|Kwon, Yong Kuk - USDA, FAS, VISITING SCI|
Submitted to: Public Library of Science for Pathogens
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 14, 2008
Publication Date: July 1, 2008
Citation: Lipatov, A.S., Kwon, Y., Sarmento, L., Lager, K.M., Spackman, E., Suarez, D.L., Swayne, D.E. 2008. Domestic pigs have low susceptibility to H5N1 highly pathogenic avian influenza viruses. Public Library of Science for Pathogens [serial online]. 4(7):e1000102. Available: http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000102. Interpretive Summary: The ability of the H5N1 highly pathogenic avian influenza viruses (HPAI) to infect and cause disease in pigs is unknown. We exposed groups of conventional 2-3-week-old domestic piglets in the nose with one of four different H5N1 HPAI viruses or swine influenza viruses (SIV) of H3N2 and H1N1 subtypes. The pigs were more resistant to infection with the H5N1 HPAI virus than to the H3N2/H1N1 SIV. None of the pigs developed disease, but with two of the H5N1 HPAI viruses, exposed pigs lost weight and developed mild pneumonia. The H5N1 viruses only grew in the respiratory tract, but a lower amount of virus was produced than with infections by the two SIV. Feeding raw H5N1 infected poultry meat to pigs transmitted the virus causing infection detected by an antibody response, but no disease. Pigs had a low susceptibility to infection with H5N1 HPAI.
Technical Abstract: Background. Genetic reassortment of H5N1 highly pathogenic avian influenza viruses (HPAI) with currently circulating human influenza A strains is one possibility that could lead to efficient human-to-human transmissibility. Domestic pigs which are susceptible to infection with both human and avian influenza A viruses are one of the natural hosts where such reassortment events could occur. The susceptibility of pigs to infection with various H5N1 HPAI viruses was characterized in this study. Methods and Findings. Two to three weeks-old domestic piglets were intranasally inoculated with 106 EID50 of A/Vietnam/1203/04 (VN/04), A/chicken/Indonesia/7/03 (Ck/Indo/03), A/Whooper swan/Mongolia/244/05 (WS/Mong/05), and A/Muscovy duck/Vietnam/ 209/06 (MDk/VN/06) viruses. Swine H3N2 and H1N1 viruses were studied as a positive control for swine influenza virus infection. The pathogenicity of the H5N1 HPAI viruses was also characterized in mouse and ferrets animal models. Inoculation of pigs with H5N1 viruses did not result in clinical signs when administered intranasally or when consumed in infected chicken meat. Mild weight loss was seen in pigs inoculated with WS/Mong/05, Ck/Indo/03 H5N1 and H1N1 swine influenza viruses. WS/Mong/05, Ck/Indo/03 and VN/04 viruses were detected in nasal swabs of inoculated pigs mainly on days 1 and 2. Titers of H5N1 viruses in nasal swabs were remarkably lower compared with swine influenza viruses. Replication of all four H5N1 viruses in pigs was restricted to the respiratory tract, mainly to the lungs. Titers of H5N1 viruses in the lungs were lower than those of swine viruses. Histological examination revealed mild to moderate bronchiolitis and focal alveolitis in the lungs of pigs infected with H5N1 viruses while infection with swine influenza viruses resulted in severe tracheobronchitis and bronchopneumonia. Conclusions. Pigs had lower susceptibility to infection with H5N1 HPAI. Inoculation of pigs with H5N1 viruses resulted in asymptomatic infection restricted to the respiratory tract in contrast to mouse and ferrets animal models, where some of the studied viruses are highly pathogenic and replicate systemically.