|ABENTE, EUGENIO - Orise Fellow|
|RAJAO, DANIELA - Non ARS Employee|
|GAUGER, PHILLIP - Iowa State University|
Submitted to: Pig Veterinary Society International Congress Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 3/1/2016
Publication Date: N/A
Technical Abstract: Introduction Influenza A viruses (IAV) periodically transmit between pigs, people, and birds. If two IAV strains infect the same host, genes can reassort to generate progeny virus with potential to be more infectious or avoid immunity. Pigs pose a risk for such reassortment. Highly pathogenic avian influenza (HPAI) viruses are a global health concern due to the high human case fatality rate observed with specific H5 lineages, such as the Euro-African lineage H5N1 that emerged in the Middle East in 2005. HPAI of Eurasian H5 lineage were recently detected in wild birds and backyard and commercial poultry in North America, with an H5N2 causing outbreaks in the Midwest. In vivo studies were performed with North American HPAI H5’s, the Euro-African H5N1, and Euro-African H5N1 and H1N1pdm09 reassortants to assess the risk of these HPAI H5 in pigs. Materials and Methods Wildtype viruses from Clade 22.214.171.124 (H5N8, H5N1, and H5N2), Clade 2.2 (H5N1), H1N1pdm09, and Clade 2.2 (H5N1) and H1N1pdm09 reassortant viruses were inoculated into primary challenged pigs. Contact pigs were comingled on 2 days post-infection (dpi). Serum was tested by ELISA and hemagglutination inhibition (HI) assays. Nasal swabs were taken to evaluate viral shedding. Lungs were removed at necropsy and bronchoalveolar lavage fluids (BALF) were collected. Lungs were examined for pneumonia and for histopathologic evaluation. Viral RNA was extracted and quantitative TaqMan real-time PCR assays were performed. Virus isolation was performed on RT-PCR positive samples. Results There was limited replication of avian HPAI of Clade 126.96.36.199 in primary pigs and no evidence for spread to contact pigs. However, Clade 2.2 lineage H5N1 showed some transmission in pigs that increased by swapping the H5 and N1 surface genes onto the H1N1pdm09 internal gene backbone. HPAI was detected by the RT-PCR screening test used by veterinary diagnostic labs in the U.S. for swine and may also be detected by H5 HI assays. However, not all primary pigs seroconverted at the time points tested, so further work is required to determine the reliability of HI to assess pig exposure to H5. Conclusions HPAI showed a restricted ability to infect pigs, but the potential for HPAI viruses to incorporate genes from H1N1pdm09 to become more infectious to pigs remains. However, no reassortant viruses with HPAI H5N2 genes were reported from the 2015 North American poultry outbreak and most avian H5 viruses fail to replicate or transmit in pigs. Infection and sustained transmission seems to be unlikely, although the risk is not zero. Continued surveillance for circulating or novel strains in swine and poultry is critical for early detection.