Cytotoxic T lymphocytes play a central role in the clearance of primary infl uenza virus infection, peaking after 7-10 days; the peak in antibody titers occurs 4-7 weeks after primary infection (6) (7) (8) . Neutralizing antibodies are completely protective against secondary challenges only with closely related strains, but they are ineffective against viruses with major antigenic divergence. For this reason, current infl uenza vaccines are prepared annually on the basis of World Health Organization forecasts on the most probable infl uenza A and B virus strains thought to be circulating in the next seasonal outbreak (5, 7) . By contrast, cellular responses to cross-reactive epitopes may provide a substantial degree of protection against serologically distinct viruses (9) . The ability of infl uenza viruses to mutate and reassort their HA-NA genome segments between different animal species is a main concern because immunity generated by previous infections or vaccinations is unable to prevent infection by itself, although it may reduce virus replication and spread (8) (9) (10) .