|LEE, DONG-HUN - Orise Fellow|
|BERTRAN, KATERI - Consultant|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 3/27/2015
Publication Date: 6/29/2015
Citation: Swayne, D.E., Lee, D., Bertran, K., Kapczynski, D.R., Pantin Jackwood, M.J., Spackman, E., Suarez, D.L. 2015. Recent intercontinental movement and reassortment of H5 clade 184.108.40.206 HPAIV and the resulting impact on pathobiology in wild birds and poultry [abstract]. Abstracts of Global Alliance for Research on Avian Diseases (GARAD) Conference, June 29-July 1, 2015, London, United Kingdom. p. 16.
Technical Abstract: H5N1 high pathogenicity avian influenza (HPAI) virus (HPAIV) emerged in 1996 in Guangdong, China, and has since spread to infect and cause deaths in wild birds, poultry, and humans in over 63 countries in Asia, Europe, and Africa; and more recently a reassortant H5N8 clade 220.127.116.11 HPAI virus has spread to Europe and North America, with further reassortment with North America low pathogenicity avian influenza virus genes. Phylogenetic network analysis and understanding of waterfowl migration patterns indicates the Eurasian H5N8 clade 18.104.22.168 avian influenza virus emerged in late 2013 in China, spread in early 2014 to South Korea and Japan, and reached Siberia and Beringia (Russian Far East and Alaska) by summer 2014 via migratory birds. Three genetically distinct subgroups emerged in late 2014; subgroup A1 moving to western Russia and Europe, subgroup A2 to North America, and subgroup A3 to Korea. All three subgroups reappeared in Japan, a wintering site for waterfowl from Eurasia and North America. Studies to understand the infectivity and transmissibility of an H5N8 and H5N2 clade 22.214.171.124 HPAI viruses in mallards, chickens, turkeys, and Japanese quail were undertaken. Chickens and Japanese quail were frequently listless and had ruffled feathers before death, but a few had neurological signs. Pancreatic necrosis, splenomegaly, renomegaly, and petechial hemorrhages on myocardium were the most common lesions in birds that died. However, some chickens also had cyanosis of combs and wattles. Neurological signs were the primary presentation of disease in turkeys. The mean death time in all species was late (3-9 days post exposure) when compared to H5N1 HPAIV (2-3 days). Infection led to death as survivors lacked H5 hemagglutination inhibiting antibodies. However, neither virus appeared to be well adapted to chickens or turkeys and required a dose of 6log10 50% egg infectious doses (EID50) per bird to achieve 50% infection and did not transmit to contact exposure birds. Quail were slightly more susceptible with a 50% infectious dose of 4 log10 EID50 per bird for each isolate. All mallard ducks became infected with both viruses at all challenge doses (bird infective dose < or = 102 EID50), and transmitted to contact ducks. Infected ducks showed decreased weight gain, and some ducks had fever, but no other clinical signs and no mortality were observed. High amounts of virus were detected in oropharyngeal swabs, with some ducks still shedding virus 14 days after inoculation. These results suggest the intercontinental H5N8 and H5N2 HPAIVs have reduced virulence and transmissibility for gallinaceous host compared to historical H5N1 HPAIV while maintaining low virulence and high infectivity for wild waterfowl.