Epidemiologic implications of changes in the influenza virus genome.
Among the molecular maneuvers that enable the influenza virus to survive are antigenic variation and functional alterations. Two kinds of minor antigenic variations, producing new strains within type A virus subtypes, have been discovered: antigenic drift, in which the amino acid sequences of the antigens are changed; and antigenic camouflage, in which the antigens are glycosylated. Both kinds of variation are caused by mutations in the viral genome. These mutations produce slightly changed antigens, which many existing antibodies cannot recognize. Major antigenic variations (so-called antigenic shift) are produced by gene reassortment. Two subtypes, coinfecting a host, can reassort their eight ribonucleoprotein gene segments into as many as 256 different combinations. Such recombinations can produce new viruses with the potential for transmission in humans, but whose surface antigens are completely unmatched by antibodies in the population, permitting a pandemic to occur. Functional changes, caused by mutations, alter the interactions between the virus and the host, including virus binding to host receptor sites and fusion of viral and host membranes. All these mechanisms allow the influenza virus to survive in humans, probably perpetually.
D000956:Antigens, Viral / Q000235:genetics*; D004196:Disease Outbreaks; D005814:Genes, Viral; D014644:Genetic Variation; D006388:Hemagglutinins / Q000235:genetics; D006801:Humans; D007251:Influenza, Human / Q000453:epidemiology* / Q000382:microbiology / Q000401:mortality; D008958:Models, Molecular; D009154:Mutation; D009975:Orthomyxoviridae / Q000235:genetics* / Q000276:immunology / Q000648:ultrastructure; D011014:Pneumonia / Q000401:mortality; D014481:United States
D000956:Antigens, Viral; D006388:Hemagglutinins