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Differential Polymerase Activity in Avian and Mammalian Cells Determines Host Range of Influenza Virus

G. Gabriel, M. Abram, B. Keiner, R. Wagner, H.-D. Klenk,^* and J. Stech

Institut fuer Virologie, Philipps-Universität Marburg, Hans-Meerwein-Str. 2, 35043 Marburg, Germany

Received 28 March 2007/ Accepted 6 June 2007

As recently shown, mutations in the polymerase genes causing increased polymerase activity in mammalian cells are responsible for the adaptation of the highly pathogenic avian influenza virus SC35 (H7N7) to mice (G. Gabriel et al., Proc. Natl. Acad. Sci. USA 102:18590-18595, 2005). We have now compared mRNA, cRNA, and viral RNA levels of SC35 and its mouse-adapted variant SC35M in avian and mammalian cells. The increase in levels of transcription and replication of SC35M in mammalian cells was linked to a decrease in avian cells. Thus, the efficiency of the viral polymerase is a determinant of both host specificity and pathogenicity.

Published ahead of print on 13 June 2007.

Present address: Paul Ehrlich Institut, Paul Ehrlich Str. 51-59, 63225 Langen, Germany.

Present address: Friedrich-Löffler-Institut, Bundesforschungsinstitut für Tiergesundheit, Institut für Molekularbiologie, Boddenblick 5a, 17493 Greifswald, Insel Riems, Germany.

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