|Event Title||First Global Alliance for Research on Avian Diseases (GARAD) Conference|
|Event Date & Time||On Wed, 01 Jul 2015 at 10:55:00 - 11:15:00|
|Venue||Edmond J. Safra Lecture Theatre|
|Abstract Title||The contribution of avian influenza virus PB1-F2 protein to viral virulence and pathogenesis in poultry|
|Affiliations||The Pirbright Institute, Compton Laboratory, Compton, UK.|
The PB1-F2 protein is translated from the +1 frame of the genetic segment that encodes the influenza virus RNA polymerase. Work in mammalian systems has shown PB1-F2 to have a range of effects dependent upon cell type and viral strain including pro-apoptotic and pro-inflammatory functions, modulation of the innate immune response, and regulation of viral polymerase activity. The PB1-F2 protein is often truncated or missing in influenza viruses isolated from mammals, however 96% of all avian influenza isolates possess a full length PB1-F2 gene, suggesting a unique function in the avian host. To date, only limited studies have been undertaken in avian systems and the role of PB1-F2 in the avian host remains to be fully elucidated. Here, we generated isogenic viruses that encoded a full length or knock out of the PB1-F2 protein in prototypical H9N2 and H5N1 influenza strains of utmost importance to the poultry industry. We show that PB1-F2 reduces the pathology of influenza viruses in chickens a direct contrast to the situation in mammals. We observed a more prolonged period of infectious virus shedding from inoculated birds when PB1-F2 was present and that this coincided with a reduction in circulating blood leukocytes. We hypothesis that PB1-F2 has a role in modulation of the innate immune response in chickens by removable of leukocytes which results in a longer infectious shedding period that in a field flock situation may result in more effective transmission. Removal of PB1-F2 may in some situations cause an uncontrolled immune response resulting immunopathology.