Archives of Virology

, Volume 155, Issue 1, pp 107–110

Readaptation of a low-virulence influenza H9 escape mutant in mice: the role of changes in hemagglutinin as revealed by site-specific mutagenesis

Authors

  • N. A. Ilyushina
    • The D.I. Ivanovsky Institute of Virology
    • Division of Virology, Department of Infectious DiseasesSt. Jude Children’s Research Hospital
  • I. A. Rudneva
    • The D.I. Ivanovsky Institute of Virology
  • A. M. Khalenkov
    • Division of Virology, Department of Infectious DiseasesSt. Jude Children’s Research Hospital
  • T. A. Timofeeva
    • The D.I. Ivanovsky Institute of Virology
  • P. S. Krylov
    • The D.I. Ivanovsky Institute of Virology
    • Division of Virology, Department of Infectious DiseasesSt. Jude Children’s Research Hospital
    • Department of PathologyUniversity of Tennessee
  • N. V. Kaverin
    • The D.I. Ivanovsky Institute of Virology
Brief Report

DOI: 10.1007/s00705-009-0535-1

Cite this article as:
Ilyushina, N.A., Rudneva, I.A., Khalenkov, A.M. et al. Arch Virol (2010) 155: 107. doi:10.1007/s00705-009-0535-1
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Abstract

In our earlier studies, we showed that an escape mutant of mouse-adapted H9N2 influenza virus carrying a T198N amino acid change in heamagglutinin (HA) has a lowered virulence for mice. The readaptation of this mutant to mice was associated with N198S or N198D reverse mutations. In this study, single-gene reassortants having HA gene of the wild-type virus, its low-virulence escape mutant, or a readapted variant were generated by site-specific mutagenesis and assayed for virulence. The results showed that antibody-selected mutations in the HA of H9 influenza virus can decrease mortality and virus accumulation in mouse lungs, though not in nasal turbinates, and the effect may be compensated by reverse mutations in the course of passaging.

Copyright information

© Springer-Verlag 2009