Abstract
THE abrupt antigenic change which led to the appearance of A2 (Asian) influenza viruses in 1957 was accompanied by the acquisition of sensitivity to a new type of non-specific inhibitor1–3, now referred to as the γ-type. Active almost exclusively against A2 strains it is easily distinguished from α- and β-type inhibitors both by its characteristic properties and its occurrence in high titre in normal horse serum. Some A2 strains and laboratory variants of A2 strains are partially or completely insensitive to it. These variations are due to the presence of two distinct types of particle which differ in their susceptibility to γ-inhibitor. Their relative proportions determine the inhibitor sensitivity of any particular virus prepara tion4,5.
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