Natural Cases of 2009 Pandemic H1N1 Influenza A Virus in Pet Ferrets

Diagnostic Virology Laboratory, National Veterinary Services Laboratories, U.S. Department of Agriculture, Animal and Plant Health Inspection Service, Ames, IA 50010, USA.
Journal of veterinary diagnostic investigation: official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc (Impact Factor: 1.35). 09/2010; 22(5):784-8. DOI: 10.1177/104063871002200525
Source: PubMed


Respiratory swab samples were collected from 5 pet ferrets (Mustela putorius furo) exhibiting influenza-like illness. The ferrets represented 3 households in 2 states. In each case, the owners reported influenza-like illness in themselves or family members prior to the onset of a similar illness in the ferrets. Real-time reverse transcription polymerase chain reaction assays designed for the detection of the 2009 H1N1 Influenza A virus were conducted in the state animal health laboratories. The assays included detection of the matrix gene of Influenza A virus and neuraminidase gene specific for 2009 H1N1 virus. Samples were positive for both screening assays. The samples were confirmed positive by the National Veterinary Services Laboratories. The history of illness in family members prior to illness in the ferrets suggests that Influenza A virus was transmitted from humans to the ferrets.

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Available from: Leo Koster, Sep 17, 2014
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    • "The pandemic H1N1 influenza A virus (pH1N1), first isolated from humans in 2009, quickly spread to numerous other species, including swine, cats and ferrets [1]–[4]. Genetic analysis of 1,516 swine influenza viruses (SIVs) isolated in 2009–2010 identified 41 viruses related to pH1N1, indicating that the pH1N1 had become established in North American swine herds [5]. "
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    ABSTRACT: The pandemic H1N1 (pH1N1) influenza virus was first reported in humans in the spring of 2009 and soon thereafter was identified in numerous species, including swine. Reassortant viruses, presumably arising from the co-infection of pH1N1 and endemic swine influenza virus (SIV), were subsequently identified from diagnostic samples collected from swine. In this study, co-infection of swine testicle (ST) cells with swine-derived endemic H1N2 (MN745) and pH1N1 (MN432) yielded two reassortant H1N2 viruses (R1 and R2), both possessing a matrix gene derived from pH1N1. In ST cells, the reassortant viruses had growth kinetics similar to the parental H1N2 virus and reached titers approximately 2 log(10) TCID(50)/mL higher than the pH1N1 virus, while in A549 cells these viruses had similar growth kinetics. Intranasal challenge of pigs with H1N2, pH1N1, R1 or R2 found that all viruses were capable of infecting and transmitting between direct contact pigs as measured by real time reverse transcription PCR of nasal swabs. Lung samples were also PCR-positive for all challenge groups and influenza-associated microscopic lesions were detected by histology. Interestingly, infectious virus was detected in lung samples for pigs challenged with the parental H1N2 and pH1N1 at levels significantly higher than either reassortant virus despite similar levels of viral RNA. Results of our experiment suggested that the reassortant viruses generated through in vitro cell culture system were attenuated without gaining any selective growth advantage in pigs over the parental lineages. Thus, reassortant influenza viruses described in this study may provide a good system to study genetic basis of the attenuation and its mechanism.
    PLoS ONE 06/2012; 7(6):e39177. DOI:10.1371/journal.pone.0039177 · 3.23 Impact Factor
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    • "Another unusual feature was that pH1N1 caused a higher morbidity and fatality in young healthy adults than the seasonal influenza viruses (Chowell et al., 2009). Equally important and unique was the ability of pH1N1 to cross species barriers, as it was detected in different animal species including dogs, turkeys, cats, swine, ferrets and other wildlife (Berhane et al., 2010; Dundon et al., 2010; Pasma & Joseph, 2010; Schrenzel et al., 2011; Sponseller et al., 2010; Swenson et al., 2010). This has raised concerns that reassortments might occur between pH1N1 and other influenza viruses, including highly pathogenic H5N1 avian influenza viruses (Kimble et al., 2011; Schrauwen et al., 2011). "
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    ABSTRACT: The 2009 pandemic H1N1 virus (pH1N1) contains neuraminidase (NA) and matrix (M) genes from Eurasian avian-like swine influenza viruses (SIVs), with the remaining six genes from North American triple-reassortant SIVs. To characterize the role of the pH1N1 NA and M genes in pathogenesis and transmission, their impact was evaluated in the background of an H1N1 triple-reassortant (tr1930) SIV in which the HA (H3) and NA (N2) of influenza A/swine/Texas/4199-2/98 virus were replaced with those from the classical H1N1 A/swine/Iowa/15/30 (1930) virus. The laboratory-adapted 1930 virus did not shed nor transmit in pigs, but tr1930 was able to shed in infected pigs. The NA, M or both genes of the tr1930 virus were then substituted by those of pH1N1. The resulting virus with both NA and M from pH1N1 grew to significantly higher titre in cell cultures than the viruses with single NA or M from pH1N1. In a pig model, only the virus containing both NA and M from pH1N1 was transmitted to and infected sentinels, whereas the viruses with single NA or M from pH1N1 did not. These results demonstrate that the right combination of NA and M genes is critical for the replication and transmissibility of influenza viruses in pigs.
    Journal of General Virology 02/2012; 93(Pt 6):1261-8. DOI:10.1099/vir.0.040535-0 · 3.18 Impact Factor
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    ABSTRACT: PB1-F2 is an 87- to 90-amino-acid-long protein expressed by certain influenza A viruses. Previous studies have shown that PB1-F2 contributes to virulence in the mouse model; however, its role in natural hosts-pigs, humans, or birds-remains largely unknown. Outbreaks of domestic pigs infected with the 2009 pandemic H1N1 influenza virus (pH1N1) have been detected worldwide. Unlike previous pandemic strains, pH1N1 viruses do not encode a functional PB1-F2 due to the presence of three stop codons resulting in premature truncation after codon 11. However, pH1N1s have the potential to acquire the full-length form of PB1-F2 through mutation or reassortment. In this study, we assessed whether restoring the full-length PB1-F2 open reading frame (ORF) in the pH1N1 background would have an effect on virus replication and virulence in pigs. Restoring the PB1-F2 ORF resulted in upregulation of viral polymerase activity at early time points in vitro and enhanced virus yields in porcine respiratory explants and in the lungs of infected pigs. There was an increase in the severity of pneumonia in pigs infected with isogenic virus expressing PB1-F2 compared to the wild-type (WT) pH1N1. The extent of microscopic pneumonia correlated with increased pulmonary levels of alpha interferon and interleukin-1β in pigs infected with pH1N1 encoding a functional PB1-F2 but only early in the infection. Together, our results indicate that PB1-F2 in the context of pH1N1 moderately modulates viral replication, lung histopathology, and local cytokine response in pigs.
    Journal of Virology 02/2012; 86(10):5523-32. DOI:10.1128/JVI.00134-12 · 4.44 Impact Factor
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