Abstract
The hemagglutinin (HA) protein of influenza virus mediates essential viral functions including the binding to host receptor and virus entry. It also has the antigenic sites required for virus neutralization by host antibodies. Here, we characterized an H3N2 triple reassortant (TR) influenza virus (A/turkey/Ohio/313053/04) with a mutation at the receptor binding domain (Asp190Ala) that occurred upon virus transmission from turkeys to pigs in an experimental infection study. The mutant virus replicated less efficiently than the parental virus in human, pig and turkey primary tracheal/bronchial epithelial cells, with more than 3-log10 difference in virus titer at 72 hours post infection. In addition, the mutant virus demonstrated lower binding efficiency to plasma membrane preparations from all three cell types compared to the parental virus. Antisera raised against the parental virus reacted equally to both homologous and heterlogous viruses, however, antisera raised against the mutant virus showed 4-8 folds lower reactivity to the parental virus.
Highlights
Influenza A viruses infect a wide range of animal species including mammals and birds [1]
We characterized an H3N2 triple reassortant (TR) influenza virus with a mutation at the receptor binding domain (RBD) (Asp190Ala) that occurred upon virus transmission from turkeys to pigs in an experimental infection study [10]
Generation of mutant viruses The H3N2 TR virus used in this study, A/turkey/Ohio/ 313053/04 (TK04), was previously isolated at our laboratory [11] and has been propagated two times in 10-dayold embryonated chicken eggs (ECE)
Summary
Influenza A viruses infect a wide range of animal species including mammals and birds [1]. Previous studies have identified key residues at the receptor binding domain (RBD) of the HA molecule that are critical in determining host range specificity of influenza viruses. Ala is rarely expressed at this position and characterization of such mutation is essential for its possible effect on antigenicity, receptor binding specificity, and interspecies transmission of H3 subtype influenza viruses [14,15,16,17].
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