Immunity to Influenza in Man

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.

Epidemiological models with age structure, proportionate mixing, and cross-immunity

“…Periods of 10 to 20 years are observed when cr is small, while periods of 3-4 years are observed when cross-immunity is intermediate. These results are consistent with the recently documented evidence on the co-circulation of strains of the same subtype (Couch and Kasel, 1983;Thacker, 1986 [Fig. 2]).…”

“…In what follows, the sub-index i indicates that the corresponding class has been infected by or recovered from strain i . If two related strains of a virus such as influenza are co-circulating in a population, then individuals who have been infected by one strain may have partial immunity (i.e., decreased susceptibility) to the other strain (see Castillo-Chavez, et al, 1987;Couch and Kasel, 1983). Assume that individuals, while infected with one strain, temporarily are not susceptible to the other, either because of temporary immunity or because of isolation from the rest of the population.…”

Evaluation of a vectored equine herpesvirus type 1 (EHV-1) vaccine expressing H3 haemagglutinin in the protection of dogs against canine influenza

“…Humoral antibody responses against HA are considered good indicators for evaluating potentially protective immunity upon natural or vaccine-induced influenza infection [24,25]. An increase in the antibody response against this influenza antigen is highest upon natural infection, moderate after vaccination with MLV and least effective after immunization with inactivated preparations [26].…”

“…In dogs, a subcutaneous inoculation, performed twice in a 4-week interval, induced a robust antibody response against CIV and antibodies could be readily detected within two weeks after the first immunization using a sensitive competitive ELISA. The HI antibody response, which is viewed as a good indicator of protection [24,25], was detected in all immunized dogs after booster vaccination.…”

Some Scaling Principles for the Immune System

“…Each antigen may have multiple epitopes, for example, the hemagglutinin molecule on the surface of influenza A has four non-overlapping antigenic regions. 8 However, for the scaling arguments made here, it suffices to assume each antigen has a single epitope. We also assume that there is a (small) volume v 0 around the antigen's representative point, such that the antigen can be eliminated by the immune system if at least one B-cell clone has its representative point inside v 0 , that is, recognition need not be perfect; 7,9 if, however, all N clones are represented in shape space by points outside v 0 , then B cells will not recognize the antigen, with a potentially fatal result for the organism.…”