No abstract

The observations summarized in this review indicate immunity to infection with type A influenza viruses is subtype specific since little or none is conveyed to subtypes possessing immunologically distinct HA and NA proteins. However, within a subtype, a prior antigenic experience with one variant may prevent or modify illness to another. The resulting degree of subtype immunity depends on the extent of relatedness between variants. Observations with H3N2 viruses indicate that homotypic resistance to subsequent infection and illness with the same virus is potent and of relatively long duration. The long lasting durability of such immunity was indicated by the epidemiologic pattern following the reappearance of H1N1 virus. Knowledge of the duration and specificity of immunity aids considerably in assessing mechanisms that account for host resistance to influenza. Recovery from influenza virus infection must involve a variety of humoral and cell-mediated immune mechanisms, and conclusions regarding the relative importance of each one are not possible at present. To prevent infection, involved immune mechanism(s) must account for: (a) subtype specificity, (b) reduced cross-reactivity of immunity for succeeding antigenic variants, (c) a long duration of immunity, and (d) immunity at the mucosal surface. Only antibody directed toward the HA molecule presently satisfies these properties and thus should be considered the major mediator of resistance to infection. Study of naturally occurring infection is needed for determining the duration and specificity of secretory IgA in nasal and lower respiratory secretions so as to establish its relative importance as a mediator of immunity. However, the described duration, specificity, and consistent relationship to immunity suggest that IgG antibody in respiratory secretions, derived entirely or partly from serum, is the most likely mediator of resistance to natural influenza.

No abstract

In Houston the temporal occurrence of infections with parainfluenza virus type 3 has evolved from an endemic to an epidemic pattern. Continuous virological surveillance for six years demonstrated that most infections occurred the late winter or spring after influenza virus activity. At least two-thirds of children observed in the Houston Family Study were infected with this virus in each of the first two years of life, and the risk of illness was about 30/100 children per year. After two years of age, the infection and illness rates dropped to 32 and 8 per 100 child-years, respectively. Most lower-respiratory-tract disease was associated with primary infection, and the risk for infection was greater during the second year for the smaller proportion of children who escaped infection during the first year. The risk during the first year may have been modified by passively acquired maternal antibody.