Title: Characterization of the 2012 highly pathogenic avian influenza H7N3 virus isolated from poultry in an outbreak in Mexico: pathobiology and vaccine protection Authors
|Guzman, Sofia -|
|Ricardez, Yardira -|
|Bertran, Kateri -|
Submitted to: Journal of Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: April 15, 2013
Publication Date: July 10, 2013
Citation: Kapczynski, D.R., Pantin Jackwood, M.J., Guzman, S.G., Ricardez, Y., Spackman, E., Bertran, K., Suarez, D.L., Swayne, D.E. 2013. Characterization of the 2012 highly pathogenic avian influenza H7N3 virus isolated from poultry in an outbreak in Mexico: pathobiology and vaccine protection. Journal of Virology. 87(15). Available:http://jvi.asm.org/content/early/2013/06/05/JVI.00666-13.long Interpretive Summary: Avian influenza (AI) viruses cause widespread morbidity and mortality in wild and domestic bird populations and threaten the U.S. poultry food supply and safety. Highly Pathogenic (HP) AI is an economically important disease of poultry that has significant impact on global trade. New outbreaks of HPAI in commercial poultry represent one of the most critical diseases to contain and require reporting to the World Organization for Animal Health. Following an outbreak of HPAI in Mexico in 2012, we determined the virulence mechanisms unique to this virus and tested a number of different vaccine formulations for protection of poultry. In these studies we demonstrate that the Mexican 2012 HPAI virus kills birds within days, but that recent USDA master seed vaccine viruses can provide complete protection from disease. These studies further our knowledge of new and ongoing HPAI outbreaks.
Technical Abstract: In June of 2012, a H7N3 highly pathogenic avian influenza (HPAI) virus was identified as the cause of a severe disease outbreak in commercial laying chicken farms in Mexico. The purpose of this study was to characterize the Mexican 2012 H7N3 HPAI virus (A/chicken/Jalisco/CPA1/2012) and determine protection conferred against the virus by different H7 inactivated vaccines in chickens. Both adult and young chickens intranasally inoculated with the virus became infected and died between 2 and 4 days post inoculation (p.i.) some without presenting clinical signs (peracute disease), some showing nonspecific clinical signs including ruffled feathers, lethargy, anorexia and prostration, and some presenting with severe respiratory distress, facial edema, cyanotic combs, wattles and legs. High virus titers and viral replication in many tissues was demonstrated at 2 days p.i. in infected birds. The Jalisco virus had high sequence similarity of greater than 97% to wild bird viruses from North America for all eight gene segments. The hemagglutinin gene of the virus contained a 24 nucleotide insert at the hemagglutinin cleavage site which had a 100% sequence identity to chicken 28s ribosomal RNA, suggesting the insert was non-homologous recombination with the host genome. For the vaccine protection studies, both U.S. H7 low pathogenic AI viruses and a virus selected for use as a vaccine seed strain in Mexico were tested as antigen in experimental oil emulsion vaccines and injected into chickens three weeks prior to challenge. All H7 vaccines tested provided >90 % protection against clinical disease after challenge and decreased the number of birds shedding and the titers of viral shedding. This study demonstrates the pathological consequence of H7 HPAI infection of chickens and provides support for effective vaccination programs in poultry against this virus.