pdm09 influenza A viruses lack extra-epitopic amino acid residues previously associated with reduced recognition by M1 58-66 -specific CD8 + T cells. During >6 years of evolution, H1N1pdm09 virus accumulated alternative mutations outside the M1 58-66 epitope that did not reduce sensitivity to M1 58-66 -specific CD8 + T cells. Abstract Extra-epitopic amino acid residues affect recognition of human influenza A viruses (IAVs) by CD8 + T-lymphocytes (CTLs) specific for the highly conserved HLA-A*0201 restricted M1 58-66 epitope located in the matrix 1 (M1) protein. These residues are absent in the M1 protein of the 2009-pandemic IAV (H1N1pdm09). Consequently, stimulation with M1 protein of H1N1pdm09 IAV resulted in stronger activation and lytic activity of M1 58-66 -specific CTLs than stimulation with seasonal H3N2 IAVs. During >6 years of circulation in the human population, descendants of the H1N1pdm09 virus had accumulated 4 other amino acid substitutions. However, these did not affect M1 58-66 -specific CTL activation.
【저자키워드】 influenza A virus, escape, extra-epitopic amino acid residues, H1N1pdm2009, CD8+ T-lymphocytes,