Transmission of pandemic influenza H1N1 (2009) in Vietnamese swine in 2009–2010
Article first published online: 30 DEC 2011
© 2011 Blackwell Publishing Ltd
Influenza and Other Respiratory Viruses
Volume 6, Issue 5, pages 348–357, September 2012
How to Cite
Trevennec, K., Leger, L., Lyazrhi, F., Baudon, E., Cheung, C. Y., Roger, F., Peiris, M. and Garcia, J.-M. (2012), Transmission of pandemic influenza H1N1 (2009) in Vietnamese swine in 2009–2010. Influenza and Other Respiratory Viruses, 6: 348–357. doi: 10.1111/j.1750-2659.2011.00324.x
- Issue published online: 14 AUG 2012
- Article first published online: 30 DEC 2011
- Accepted 9 November 2011. Published Online 30 December 2011.
- Cross-species transmission;
- influenza pandemic H1N1;
Please cite this paper as: Trevennec et al. (2012) Transmission of pandemic influenza H1N1 (2009) in Vietnamese swine in 2009–2010. Influenza and Other Respiratory Viruses 6(5), 348–357.
Background The pandemic of 2009 was caused by an H1N1 (H1N1pdm) virus of swine origin. This pandemic virus has repeatedly infected swine through reverse zoonosis, although the extent of such infection in swine remains unclear.
Objective This study targets small and commercial pig producers in North Vietnam, in order to estimate the extent of H1N1pdm infection in swine and to identify the risk factors of infection.
Methods Virologic and serologic surveillance of swine was carried out in 2009–2010 in pig farms (38 swabs and 1732 sera) and at a pig slaughterhouse (710 swabs and 459 sera) in North Vietnam. The sera were screened using a influenza type A-reactive ELISA assay, and positive sera were tested using hemagglutination inhibition tests for antibody to a panel of H1-subtype viruses representing pandemic (H1N1) 2009 (H1N1pdm), triple reassortant (TRIG), classical swine (CS), and Eurasian avian-like (EA) swine lineages. Farm-level risk factors were identified using a zero-inflated negative binomial model.
Results We found a maximal seroprevalence of H1N1pdm of 55·6% [95% CI: 38·1–72·1] in the slaughterhouse at the end of December 2009, 2 weeks after the peak of reported human fatalities with H1N1pdm. Farm-level seroprevalence was 29% [95% CI: 23·2–35·7]. In seropositive farms, within-herd seroprevalence ranged from 10 to 100%. We identified an increased risk of infection for farms that specialized in fattening and a decreased risk of infection in farms hiring external swine workers.
Conclusions Our findings suggest extensive reverse-zoonotic transmission from humans to pigs with subsequent onward transmission within pig herds.