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Review
. 2014:385:243-74.
doi: 10.1007/82_2014_388.

Molecular determinants of influenza virus pathogenesis in mice

Ram P Kamal  1 , Jaqueline M Katz, Ian A York
Affiliations
Review

Molecular determinants of influenza virus pathogenesis in mice

Ram P Kamal et al. Curr Top Microbiol Immunol. 2014.

Abstract

Mice are widely used for studying influenza virus pathogenesis and immunology because of their low cost, the wide availability of mouse-specific reagents, and the large number of mouse strains available, including knockout and transgenic strains. However, mice do not fully recapitulate the signs of influenza infection of humans: transmission of influenza between mice is much less efficient than in humans, and influenza viruses often require adaptation before they are able to efficiently replicate in mice. In the process of mouse adaptation, influenza viruses acquire mutations that enhance their ability to attach to mouse cells, replicate within the cells, and suppress immunity, among other functions. Many such mouse-adaptive mutations have been identified, covering all 8 genomic segments of the virus. Identification and analysis of these mutations have provided insight into the molecular determinants of influenza virulence and pathogenesis, not only in mice but also in humans and other species. In particular, several mouse-adaptive mutations of avian influenza viruses have proved to be general mammalian-adaptive changes that are potential markers of pre-pandemic viruses. As well as evaluating influenza pathogenesis, mice have also been used as models for evaluation of novel vaccines and anti-viral therapies. Mice can be a useful animal model for studying influenza biology as long as differences between human and mice infections are taken into account.

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References

    1. Abed Y, Pizzorno A, Hamelin ME, Leung A, Joubert P, Couture C, Kobasa D, Boivin G. The 2009 pandemic H1N1 D222G hemagglutinin mutation alters receptor specificity and increases virulence in mice but not in ferrets. J Infect Dis. 2011;204:1008–1016. doi: 10.1093/infdis/jir483. - DOI - PubMed
    1. Alberts R, Srivastava B, Wu H, Viegas N, Geffers R, Klawonn F, Novoselova N, do Valle TZ, Panthier JJ, Schughart K. Gene expression changes in the host response between resistant and susceptible inbred mouse strains after influenza A infection. Microbes Infect. 2010;12:309–318. doi: 10.1016/j.micinf.2010.01.008. - DOI - PubMed
    1. Alymova IV, Green AM, van de Velde N, McAuley JL, Boyd KL, Ghoneim HE, McCullers JA. Immunopathogenic and antibacterial effects of H3N2 influenza A virus PB1-F2 map to amino acid residues 62, 75, 79, and 82. J Virol. 2011;85:12324–12333. doi: 10.1128/JVI.05872-11. - DOI - PMC - PubMed
    1. Alymova IV, Samarasinghe A, Vogel P, Green AM, Weinlich R, McCullers JA. A novel cytotoxic sequence contributes to influenza A viral protein PB1-F2 pathogenicity and predisposition to secondary bacterial infection. J Virol. 2014;88:503–515. doi: 10.1128/JVI.01373-13. - DOI - PMC - PubMed
    1. Andrewes CH, Laidlaw PP, Smith W. The susceptibility of mice to the viruses of human and swine influenza. The Lancet. 1934;224:859–862.