|RAJAO, DANIELA - Non ARS Employee|
|CULHANE, MARIE - University Of Minnesota|
|LEWIS, NICOLA - University Of Cambridge|
Submitted to: Veterinary Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/21/2014
Publication Date: 3/1/2015
Citation: Henningson, J.N., Rajao, D.S., Kitikoon, P., Lorusso, A., Culhane, M.R., Lewis, N.S., Anderson, T.K., Vincent, A.L. 2015. Comparative virulence of wild-type H1N1pdm09 influenza A isolates in swine. Veterinary Microbiology. 176(1-2):40-49.
Interpretive Summary: The H1N1 influenza virus (H1N1pdm09) that led to the human pandemic of 2009 spread to pigs in the U.S. and globally, contributing to the great diversity of influenza A viruses (IAV) in swine. Understanding how genetic variation influences properties of the virus is important to aid in predicting the impact of the genetic changes on the disease in pigs. Three swine H1N1pdm09 viruses (IL/09, IL/10, MN/10) were shown to have genetic changes in the hemagglutinin (HA) gene. The viruses caused lung lesions in pigs and replicated to levels similar to an early human H1N1pdm09 (CA/09), however one of the viruses resulted in lower levels of virus in the nose and lungs. Changes in the HA gene may have the potential to alter the virulence of H1N1pdm09 in swine, but additional factors (i.e., the whole virus genome, host ecology) are likely important.
Technical Abstract: In 2009, a novel swine-origin H1N1 (H1N1pdm09) influenza A virus (IAV) reached pandemic status and was soon after detected in pigs worldwide. The objective of this study was to evaluate whether differences in the HA protein can affect pathogenicity and antigenicity of H1N1pdm09 in swine. We compared lung pathology, viral replication and shedding and the antigenic relationships of four wild-type H1N1pdm09 viruses in pigs: one human (CA/09) and three isolated in swine after the pandemic (IL/09, IL/10, and MN/10). The swine strains were selected based upon unique amino acid substitutions in the HA protein. All selected viruses resulted in mild disease and viral shedding through nasal and oral fluids, however, viral replication and the degree of pathology varied between the isolates. A/Swine/IL/5265/2010 (IL/10), with substitutions I120M, S146G, S186P, V252M, had lower viral titers in the lungs and nasal secretions and fewer lung lesions. The other two swine viruses caused respiratory pathology and replicated to titers similar to the human CA/09, although MN/10 (with mutations D45Y, K304E, A425S) had lower nasal shedding. Swine-adapted H1N1pdm09 have zoonotic potential, and have reassorted with other co-circulating swine viruses, influencing the evolution of IAV in swine globally. Further, our results suggest that amino acid changes in the HA gene have the potential to alter the virulence of H1N1pdm09 in swine. Importantly, the reduction in clinical signs in pigs could result in continued circulation of these viruses with other endemic swine IAVs providing opportunities for reassortment.