|GAUGER, PHILLIP - Iowa State University|
|SENNE, DENNIS - Animal And Plant Health Inspection Service (APHIS)|
|MA, WENJUN - Kansas State University|
|Kehrli Jr, Marcus|
Submitted to: Pig Veterinary Society International Congress Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 3/31/2010
Publication Date: 7/18/2010
Citation: Lager, K.M., Vincent, A.L., Gauger, P.C., Senne, D.A., Swayne, D.E., Miller, L.C., Richt, J., Ma, W., Suarez, D.L., Kehrli Jr, M.E. 2010. Susceptibility of Swine to Low Pathogenic H5 and H7 Avian Influenza Viruses. In: Proceedings of the International Pig Veterinary Society Congress, July 18-21, 2010, Vancouver, Canada. p. 79.
Technical Abstract: Introduction: The emergence of the 2009 pandemic H1N1 influenza virus from swine origin viruses (1) reinforced the concern about transmission of animal influenza viruses to man. This follows the transmission of highly pathogenic H5N1 viruses from birds to people identified in the late 1990s and continuing today (2). These two events demonstrate the transmission of novel influenza viruses to man. In addition, the discovery of a unique H2N3 reassortant virus in swine (3) provided insight into the introduction and adaptation of low pathogenic avian influenza virus (AIV) genes into a mammalian host. To explore the likelihood of swine serving as an indirect host for AIV, we tested the susceptibility of swine to low pathogenic H5 and H7 viruses isolated from North America. Materials and Methods: Four-week-old influenza-free pigs were randomly allotted to one of 12 groups. All pigs in each group (n=12) were inoculated with a sham (Group 1) or virus inoculum (Groups 2-12). Virus challenge dose was about 1 x 10**6 EID50 in a 2 ml volume that was dripped behind each lower eyelid and into each naris. Group 6 was given a swine virus to serve as a positive control; the remaining groups received either an H5 or H7 AIV. At 3, 5, 7, and 28 days-post-inoculation (dpi), three pigs were euthanized in each group for virus detection and lesion evaluation. At 2 dpi, five contact pigs were comingled with each group and maintained as a group until 28 dpi when all pigs were euthanized. Nasal swabs were collected on days 2, 4, and 6 pi from all live pigs in each group. Bronchioalveolar lavage fluid (BALF) was collected at necropsy. Nasal swabs and BALF were tested for viral nucleic acid with real-time RT-PCR (4). Day 28 pi sera was tested for influenza virus antibody with a commercially available ELISA (5). Results: No virus, antibody, or lesions were found in the negative control group, Group 1 pigs. Challenge virus was only detected in NS from group 6 pigs challenged with the swine H1N1 at 2, 4, and 6 dpi (data not shown). Group 6 contact pigs were the only contact pigs that seroconverted by 28 dpi. AIV challenge virus was detected in the BALF from one or more pigs in each challenge group. Except for group 7, one or more inoculated pigs developed antibody by 28 dpi: however; no contact pigs in the AIV groups seroconverted. Mild lung lesions were observed in each group of pigs. Discussion: Challenge virus was detected in the BALF from one or more pigs in each of the AIV-challenged groups indicating that swine were susceptible to infection via a mucosal exposure. Although pigs were susceptible to infection, lung lesions were mild and variable. There was no virus detected from or serologic evidence of virus transmission from AIV-inoculated pigs to their respective contacts. In contrast, the contact pigs for group 6 were infected with the swine challenge virus and each pig seroconverted. Moreover, this was the only contact group from which viral nucleic acid was detected in nasal swabs. Some pigs were negative following mucosal challenge with AIV suggesting innate resistance or a challenge dose at the minimal threshold of infection. Acknowledgements: Funding was provided by USDA ARS and a USDA APHIS AIV Supplemental Fund. References 1. Garten, R. J. et al., Science 2009:325;197. 2. Duan, L. et al., Virology 2008:380;243. 3. Ma, W., et al., Proc Natl Acad Sci 2007:104;20949. 4. Spackman, E., et al., J Clin Microbiol 2002:40;3256. 5. Ciacci-Zanella, J., et al., J Vet Diagn Inv 2010:22;3.