Abstract
Avian influenza viruses (AIVs) evolve in nature through the accumulation of point mutations (antigenic drift) or the exchange of gene segments (reassortment) between two different influenza viruses upon infection of a host cell. Vaccination accelerates the antigenic drift of the viral hemagglutinin (HA), which contains the immunogenic epitopes, to evade the host immune response.
In Italy, H7N1 outbreaks in 1999 devastated the poultry industry and vaccination of chickens and turkeys was used to mitigate the economic impact of the virus. However, vaccination did not prevent the infection and the virus circulated in (vaccinated) poultry for three years. The aim of this study was to investigate the effect of HA mutations on virus fitness.
Sequence analysis of the HA protein of viruses isolated in 2002 compared to those originally introduced into poultry in 1999 was done. Reverse genetics was used to generate different H7N1 AIVs carrying the 1999 parenteral HA with or without single mutations similar to the viruses detected under vaccination pressure in 2002. Replication kinetics in chicken and turkey cells, receptor binding affinity, cell-to-cell spread, and antigenic drift against homologous or heterologous serum were studied.
Seven mutations were fixed in viruses after 1999. Mutations in the HA resulted in antigenic drift of the virus from serum raised against the HA of the vaccine strain. Mutations in the HA reduced virus affinity for avian-type sialic acid receptors and modulated virus replication and spread in cell culture.
In Italy, H7N1 outbreaks in 1999 devastated the poultry industry and vaccination of chickens and turkeys was used to mitigate the economic impact of the virus. However, vaccination did not prevent the infection and the virus circulated in (vaccinated) poultry for three years. The aim of this study was to investigate the effect of HA mutations on virus fitness.
Sequence analysis of the HA protein of viruses isolated in 2002 compared to those originally introduced into poultry in 1999 was done. Reverse genetics was used to generate different H7N1 AIVs carrying the 1999 parenteral HA with or without single mutations similar to the viruses detected under vaccination pressure in 2002. Replication kinetics in chicken and turkey cells, receptor binding affinity, cell-to-cell spread, and antigenic drift against homologous or heterologous serum were studied.
Seven mutations were fixed in viruses after 1999. Mutations in the HA resulted in antigenic drift of the virus from serum raised against the HA of the vaccine strain. Mutations in the HA reduced virus affinity for avian-type sialic acid receptors and modulated virus replication and spread in cell culture.
Co-Author(s)
Juliane Lang1, and Elsayed M. Abdelwhab1
1Institute of Molecular Virology and Cell Biology, Friedrich-Loeffler-Institut, Federal Research Institute for Animal Health, Südufer 10, 17493 Greifswald-Insel Riems, Germany
Abstract Category
Diagnostics, vaccination, or other mitigation strategies for poultry and wildlife