Abstract
Influenza A virus causes annual epidemics and occasional pandemics of short-term respiratory infections associated with considerable morbidity and mortality. The pandemics occur when new human-transmissible viruses that have the major surface protein of influenza A viruses from other host species are introduced into the human population. Between such rare events, the evolution of influenza is shaped by antigenic drift: the accumulation of mutations that result in changes in exposed regions of the viral surface proteins. Antigenic drift makes the virus less susceptible to immediate neutralization by the immune system in individuals who have had a previous influenza infection or vaccination. A biannual reevaluation of the vaccine composition is essential to maintain its effectiveness due to this immune escape. The study of influenza genomes is key to this endeavor, increasing our understanding of antigenic drift and enhancing the accuracy of vaccine strain selection. Recent large-scale genome sequencing and antigenic typing has considerably improved our understanding of influenza evolution: epidemics around the globe are seeded from a reservoir in East-Southeast Asia with year-round prevalence of influenza viruses; antigenically similar strains predominate in epidemics worldwide for several years before being replaced by a new antigenic cluster of strains. Future in-depth studies of the influenza reservoir, along with large-scale data mining of genomic resources and the integration of epidemiological, genomic, and antigenic data, should enhance our understanding of antigenic drift and improve the detection and control of antigenically novel emerging strains.
Highlights
Influenza is a single-stranded, negative-sense RNA virus that causes acute respiratory illness in humans
Segment 4 encodes the major surface glycoprotein called hemagglutinin (H), which is responsible for attaching the virus to sialic acid residues on the host cell surface and fusing the virus membrane envelope with the host cell membrane, delivering the viral genome into the cell (Figure 1)
Influenza A viruses are further classified into distinct subtypes based on the genetic and antigenic characteristics of these two surface glycoproteins
Summary
Influenza viruses can rapidly acquire genetic diversity because of high replication rates in infected hosts, an error-prone RNA polymerase (which introduces mutations during genome replication), and segment reassortment (Figure 2). Major changes in antigenicity (antigenic shift) are associated with the introduction of novel viruses into the human population that have a hemagglutinin segment of an influenza A virus from another host species and can be transmitted efficiently among humans [5]. The emergence of a novel pandemic virus, which may have been circulating undetected in swine for a decade [14,45], has highlighted the need for increased genomic surveillance of the viral populations in mammalian hosts such as swine These hosts could be a vessel for mammalian adaptation of avian viruses, either by reassortment with human or swine viruses or through adaptive changes [8], but have been monitored less intensely than avian populations. The latest emergence of a pandemic H1N1 virus has underscored the vital importance of further research into the molecular factors that determine the host range and capacity for sustained human-tohuman transmission of influenza A viruses
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