Archives of Virology

, Volume 158, Issue 6, pp 1297–1303

Influenza virus A(H1N1)pdm09 hemagglutinin polymorphism and associated disease in southern Germany during the 2010/11 influenza season

Authors

  • Valeria Falcone
    • Department of VirologyInstitute for Medical Microbiology and Hygiene, University Medical Center
  • Sibylle Bierbaum
    • Department of VirologyInstitute for Medical Microbiology and Hygiene, University Medical Center
  • Winfried Kern
    • Department of MedicineUniversity Medical Center
  • Udo Kontny
    • Center for Paediatrics and Adolescent MedicineUniversity Medical Center
  • Hartmut Bertz
    • Department of Haematology/OncologyUniversity Medical Center
  • Daniela Huzly
    • Department of VirologyInstitute for Medical Microbiology and Hygiene, University Medical Center
    • Department of VirologyInstitute for Medical Microbiology and Hygiene, University Medical Center
Original Article

DOI: 10.1007/s00705-013-1610-1

Cite this article as:
Falcone, V., Bierbaum, S., Kern, W. et al. Arch Virol (2013) 158: 1297. doi:10.1007/s00705-013-1610-1

Abstract

A novel influenza A virus emerged in early 2009 to cause the first influenza pandemic of the 21st century. Understanding the evolution of influenza virus is crucial to determine pathogenesis, vaccine efficacy, and resistance to antiviral drugs. In this study, we investigated the molecular evolution of influenza virus A(H1N1)pdm09 in the 2010/11 influenza season in southern Germany by sequence analysis of the influenza virus hemagglutinin gene from 25 patients with mild, moderate, and severe disease. Phylogenetic analysis revealed co-circulation of different genetic groups. The D222G mutation, which had previously been observed in severe cases, was not detected. Immunocompromised patients were not affected more severely than non-immunocompromised patients (p>0.05), although longer shedding was observed in some of them. Interestingly, additional mutations and potential glycosylation sites were detected in samples from the lower respiratory tract in two patients, but not in the corresponding upper respiratory tract specimens. The H275Y mutation in the influenza virus neuraminidase gene, known to confer resistance to the neuraminidase inhibitor oseltamivir, was detected in one patient.

Copyright information

© Springer-Verlag Wien 2013