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The sudden emergence of the novel reassortant A(H1N1) 2009 influenza virus led to rapid global spread, due to minimal pre-existing antibody levels in those born after 1950. Memory T cells specific for more conserved viral peptides elicit broad immunity and can promote more rapid recovery. However, mutations within T-cell immunogenic peptides occur, although less commonly than at antibody-binding sites. Comparison of human T-cell peptides between the pandemic H1N1 2009 and seasonal strains showed 50–70% conservation, depending on the particular virus protein and influenza strains. Experimental analysis demonstrated cross-recognition of some T-cell epitopes (for example, HLA-A2+M158-66), although there was also evidence of immune escape by other immunodominant peptides (for example, NP418-426 presented by the HLA-B7 family). Non-conserved T-cell regions of A(H1N1) 2009 highly resembled those derived from H1N1-1918 rather than recent seasonal viruses, reflecting protein conservation (in the parent swine virus) from influenza strains circulating early in the 20th century. As a consequence, individuals with HLA types presenting variable T-cell peptides had diminished pre-existing T-cell memory towards the A(H1N1) 2009 virus.

T-cell immunity against the A(H1N1) 2009 pandemic virus