Effect of age on the pathogenesis and innate immune responses in Pekin ducks infected with different H5N1 highly pathogenic avian influenza viruses

Pantin‐Jackwood, Mary J.; Smith, Diane; Wasilenko, Jamie; Cagle, Caran; Shepherd, Eric; Sarmento, Luciana; Kapczynski, Darrell R.; Afonso, Claudio L.

doi:10.1016/j.virusres.2012.04.015

Cited by 41 publications

(37 citation statements)

References 55 publications

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“…The level of inducible nitric oxide synthase expression has been demonstrated to be associated with the severity of the pathology (22). The difference in disease severity following HPAIV infection in ducks is associated with the difference in viral replication and host gene expression (34). Our results highlight the importance of the innate immune status in the brain to the pathogenicity of H5N1 virus, furthering the understanding of the pathogenesis of H5N1 virus in ducks.…”

Section: Discussionmentioning

confidence: 53%

“…Results from two independent studies have demonstrated that viral replication is associated with the increased inflammatory response in ducks infected with H5N1 HPAIVs (22,33). Recently, PantinJackwood et al have shown that ducks of various ages mount distinct host immune responses to H5N1 virus infection, which may be related to the different virulence (34). However, the role of the host immune response in disease severity and outcome in ducks infected with H5N1 AIVs is largely unknown.…”

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confidence: 99%

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The PA and HA Gene-Mediated High Viral Load and Intense Innate Immune Response in the Brain Contribute to the High Pathogenicity of H5N1 Avian Influenza Virus in Mallard Ducks

et al. 2013

J Virol

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Most highly pathogenic avian influenza A viruses cause only mild clinical signs in ducks, serving as an important natural reservoir of influenza A viruses. However, we isolated two H5N1 viruses that are genetically similar but differ greatly in virulence in ducks. A/Chicken/Jiangsu/k0402/2010 (CK10) is highly pathogenic, whereas A/Goose/Jiangsu/k0403/2010 (GS10) is low pathogenic. To determine the genetic basis for the high virulence of CK10 in ducks, we generated a series of single-gene reassortants between CK10 and GS10 and tested their virulence in ducks. Expression of the CK10 PA or hemagglutinin (HA) gene in the GS10 context resulted in increased virulence and virus replication. Conversely, inclusion of the GS10 PA or HA gene in the CK10 background attenuated the virulence and virus replication. Moreover, the PA gene had a greater contribution. We further determined that residues 101G and 237E in the PA gene contribute to the high virulence of CK10. Mutations at these two positions produced changes in virulence, virus replication, and polymerase activity of CK10 or GS10. Position 237 plays a greater role in determining these phenotypes. Moreover, the K237E mutation in the GS10 PA gene increased PA nuclear accumulation. Mutant GS10 viruses carrying the CK10 HA gene or the PA101G or PA237E mutation induced an enhanced innate immune response. A sustained innate response was detected in the brain rather than in the lung and spleen. Our results suggest that the PA and HA gene-mediated high virus replication and the intense innate immune response in the brain contribute to the high virulence of H5N1 virus in ducks.

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Section: Discussionmentioning

confidence: 53%

mentioning

confidence: 99%

The PA and HA Gene-Mediated High Viral Load and Intense Innate Immune Response in the Brain Contribute to the High Pathogenicity of H5N1 Avian Influenza Virus in Mallard Ducks

et al. 2013

J Virol

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“…Several studies have demonstrated that expression of immune-related genes varied with different types of ducks, different origins of AIV isolates and different tissues Cornelissen et al, 2012;Maughan et al, 2013). Furthermore, age-related differences in immune responses to AIV infection have also reported in chickens and ducks (Reemers et al, 2010;Pantin-Jackwood et al, 2012). We, therefore, hypothesized that immune responses and pathogenesis in chickens and ducks in response to H9N2 infection may be affected by these factors.…”

Section: Discussionmentioning

confidence: 90%

Different outcomes of infection of chickens and ducks with a duck-origin H9N2 influenza A virus

Wang¹,

Li²,

Diao³

et al. 2014

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Summary. -As the major aquatic and terrestrial hosts for avian influenza viruses (AIVs), ducks and chickens play a critical role in the evolution and spread of the H9N2 virus. However, the outcomes of infection of ducks and chickens with the H9N2 virus are not sufficiently documented. In this study, we compared the outcomes of infection of chickens and Peking ducks with a duck-origin H9N2 virus. The results showed that this virus caused more pronounced clinical signs and histological lesions in chickens. As for the virus shedding, chickens shed more virus in the trachea and less virus in the cloaca in levels of interferon (IFN) γ were found in the trachea of ducks compared with chickens, while comparison with ducks. As for cytokines, namely IFNs and interleukins (IL), higher higher levels of IFN-β, IFN-γ, IL-1β, and IL-6 were observed in the ileum of chickens compared with ducks. Eventually, serum hemagglutination-inhibition (HI) antibody titers were higher in chickens than in ducks. Taken together, ducks and chickens use different strategies in response to the H9N2 virus infection in tissues representing main replication sites of low-pathogenic AIVs. Given the different outcomes of the H9N2 virus infection in ducks and chickens, different measures should be taken in vaccination and treatment.Keywords: duck-origin influenza A virus; H9N2 subtype; chicken; duck * Corresponding author. E-mail: yxdiao@126.com; phone: +86 0538 8249851-8210.# These authors contributed equally to this work. Abbreviations: AIV(s) = avian influenza virus(es); CL = cloacal; HA = hemagglutinin; HI = hemagglutination-inhibition; HPAIVs = highly pathogenic avian influenza viruses; IFN = interferon; IL = interleukin; LPAIV(s) = low pathogenic avian influenza virus(es); NA = neuraminidase; OP = oropharyngeal; p.i. = post infection

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“…On the other hand, the role of cytokines in the pathology caused by H5N1 HPAIVs in avian species is less well understood. To date, several studies have shown that different avian species exhibit different pathologies and cytokine responses from H5N1 virus infection [7,11,15,17,18]. Type I interferon (IFN) was induced by H5N1 HPAIV in lung, spleen and plasma of 6-week-old chickens [15].…”

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confidence: 99%

“…Furthermore, a recently emerged Asian H5N1 HPAIV was shown to quickly induce antiviral and pro-inflammatory cytokines in the lung of 4-week-old chickens as early as 24 hr after inoculation, but 8 hr later, just before death, their mRNA levels decreased dramatically [18]. In Pekin duck infected with three H5N1 strains, younger ducks expressed cytokine mRNA more weakly than older ducks, which were more resistant to the pathological conditions caused by HPAIV infection [17]. In pigeons, which are thought to be less susceptible to H5N1 HPAIV, H5N1 HPAIV infection did not strongly induce the expression of innate immune and inflammatory-related genes in the lung [7].…”

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confidence: 99%

The Pathogenicity and Host Immune Response Associated with H5N1 Highly Pathogenic Avian Influenza Virus in Quail

Uno

Usui

Soda

et al. 2013

The Journal of Veterinary Medical Science

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ABSTRACT. Quail, like chickens, are susceptible to H5N1 subtype highly pathogenic avian influenza virus (HPAIV). Both birds experience high mortality, but quail usually survive a few more days than chicken. To understand why, we monitored quail and chickens after inoculation with 10 6 fifty-percent egg infectious doses of HPAIV A/whooper swan/Aomori/1/2008 (H5N1). The clinical course initiated as depression at 48 hr post inoculation (h.p.i.) in quail and at 36 h.p.i. in chicken, and all infected birds died. Mean death time of quail (91 hr) was significantly longer than that of chicken (66 hr). The virus titers of most tissue samples collected before death were not significantly different. At 24 h.p.i., interferon gamma (IFN-γ) mRNA expression in peripheral blood mononuclear cells (PBMC) was up-regulated in the quail but down-regulated in the chicken, although TLR-7 and seven other cytokines showed no significant differences between quail and chicken. The viral load in quail PBMC was significantly lower than that in chickens. These results suggest that the induction of IFN-γ after HPAIV infection in quail is related to lower titer of HPAIV. In conclusion, the different clinical courses observed between quail and chicken infected with H5N1 HPAIV might be caused by different IFN-γ responses against the HPAIV infection.

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Effect of age on the pathogenesis and innate immune responses in Pekin ducks infected with different H5N1 highly pathogenic avian influenza viruses

Cited by 41 publications

References 55 publications

The PA and HA Gene-Mediated High Viral Load and Intense Innate Immune Response in the Brain Contribute to the High Pathogenicity of H5N1 Avian Influenza Virus in Mallard Ducks

The PA and HA Gene-Mediated High Viral Load and Intense Innate Immune Response in the Brain Contribute to the High Pathogenicity of H5N1 Avian Influenza Virus in Mallard Ducks

Different outcomes of infection of chickens and ducks with a duck-origin H9N2 influenza A virus

The Pathogenicity and Host Immune Response Associated with H5N1 Highly Pathogenic Avian Influenza Virus in Quail

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