An uncommon but devastating condition associated with influenza is Reye’s syndrome (Sullivan-Bolyai and Corey, 1981).
The clinical syndromes of influenza A and B often are not distinguishable; however, influenza B is less often associated with the excess morbidity and mortality that may accompany outbreaks of influenza A infections (Davenport, 1982). Characteristically, influenza outbreaks occur during the winter months. They may be limited to small communities or spread to cause epidemics in several states, throughout the nation, or throughout the world (pandemics). During epidemics of influenza A infection, respiratory tract infections in a community tend to be overwhelmed by the presence of influenza and almost all cases of diagnosed viral respiratory tract illness can be associated with influenza virus. This rapid spread presents a significant practical problem for those attempting to design appropriate vaccination programs.
Influenza virions are spherical particles containing a nucleocapsid with segmented pieces of single-stranded RNA. The surface membrane contains two major glycoproteins, hemagglutinin and neuraminidase, which are also the antigens important for immunization.
The key problem facing public health authorities in terms of influenza control is that the surface antigens on influenza A viruses change frequently. This is true of both hemagglutinin and neuraminidase. When the antigenic changes are so great that the virus is no longer recognized by antisera raised against earlier strains, the antigens are said to have undergone “shift.” This has occurred with influenza A viruses several times in the past few decades (Davenport, 1982). In intervening years, a more limited “drift” has occurred, associated with less striking changes in the amino acid sequences of the surface glycoproteins. Influenza B viruses undergo less frequent changes, which are characterized as “drift” rather than “shift” to antigenically new subtypes (Davenport, 1982). The viruses can be grown easily in embryonated eggs, which have been the source of the inactivated vaccine for the past four decades. Growth of the viruses in several cell culture systems is possible.
Infection with influenza viruses induces antibody and cell-mediated immune responses. The exact duration of these responses and the degree of protection they afford following primary infection is not certain, because the viruses change their surface antigens with such great frequency. Repeated infections have been demonstrated even with one subtype (Sigel et al., 1950). Protection against homologous virus challenge can be quite lasting, however (Davenport, 1982). The virus that caused the 1977 “Russian Flu” epidemic was identical to an H1N1 type that circulated first in 1950. Individuals who had experienced infection in the 1950s were resistant against the later challenge