DISPATCHES Pandemic (H1N1) 2009 Outbreak on Pig Farm (original) (raw)

Identification of novel human derived influenza viruses in pigs with zoonotic potential

bioRxiv, 2021

In 2009, a novel swine influenza A virus (IAV) emerged causing a global pandemic that highlighted the role of swine as a reservoir. To date, there is limited information about swine IAV circulating in Latin America. We identified two swine H1N2 and one divergent swine H3N2 viruses that co-circulated in Chilean swine together with the 2009 H1N1 pandemic strain (A(H1N1)pdm09). Phylogenetic analysis revealed several human-to-swine IAV introductions occurring as early as the mid-1980s, and since 2009, several introductions of the A(H1N1)pdm09 strain. Antigenic cartography confirmed that these viruses were antigenically unique and identified drifted variants within the clusters. Human sera from the Chilean general population showed an age dependent mid to low-level antibody mediated protection against swine H1N2 and A(H1N1)pdm09-like viruses and a poor protection against the swine H3N2 virus, highlighting the zoonotic potential of this strain. Our results underscore the epidemiological i...

Swine Outbreak of Pandemic Influenza A Virus on a Canadian Research Farm Supports Human-to-Swine Transmission

Clinical Infectious Diseases, 2011

Background. Swine outbreaks of pandemic influenza A (pH1N1) suggest human introduction of the virus into herds. This study investigates a pH1N1 outbreak occurring on a swine research farm with 37 humans and 1300 swine in Alberta, Canada, from 12 June through 4 July 2009. Methods. The staff was surveyed about symptoms, vaccinations, and livestock exposures. Clinical findings were recorded, and viral testing and molecular characterization of isolates from humans and swine were performed. Human serological testing and performance of the human influenza-like illness (ILI) case definition were also studied. Results. Humans were infected before swine. Seven of 37 humans developed ILI, and 2 (including the index case) were positive for pH1N1 by reverse-transcriptase polymerase chain reaction (RT-PCR). Swine were positive for pH1N1 by RT-PCR 6 days after contact with the human index case and developed symptoms within 24 h of their positive viral test results. Molecular characterization of the entire viral genomes from both species showed minor nucleotide heterogeneity, with 1 amino acid change each in the hemagglutinin and nucleoprotein genes. Sixty-seven percent of humans with positive serological test results and 94% of swine with positive swab specimens had few or no symptoms. Compared with serological testing, the human ILI case definition had a specificity of 100% and sensitivity of 33.3%. The only factor associated with seropositivity was working in the swine nursery. Conclusions. Epidemiologic data support human-to-swine transmission, and molecular characterization confirms that virtually identical viruses infected humans and swine in this outbreak. Both species had mild illness and recovered without sequelae. Between 2 May 2009 and 5 March 2010, many countries reported pandemic influenza A H1N1 (pH1N1) infection in swine, including the first observation from Canada [1]. Some mentioned human involvement [2,

Reassortment of Pandemic H1N1/2009 Influenza A Virus in Swine

2010

The emergence of pandemic H1N1/2009 influenza demonstrated that pandemic viruses could be generated in swine. Subsequent re-introduction of H1N1/2009 to swine has occurred in multiple countries. Through systematic surveillance of influenza viruses in swine from a Hong Kong abattoir, we characterize a reassortant progeny of H1N1/2009 with swine viruses. Continued reassortment of H1N1/2009 with swine influenza viruses could produce variants with transmissibility and altered virulence for humans. Global systematic surveillance of influenza viruses in swine is warranted.

North American triple reassortant and Eurasian H1N1 swine influenza viruses do not readily reassort to generate a 2009 pandemic H1N1-like virus

mBio, 2014

The 2009 pandemic H1N1 virus (pH1N1) was derived through reassortment of North American triple reassortant and Eurasian avian-like swine influenza viruses (SIVs). To date, when, how and where the pH1N1 arose is not understood. To investigate viral reassortment, we coinfected cell cultures and a group of pigs with or without preexisting immunity with a Eurasian H1N1 virus, A/Swine/Spain/53207/2004 (SP04), and a North American triple reassortant H1N1 virus, A/Swine/Kansas/77778/2007 (KS07). The infected pigs were cohoused with one or two groups of contact animals to investigate viral transmission. In coinfected MDCK or PK15 continuous cell lines with KS07 and SP04 viruses, more than 20 different reassortant viruses were found. In pigs without or with preexisting immunity (immunized with commercial inactivated swine influenza vaccines) and coinfected with both viruses, six or seven reassortant viruses, as well as the parental viruses, were identified in bronchoalveolar lavage fluid sam...

Epidemiological update on swine influenza (H1N1) in pigs

Indian Journal of Microbiology, 2009

The 2009 H1N1 pandemic has slowed down its spread after initial speed of transmission. The conventional swine infl uenza H1N1 virus (SIV) in pig populations worldwide needs to be differentiated from pandemic H1N1 infl uenza virus, however it is also essential to know about the exact role of pigs in the spread and mutations taking place in pig-to-pig transmission. The present paper reviews epidemiological features of classical SIV and its differentiation with pandemic infl uenza.