Evolution of influenza

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The virus causing influenza is one of the best known pathogens found in various species. In particular, the virus is found in birds as well as mammals including horses, pigs, and humans.[1] The phylogeny, or the evolutionary history of a particular species, is an important component when analyzing the evolution of influenza. Phylogenetic trees are graphical models of the relationships between various species. They can be used to trace the virus back to particular species and show how organisms that look so different may be so closely related.[1]

Mechanisms of evolution[edit]

Two common mechanisms by which viruses evolve are reassortment and genetic drift.[2]

Reassortment[edit]

Reassortment allows new viruses to evolve under both natural conditions and in artificial cultures.[2] In fact, the 1957 evolution of the H2N2 virus is thought to be a result of reassortment.[2] In this case, human H1N1 strains and avian influenza A genes were mixed.[2] Infecting tissue cultures can demonstrate how pathogenic qualities can evolve for a particular species even though the reassorted virus may be nonpathogenic for another species.[2] A prime example of evolution under natural conditions is the reassortment of two avian influenza strains that were discovered in dead seals back in 1979.[2]

Drift[edit]

New viruses can also emerge by drift. Drift can refer to genetic drift or antigenic drift.[2] Mutation and selection for the most advantageous variation of the virus takes place during this form of evolution.[2] Antigenic mutants can evolve quickly due to the high mutation rate in viruses. Influenza antigenic drift happens when two influenza viruses infect one cell. When new ones come out they have a segment from the others genome that could let some but not enough antibodies to bind. Also the receptor could not bind to antibodies.[2] This evolution occurs under the pressure of antibodies or immune system responses.[2]

Transmission[edit]

Species and barriers[edit]

The transmission, or how the influenza virus is passed from one species to another, varies. There are barriers that prevent the flow of the virus between some species ranging from high to low transmission. For example, there is no direct pathway between humans and birds.[2] Pigs however, serve as an open pathway. There is a limited barrier for them to spread the virus.[2] Therefore, pigs act as a donator of the virus relatively easily.

Geographic differences[edit]

Phylogenetic maps are a graphical representation of the geographic relationships among species. They indicate that the human influenza virus is minimally impacted by geographic differences.[1] However, both swine and avian influenza does appear to be geographically dependent.[1] All three groups (avian, swine, and human) show chronological differences. The human influenza virus is retained in humans only, meaning it does not spread to other species.[1] Some lineages and sublineages of the virus emerge and may be more prevalent in certain locations. For instance, many human influenza outbreaks begin in Southeast Asia.[2]

Phylogenetic analysis[edit]

Phylogenetic analysis can help determine past viruses and their patterns as well as determining a common ancestor of the virus. Past studies reveal that an avian virus spread to pigs and then to humans approximately 100 years ago.[2] This resulted in human lineages further evolving and becoming more prominent and stable.[2]

Analysis can also feature relationships between species. The 1918 Spanish influenza virus demonstrates this. The hemagglutinin (HA) gene of the 1918 pandemic virus was closer in sequence to avian strains than other mammalian ones. Despite this genetic similarity, it is obviously a mammalian virus.[3] The gene may have been adapting in humans even prior to 1918.[3] Breaking down the phylogenetic history of the influenza virus shows that there is a common ancestor that reaches back before the 1918 outbreak that links the current human virus to the swine virus.[4] The ancestor was derived from an avian host.[2]

Future impact[edit]

Looking at the past phylogenetic relationships of the influenza virus can help lead to information regarding treatment resistance, selecting vaccine strains, and future influenza strains.

In current years, there has been a huge increase in the amount of resistance to certain drugs, including the antiviral compound adamantane.[5] In fact, its resistance has recently climbed from 2 percent to nearly 90 percent.[5] These records of built up resistance infer that drugs, such as adamantine, will not be useful against the influenza virus in the future.

Various lineages may continue their presence and reassort indicating the importance of a complete-genome approach to determine new influenza strains and future epidemics.[6][7] In terms of vaccine strain selection, antigenic clades evolve by reassortment, not by antigenic drift.[6] This was shown in the 2003-2004 influenza outbreak.[6]

Phylogenetic trees can help determine what codons in the HA gene of the influenza A virus have changed in past outbreaks.[8] The more mutations there are in a virus strain, the more likely that strain is to be a generator of a new lineage in future influenza seasons.[8]

References[edit]

  1. ^ a b c d e Liu, S; Kang, J; Chen, J; Tai, D; Jiang, W; Hou, G; Chen, J; Li, J; Huang, B (2009). "Panorama phylogenetic diversity and distribution of type A influenza virus". In Field, Dawn. PLoS ONE 4 (3): 1–20. doi:10.1371/journal.pone.0005022. 
  2. ^ a b c d e f g h i j k l m n o p Scholtissek, C (1995). "Molecular evolution of influenza viruses". Virus Genes 11 (2–3): 209–215. doi:10.1007/BF01728660. PMID 8828147. 
  3. ^ a b Reid, A; Fanning, T; Hultin, J; Taubenberger, J (1999). "Origin and evolution of the 1918 "Spanish" influenza virus hemagglutinin gene". Proceedings of the National Academy of Sciences USA 96 (4): 1651–1656. doi:10.1073/pnas.96.4.1651. PMC 15547. PMID 9990079. 
  4. ^ Gorman, O; Donis, R; Kawaoka, Y; Webster, R (1990). "Evolution of influenza A virus PB2 genes: implications for evolution of the ribonucleoprotein complex and origin of human influenza A virus". Journal of Virology 64 (10): 4893–4902. PMC 247979. PMID 2398532. 
  5. ^ a b Simonsen, L; Viboud, C; Grenfell, B; Dushoff, J; Jennings, L; Smit, M; Macken, C; Hata, M et al. (2007). "The genesis and spread of reassortment human influenza A/H3N2 viruses conferring adamantane resistance". Molecular Biology and Evolution 24 (8): 1811–20. doi:10.1093/molbev/msm103. PMID 17522084. 
  6. ^ a b c Holmes, E; Ghedin, E; Miller, N; Taylor, J; Bao, Y; St George, K; Grenfell, B; Salzberg, S; Fraser, C; Lipman, D; Taubenberger, J (2005). "Whole-Genome Analysis of Human Influenza A Virus Reveals Multiple Persistent Lineages and Reassortment among Recent H3N2 Viruses". PLoS Biology 3 (9): 1579–1589. doi:10.1371/journal.pbio.0030300. PMC 1180517. PMID 16026181. 
  7. ^ Vana, G; Westover, K (2008). "Origin of the 1918 Spanish influenza virus: A comparative genomic analysis". Molecular Phylogenetics and Evolution 3 (3): 1100–1110. doi:10.1016/j.ympev.2008.02.003. PMID 18353690. 
  8. ^ a b Fitch, W; Bush, R; Bender, C; Subbarao, K; Cox, N (2000). "Predicting the evolution of human influenza A". Journal of Heredity 91 (3): 183–185. doi:10.1093/jhered/91.3.183. PMID 10833042.