
Differential Polymerase Activity in Avian and Mammalian Cells Determines Host Range of Influenza Virus
Author(s) -
Gülşah Gabriel,
Michael E. Abram,
Bjoern Keiner,
Ralf Wagner,
HansDieter Klenk,
Jürgen Stech
Publication year - 2007
Publication title -
journal of virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.617
H-Index - 292
eISSN - 1070-6321
pISSN - 0022-538X
DOI - 10.1128/jvi.00666-07
Subject(s) - biology , virology , polymerase , viral replication , virus , influenza a virus , rna polymerase , influenza a virus subtype h5n1 , transcription (linguistics) , gene , rna polymerase ii , orthomyxoviridae , viral shedding , microbiology and biotechnology , gene expression , rna , genetics , promoter , linguistics , philosophy
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.