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We investigated possible associations of HL-A types and antibody-response patterns during clinical trials with a live, attenuated intranasal influenza A vaccine. After vaccination, subjects with HL-A type W16 had, as a group, a mean convalescent-phase hemagglutination-inhibiting antibody titer of 14, which was significantly lower (P less than 0.001) than the mean titer of 36 in subjects without Type W16. Of 25 subjects with a poor antibody response, 32 per cent had HL-A type W16, whereas only 5 per cent with a good response had Type W16. The mean titers in nasal secretions of five W16 subjects at 13 and 30 days were less than 3; in contrast, similar titers of 22 subjects without W16 were 8 and 9 respectively. The results suggest that the lower antibody response in W16 subjects is due to increased cellular resistance to infection rather than to a suppressed immune response because other subjects with W16 had normal antibody responses after vaccination with killed influenza vaccine.
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Spencer et al. (1976) studied this question.
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