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The Role of Punctuated Evolution in the Pathogenicity of Influenza Viruses

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  • Author: Jonathan A. McCullers1
  • Editors: W. Michael Scheld2, James M. Hughes3, Richard J. Whitley4
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Department of Pediatrics, The University of Tennessee Health Sciences Center, Memphis, TN 38103; 2: Department of Infectious Diseases, University of Virginia Health System, Charlottesville, VA; 3: Division of Infectious Diseases, Department of Medicine, Emory University School of Medicine, Atlanta, GA; 4: Department of Pediatrics, University of Alabama at Birmingham, Birmingham, AL
    • Source: microbiolspec March 2016 vol. 4 no. 2 doi:10.1128/microbiolspec.EI10-0001-2015
  • Received 07 July 2015 Accepted 11 August 2015 Published 25 March 2016
  • Jonathan A. McCullers, [email protected]
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  • Abstract:

    Influenza is an acute respiratory disease caused by influenza viruses. Evolutionarily, all influenza viruses are zoonoses, arising in the animal reservoir and spilling over into the human population. Several times a century, one of these zoonotic events results in a new influenza virus lineage becoming established in humans and circulating for years or decades as an endemic strain. The worldwide pandemic that occurs shortly after the nascent virus becomes established can have a profound impact on morbidity and mortality. Because influenza viruses continually evolve and the illness they engender can vary considerably based on characteristics of the strain, the weather, other circulating or endemic pathogens, as well as the number of susceptible hosts, the impact of each season on human health is unpredictable. Over time, the general pattern is for pandemic strains to adapt and gradually take on characteristics of seasonal strains with lower virulence and a diminished synergism with bacterial pathogens. Study of this punctuated evolution yields a number of insights into the overall pathogenicity of influenza viruses.

  • Citation: McCullers J. 2016. The Role of Punctuated Evolution in the Pathogenicity of Influenza Viruses. Microbiol Spectrum 4(2):EI10-0001-2015. doi:10.1128/microbiolspec.EI10-0001-2015.

References

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2. Greenbaum A, Quinn C, Bailer J, Su S, Havers F, Durand LO, Jiang V, Page S, Budd J, Shaw M, Biggerstaff M, de Fijter S, Smith K, Reed C, Epperson S, Brammer L, Feltz D, Sohner K, Ford J, Jain S, Gargiullo P, Weiss E, Burg P, DiOrio M, Fowler B, Finelli L, Jhung MA. 5 May 2015. Investigation of an outbreak of variant influenza A(H3N2) virus infection associated with an agricultural fair—Ohio, August 2012. J Infect Dis 2012:1592–1599. [PubMed][CrossRef]
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4. Osterhaus AD, Rimmelzwaan GF, Martina BE, Bestebroer TM, Fouchier RA. 2000. Influenza B virus in seals. Science 288:1051–1053. [PubMed][CrossRef]
5. Smith AM, McCullers JA. 2013. Molecular signatures of virulence in the PB1-F2 proteins of H5N1 influenza viruses. Virus Res 178:146–150. [PubMed][CrossRef]
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7. McAuley JL, Chipuk JE, Boyd KL, Van De Velde N, Green DR, McCullers JA. 2010. PB1-F2 proteins from H5N1 and 20 century pandemic influenza viruses cause immunopathology. PLoS Pathog 6:e1001014. [PubMed][CrossRef]
8. Jhung MA, Nelson DI. 2015. Outbreaks of avian influenza A (H5N2), (H5N8), and (H5N1) among birds—United States, December 2014–January 2015. MMWR Morb Mortal Wkly Rep 64:111. [PubMed]
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12. Xu J, Davis CT, Christman MC, Rivailler P, Zhong H, Donis RO, Lu G. 2012. Evolutionary history and phylodynamics of influenza A and B neuraminidase (NA) genes inferred from large-scale sequence analyses. PLoS One 7:e38665. [PubMed][CrossRef]
13. Ward MJ, Lycett SJ, Avila D, Bollback JP, Leigh Brown AJ. 2013. Evolutionary interactions between haemagglutinin and neuraminidase in avian influenza. BMC Evol Biol 13:222. [PubMed][CrossRef]
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15. Elderfield RA, Watson SJ, Godlee A, Adamson WE, Thompson CI, Dunning J, Fernandez-Alonso M, Blumenkrantz D, Hussell T, Zambon M, Openshaw P, Kellam P, Barclay WS. 2014. Accumulation of human-adapting mutations during circulation of A(H1N1)pdm09 influenza virus in humans in the United Kingdom. J Virol 88:13269–13283. [PubMed][CrossRef]
16. Castelan-Vega JA, Magana-Hernandez A, Jimenez-Alberto A, Ribas-Aparicio RM. 2014. The hemagglutinin of the influenza A(H1N1)pdm09 is mutating towards stability. Adv Appl Bioinform Chem 7:37–44. [PubMed]
17. Vigerust DJ, Ulett KB, Boyd KL, Madsen J, Hawgood S, McCullers JA. 2007. N-linked glycosylation attenuates H3N2 influenza viruses. J Virol 81:8593–8600. [PubMed][CrossRef]
18. Marth JD, Grewal PK. 2008. Mammalian glycosylation in immunity. Nat Rev Immunol 8:874–887. [PubMed][CrossRef]
19. Kornfeld R, Kornfeld S. 1985. Assembly of asparagine-linked oligosaccharides. Annu Rev Biochem 54:631–664. [PubMed][CrossRef]
20. Daniels R, Kurowski B, Johnson AE, Hebert DN. 2003. N-linked glycans direct the cotranslational folding pathway of influenza hemagglutinin. Mol Cell 11:79–90. [PubMed][CrossRef]
21. Reading PC, Tate MD, Pickett DL, Brooks AG. 2007. Glycosylation as a target for recognition of influenza viruses by the innate immune system. Adv Exp Med Biol 598:279–292. [PubMed][CrossRef]
22. Wanzeck K, Boyd KL, McCullers JA. 2011. Glycan shielding of the influenza virus hemagglutinin contributes to immunopathology in mice. Am J Respir Crit Care Med 183:767–773. [PubMed][CrossRef]
23. Hrincius ER, Liedmann S, Finkelstein D, Vogel P, Gansebom S, Samarasinghe AE, You D, Cormier SA, McCullers JA. 2015. Acute lung injury results from innate sensing of viruses by an ER stress pathway. Cell Rep 11:1591–1603. [PubMed][CrossRef]
24. Peltola VT, Murti KG, McCullers JA. 2005. Influenza virus neuraminidase contributes to secondary bacterial pneumonia. J Infect Dis 192:249–257. [PubMed][CrossRef]
25. McCullers JA, Bartmess KC. 2003. Role of neuraminidase in lethal synergism between influenza virus and Streptococcus pneumoniae. J Infect Dis 187:1000–1009. [PubMed][CrossRef]
26. Siegel SJ, Roche AM, Weiser JN. 2014. Influenza promotes pneumococcal growth during coinfection by providing host sialylated substrates as a nutrient source. Cell Host Microbe 16:55–67. [PubMed][CrossRef]
27. Peltola VT, McCullers JA. 2004. Respiratory viruses predisposing to bacterial infections: role of neuraminidase. Pediatr Infect Dis J 23:S87–S97. [PubMed][CrossRef]
28. Gubareva LV, Kaiser L, Matrosovich MN, Soo-Hoo Y, Hayden FG. 2001. Selection of influenza virus mutants in experimentally infected volunteers treated with oseltamivir. J Infect Dis 183:523–531. [PubMed][CrossRef]
29. Gubareva LV, Nedyalkova MS, Novikov DV, Murti KG, Hoffmann E, Hayden FG. 2002. A release-competent influenza A virus mutant lacking the coding capacity for the neuraminidase active site. J Gen Virol 83:2683–2692. [PubMed][CrossRef]
30. Smith AM, McCullers JA. 2013. Molecular signatures of virulence in the PB1-F2 proteins of H5N1 influenza viruses. Virus Res 178:146–150. [PubMed][CrossRef]
31. McAuley JL, Hornung F, Boyd KL, Smith AM, McKeon R, Bennink J, Yewdell JW, McCullers JA. 2007. Expression of the 1918 influenza A virus PB1-F2 enhances the pathogenesis of viral and secondary bacterial pneumonia. Cell Host Microbe 2:240–249. [PubMed][CrossRef]
32. Alymova IV, Green AM, Van De Velde N, McAuley JL, Boyd KL, Ghoneim HE, McCullers JA. 2011. Immunopathogenic and antibacterial effects of H3N2 influenza A virus PB1-F2 map to amino acid residues 62, 75, 79, and 82. J Virol 85:12324–12333. [PubMed][CrossRef]
33. McAuley JL, Hornung F, Boyd KL, Smith AM, McKeon R, Bennink J, Yewdell JW, McCullers JA. 2007. Expression of the 1918 influenza A virus PB1-F2 enhances the pathogenesis of viral and secondary bacterial pneumonia. Cell Host Microbe 2:240–249. [PubMed][CrossRef]
34. Hrincius ER, Liedmann S, Anhlan D, Wolff T, Ludwig S, Ehrhardt C. 2014. Avian influenza viruses inhibit the major cellular signalling integrator c-Abl. Cell Microbiol 16:1854–1874. [PubMed][CrossRef]
35. Hrincius ER, Liedmann S, Finkelstein D, Vogel P, Gansebom S, Ehrhardt C, Ludwig S, Hains DS, Webby R, McCullers JA. 2015. Nonstructural protein 1 (NS1)-mediated inhibition of c-Abl results in acute lung injury and priming for bacterial co-infections: insights into 1918 H1N1 pandemic? J Infect Dis 211:1418–1428. [PubMed][CrossRef]
36. Hrincius ER, Hennecke AK, Gensler L, Nordhoff C, Anhlan D, Vogel P, McCullers JA, Ludwig S, Ehrhardt C. 2012. A single point mutation (Y89F) within the non-structural protein 1 of influenza A viruses limits epithelial cell tropism and virulence in mice. Am J Pathol 180:2361–2374. [PubMed][CrossRef]
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2016-03-25
2021-01-19

Abstract:

Influenza is an acute respiratory disease caused by influenza viruses. Evolutionarily, all influenza viruses are zoonoses, arising in the animal reservoir and spilling over into the human population. Several times a century, one of these zoonotic events results in a new influenza virus lineage becoming established in humans and circulating for years or decades as an endemic strain. The worldwide pandemic that occurs shortly after the nascent virus becomes established can have a profound impact on morbidity and mortality. Because influenza viruses continually evolve and the illness they engender can vary considerably based on characteristics of the strain, the weather, other circulating or endemic pathogens, as well as the number of susceptible hosts, the impact of each season on human health is unpredictable. Over time, the general pattern is for pandemic strains to adapt and gradually take on characteristics of seasonal strains with lower virulence and a diminished synergism with bacterial pathogens. Study of this punctuated evolution yields a number of insights into the overall pathogenicity of influenza viruses.

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Figures

The Role of Punctuated Evolution in the Pathogenicity of Influenza Viruses
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Citation: McCullers J. 2016. The role of punctuated evolution in the pathogenicity of influenza viruses. microbiolspec 4(2): doi:10.1128/microbiolspec.EI10-0001-2015
/content/microbiolspec/10.1128/microbiolspec.EI10-0001-2015.fig1
FIGURE 1

Influenza A virus life cycle in cells.

microbiolspec/4/2/EI10-0001-2015-fig1_thmb.gif
microbiolspec/4/2/EI10-0001-2015-fig1.gif
Image of FIGURE 1

Click to view

FIGURE 1

Influenza A virus life cycle in cells.

Source: microbiolspec March 2016 vol. 4 no. 2 doi:10.1128/microbiolspec.EI10-0001-2015
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/content/microbiolspec/10.1128/microbiolspec.EI10-0001-2015.fig2
FIGURE 2

Influenza A virus ecology. The wild-bird reservoir is the source of all zoonotic influenza A viruses. These viruses cross over into humans through intermediate species, such as domestic poultry and swine. Farm animal silhouettes by Otutor, used under License CC BY 3.0 (https://creativecommons.org/licenses/by/3.0/us/); oyster catcher silhouette courtesy of Rachison Alexandra; human silhouettes courtesy of Mackey Creations.

microbiolspec/4/2/EI10-0001-2015-fig2_thmb.gif
microbiolspec/4/2/EI10-0001-2015-fig2.gif
Image of FIGURE 2

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FIGURE 2

Influenza A virus ecology. The wild-bird reservoir is the source of all zoonotic influenza A viruses. These viruses cross over into humans through intermediate species, such as domestic poultry and swine. Farm animal silhouettes by Otutor, used under License CC BY 3.0 (https://creativecommons.org/licenses/by/3.0/us/); oyster catcher silhouette courtesy of Rachison Alexandra; human silhouettes courtesy of Mackey Creations.

Source: microbiolspec March 2016 vol. 4 no. 2 doi:10.1128/microbiolspec.EI10-0001-2015
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Download as Powerpoint
/content/microbiolspec/10.1128/microbiolspec.EI10-0001-2015.fig3
FIGURE 3

Pandemic timeline. Four major lineages of influenza A virus have established endemicity in humans in the last century. The 1957 and 1968 pandemic viruses were reassortants which included genes from the previously circulating viruses which they replaced. The 1918 and 2009 pandemic strains came directly from animal reservoirs. The seasonal H1N1 lineage which circulated early in the 20th century was replaced in 1957 but reemerged in 1976 and cocirculated for 32 years with seasonal H3N2 strains.

microbiolspec/4/2/EI10-0001-2015-fig3_thmb.gif
microbiolspec/4/2/EI10-0001-2015-fig3.gif
Image of FIGURE 3

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FIGURE 3

Pandemic timeline. Four major lineages of influenza A virus have established endemicity in humans in the last century. The 1957 and 1968 pandemic viruses were reassortants which included genes from the previously circulating viruses which they replaced. The 1918 and 2009 pandemic strains came directly from animal reservoirs. The seasonal H1N1 lineage which circulated early in the 20th century was replaced in 1957 but reemerged in 1976 and cocirculated for 32 years with seasonal H3N2 strains.

Source: microbiolspec March 2016 vol. 4 no. 2 doi:10.1128/microbiolspec.EI10-0001-2015
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Download as Powerpoint

Tables

The Role of Punctuated Evolution in the Pathogenicity of Influenza Viruses
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Citation: McCullers J. 2016. The role of punctuated evolution in the pathogenicity of influenza viruses. microbiolspec 4(2): doi:10.1128/microbiolspec.EI10-0001-2015
/content/microbiolspec/10.1128/microbiolspec.EI10-0001-2015.T1
TABLE 1

Influenza A virus gene functions

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TABLE 1

Influenza A virus gene functions

Source: microbiolspec March 2016 vol. 4 no. 2 doi:10.1128/microbiolspec.EI10-0001-2015

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