![]() ![]() A large proportion of the disease burden of influenza stems from antigenic drift, which allows individuals to be infected multiple times throughout their lives. The influenza virus population continually evolves in antigenic phenotype in a process known as antigenic drift. ![]() Although individuals develop long-lasting immunity to particular influenza strains after infection, antigenic mutations to the influenza virus genome result in proteins that are recognized to a lesser degree by the human immune system, leaving individuals susceptible to future infection. Seasonal influenza infects between 10% and 20% of the human population every year, causing an estimated 250,000 to 500,000 deaths annually ( Influenza Fact sheet, 2009). ![]() This information could potentially speed up the development of new flu vaccines for each flu season. provides a useful framework to study influenza, and could help to pinpoint which changes in viral genes cause the changes in antigens. This suggests that knowing which antigenic phenotypes are present at the start of flu season could help predict which strains of the virus will predominate later on. Further, a correlation was observed between antigenic drift and the number of new influenza cases per year for each flu strain. This revealed that the antigenic phenotype of H3N2-a subtype that is becoming increasingly common-evolved faster than the other three subtypes. have now developed an approach to combine antigenic maps with genetic information about the four subtypes of the human flu virus. Gene sequencing has shown that there are four subtypes of the flu virus that commonly infect people but the relationship between changes in antigenic phenotype and changes in gene sequences of the influenza virus is poorly understood.īedford et al. This information about the “antigenic phenotype” of the virus can be plotted on an antigenic map in which strains with similar antigens cluster together. It is possible to determine which antigens are displayed by a new strain of the virus by observing how blood samples that respond to known strains respond to the new strain. This antigenic drift-so-called because the antigens displayed by the virus keep changing-also explains why influenza vaccines become less effective over time and need to be reformulated every year. Even though the human immune system can detect and destroy the virus that causes influenza, people can catch flu many times throughout their lifetimes because the virus keeps evolving in an effort to avoid the immune system. This work makes possible substantial future advances in investigating the dynamics of influenza and other antigenically-variable pathogens by providing a model that intimately combines molecular and antigenic evolution.Įvery year, seasonal influenza, commonly called flu, infects up to one in five people around the world, and causes up to half a million deaths. We also show that year-to-year antigenic drift appears to drive incidence patterns within each influenza lineage. Using HI data from influenza lineages A/H3N2, A/H1N1, B/Victoria and B/Yamagata, we determine patterns of antigenic drift across viral lineages, showing that A/H3N2 evolves faster and in a more punctuated fashion than other influenza lineages. Here, we extend previous approaches to antigenic cartography, and simultaneously characterize antigenic and genetic evolution by modeling the diffusion of antigenic phenotype over a shared virus phylogeny. Antigenic phenotype is often assessed through pairwise measurement of cross-reactivity between influenza strains using the hemagglutination inhibition (HI) assay. Influenza viruses undergo continual antigenic evolution allowing mutant viruses to evade host immunity acquired to previous virus strains. ![]()
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