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PR8 virus harbouring H5N1 NS gene contributed for THP-1 cell tropism

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Abstract

Innate immune cells are key player in immune response to influenza virus infection. Influenza infected monocytes exacerbate the disease pathology. However, monocytes differ in susceptibilities to influenza virus infection. Herein, susceptibilities of U937 and THP-1 monocytic cells to PR8 virus infection, the associated cellular factor- sialic acid (SA) receptor distribution and viral factor were determined. Moreover, amino acid sequences in hemagglutinin (HA) receptor binding domain (RBD) of PR8 virus that determine SA preferences were analysed. PR8 infected U937 cells express significantly higher numbers of nucleoprotein positive cells suggesting U937 cells being more susceptible to influenza virus than THP-1 cells. Lectin staining suggested similar pattern of SA receptor distribution in both cells. Interestingly, sequence analysis of RBD suggested their preferences for alpha 2,3 SA receptors suggesting RBD sequences are not always determining for SA preferences. Furthermore, the resistance barrier on THP-1 cells was overcome by H5N1 NS gene. In conclusion, the study demonstrated that decreased susceptibility of THP-1 cells to PR8 virus could not be related to the SA receptor distribution, and H5N1 NS gene was sufficient to determine tropism for THP-1 cells. Hence, mechanistic basis of NS gene on cell tropism and contribution of other internal genes remained to be determined.

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References

  1. Cole SL, Ho LP. Contribution of innate immune cells to pathogenesis of severe influenza virus infection. Clin Sci (Lond). 2017;131(4):269–83. https://doi.org/10.1042/CS20160484.

    Article  CAS  Google Scholar 

  2. Herold S, Steinmueller M, von Wulffen W, Cakarova L, Pinto R, Pleschka S, et al. Lung epithelial apoptosis in influenza virus pneumonia: the role of macrophage-expressed TNF-related apoptosis-inducing ligand. J Exp Med. 2008;205(13):3065–77. https://doi.org/10.1084/jem.20080201.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  3. Duan M, Hibbs ML, Chen W. The contributions of lung macrophage and monocyte heterogeneity to influenza pathogenesis. Immunol Cell Biol. 2017;95(3):225–35. https://doi.org/10.1038/icb.2016.97.

    Article  CAS  PubMed  Google Scholar 

  4. Nicholls JM, Chan RW, Russell RJ, Air GM, Peiris JS. Evolving complexities of influenza virus and its receptors. Trends Microbiol. 2008;16(4):149–57. https://doi.org/10.1016/j.tim.2008.01.008.

    Article  CAS  PubMed  Google Scholar 

  5. Rogers GN, Paulson JC, Daniels RS, Skehel JJ, Wilson IA, Wiley DC. Single amino acid substitutions in influenza haemagglutinin change receptor binding specificity. Nature. 1983;304(5921):76–8.

    Article  CAS  Google Scholar 

  6. Nobusawa E, Ishihara H, Morishita T, Sato K, Nakajima K. Change in receptor-binding specificity of recent human influenza A viruses (H3N2): a single amino acid change in hemagglutinin altered its recognition of sialyloligosaccharides. Virology. 2000;278(2):587–96. https://doi.org/10.1006/viro.2000.0679.

    Article  CAS  PubMed  Google Scholar 

  7. Vines A, Wells K, Matrosovich M, Castrucci MR, Ito T, Kawaoka Y. The role of influenza A virus hemagglutinin residues 226 and 228 in receptor specificity and host range restriction. J Virol. 1998;72(9):7626–31.

    CAS  PubMed  PubMed Central  Google Scholar 

  8. Lamichhane PP, Boonnak K, Changsom D, Noisumdaeng P, Sangsiriwut K, Pattanakitsakul SN, et al. H5N1 NS genomic segment distinctly governs the influenza virus infectivity and cytokine induction in monocytic cells. Asian Pac J Allergy Immunol. 2018;36(1):58–68. https://doi.org/10.12932/AP0870.

    Article  PubMed  Google Scholar 

  9. Ana-Sosa-Batiz F, Vanderven H, Jegaskanda S, Johnston A, Rockman S, Laurie K, et al. Influenza-specific antibody-dependent phagocytosis. PLoS ONE. 2016;11(4):e0154461. https://doi.org/10.1371/journal.pone.0154461.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  10. Petersen H, Wang Z, Lenz E, Pleschka S, Rautenschlein S. Reassortment of NS segments modifies highly pathogenic avian influenza virus interaction with avian hosts and host cells. J Virol. 2013;87(10):5362–71. https://doi.org/10.1128/JVI.02969-12.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  11. Twu KY, Kuo RL, Marklund J, Krug RM. The H5N1 influenza virus NS genes selected after 1998 enhance virus replication in mammalian cells. J Virol. 2007;81(15):8112–21. https://doi.org/10.1128/JVI.00006-07.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  12. Ma W, Brenner D, Wang Z, Dauber B, Ehrhardt C, Hogner K, et al. The NS segment of an H5N1 highly pathogenic avian influenza virus (HPAIV) is sufficient to alter replication efficiency, cell tropism, and host range of an H7N1 HPAIV. J Virol. 2010;84(4):2122–33. https://doi.org/10.1128/JVI.01668-09.

    Article  CAS  PubMed  Google Scholar 

  13. Lipatov AS, Andreansky S, Webby RJ, Hulse DJ, Rehg JE, Krauss S, et al. Pathogenesis of Hong Kong H5N1 influenza virus NS gene reassortants in mice: the role of cytokines and B- and T-cell responses. J Gen Virol. 2005;86(Pt 4):1121–30. https://doi.org/10.1099/vir.0.80663-0.

    Article  CAS  PubMed  Google Scholar 

  14. Yan X, Wang Q, Zhang Z, Xie Y, Zhang H, Razi M, et al. Involvement of non-structural proteins (NS) in influenza A infection and viral tropism. Biochem Biophys Res Commun. 2012;428(1):62–7. https://doi.org/10.1016/j.bbrc.2012.10.006.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  15. Hoeve MA, Nash AA, Jackson D, Randall RE, Dransfield I. Influenza virus A infection of human monocyte and macrophage subpopulations reveals increased susceptibility associated with cell differentiation. PLoS ONE. 2012;7(1):e29443. https://doi.org/10.1371/journal.pone.0029443.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

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Acknowledgements

PPL was supported by Siriraj Graduate Studentship for international students. Eight recombinant pHW2000 plasmids carrying each genomic segment of PR8 virus for construction of reassortant viruses was kindly provided by Prof. Robert G. Webster, St. Jude Children’s Research Hospital, Memphis, TN, USA.

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  1. Prem Prasad Lamichhane

    Present address: Department of Laboratory Medicine, A & B International Hospital, Pokhara-2, Nepal

Authors and Affiliations

  1. Department of Microbiology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok Noi, Bangkok, Thailand

    Prem Prasad Lamichhane & Pilaipan Puthavathana

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  1. Prem Prasad Lamichhane
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  2. Pilaipan Puthavathana
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Correspondence to Prem Prasad Lamichhane.

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Lamichhane, P.P., Puthavathana, P. PR8 virus harbouring H5N1 NS gene contributed for THP-1 cell tropism. VirusDis. 29, 548–552 (2018). https://doi.org/10.1007/s13337-018-0499-4

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