Genome-wide gene expression pattern underlying differential host response to high or low pathogenic H5N1 avian influenza virus in ducks

Kumar, Ayush; Vijayakumar, P.; Gandhale, Pradeep N.; Ranaware, P.B.; Kumar, Himanshu; Kulkarni, D. D.; Raut, Ashwin Ashok; Mishra, Anamika

doi:10.4149/av_2017_01_66

Cited by 20 publications

(19 citation statements)

References 49 publications

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“…Despite a pronounced similarity in host response across species following infection by highly pathogenic H5N1 virus, there were notable fine differences in certain aspects of the observed response. In duck, for example, induced expression of antiviral gene IFIT5 was observed only following infection with low pathogenic virus, whereas highly pathogenic H5N1 virus strain did not induce expression of this gene [30]. By contrast, our present study with human macrophages observed a significant up-regulation of IFIT5 in response to highly pathogenic H5N1 virus infection.…”

Section: Discussioncontrasting

confidence: 69%

“…[22, 23, 27, 28]. In vivo experiments employing mice [29], ferrets [7], or ducks [30] to investigate the host gene expression profiles after H5N1 virus infection, have revealed a general phenomenon, whereby IFN and chemokine pathways are significantly up-regulated in lungs after H5N1 virus infection. Despite a pronounced similarity in host response across species following infection by highly pathogenic H5N1 virus, there were notable fine differences in certain aspects of the observed response.…”

Section: Discussionmentioning

confidence: 99%

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Whole transcriptome analysis reveals differential gene expression profile reflecting macrophage polarization in response to influenza A H5N1 virus infection

et al. 2018

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Section: Discussioncontrasting

confidence: 69%

Section: Discussionmentioning

confidence: 99%

Whole transcriptome analysis reveals differential gene expression profile reflecting macrophage polarization in response to influenza A H5N1 virus infection

et al. 2018

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“…TRIM23 was identified as a differentially expressed gene in a microarray study from ducks infected with both HPAI and LPAI strains of IAV, as upregulated 5 DPI in LPAI but not HPAI infections (Kumar et al, 2017). TRIM23 is an ancient TRIM with well-conserved structural homology, and uses its ADP-ribosylation factor (ARF) domain to activate TBK1 through GTPase activity (Sparrer et al, 2017).…”

Section: Other Antiviral Proteins Of Interest Trim Proteinsmentioning

confidence: 99%

Pattern Recognition Receptor Signaling and Innate Responses to Influenza A Viruses in the Mallard Duck, Compared to Humans and Chickens

Campbell

Magor

2020

Front. Cell. Infect. Microbiol.

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Mallard ducks are a natural host and reservoir of avian Influenza A viruses. While most influenza strains can replicate in mallards, the virus typically does not cause substantial disease in this host. Mallards are often resistant to disease caused by highly pathogenic avian influenza viruses, while the same strains can cause severe infection in humans, chickens, and even other species of ducks, resulting in systemic spread of the virus and even death. The differences in influenza detection and antiviral effectors responsible for limiting damage in the mallards are largely unknown. Domestic mallards have an early and robust innate response to infection that seems to limit replication and clear highly pathogenic strains. The regulation and timing of the response to influenza also seems to circumvent damage done by a prolonged or dysregulated immune response. Rapid initiation of innate immune responses depends on viral recognition by pattern recognition receptors (PRRs) expressed in tissues where the virus replicates. RIG-like receptors (RLRs), Toll-like receptors (TLRs), and Nod-like receptors (NLRs) are all important influenza sensors in mammals during infection. Ducks utilize many of the same PRRs to detect influenza, namely RIG-I, TLR7, and TLR3 and their downstream adaptors. Ducks also express many of the same signal transduction proteins including TBK1, TRIF, and TRAF3. Some antiviral effectors expressed downstream of these signaling pathways inhibit influenza replication in ducks. In this review, we summarize the recent advances in our understanding of influenza recognition and response through duck PRRs and their adaptors. We compare basal tissue expression and regulation of these signaling components in birds, to better understand what contributes to influenza resistance in the duck.

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“…Direct comparison is complicated by the need to challenge highly susceptible chickens with a much lower infecting dose than ducks. Kumar et al [96] infected domestic ducks with two highly pathogenic Eurasian lineage IAV strains that differed in the severity of disease that they caused. A/duck/Tripura/103597/2008 (H5N1) is a HPAI strain that belongs to clade 2.2.2.1 [97,98] and possesses a polybasic HA cleavage site (residues RRRKKR at positions 341–346, GenBank accession: GU252822).…”

Section: Innate Immune Signaling—pro-inflammatory and Interferon Rmentioning

confidence: 99%

“…However, it caused milder disease in experimentally infected ducks compared to A/duck/India/02CA10/2011 (H5N1) (clade 2.3.2). The authors found upregulation of important antiviral interferon-stimulated genes in the lungs of Tripura/103597-infected ducks, but not in India/02CA10-infected ducks at 5 dpi, showing that ISG expression correlates inversely with disease severity in ducks [96]. Muscovy ducks, which are more susceptible to influenza pathology, have higher pro-inflammatory responses to HPAI viruses compared to Pekin and wild mallard ducks, and also have lower IFN-α responses in their spleens [51].…”

Section: Innate Immune Signaling—pro-inflammatory and Interferon Rmentioning

confidence: 99%

Innate Immune Responses to Avian Influenza Viruses in Ducks and Chickens

Evseev

Magor

2019

Veterinary Sciences

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Mallard ducks are important natural hosts of low pathogenic avian influenza (LPAI) viruses and many strains circulate in this reservoir and cause little harm. Some strains can be transmitted to other hosts, including chickens, and cause respiratory and systemic disease. Rarely, these highly pathogenic avian influenza (HPAI) viruses cause disease in mallards, while chickens are highly susceptible. The long co-evolution of mallard ducks with influenza viruses has undoubtedly fine-tuned many immunological host–pathogen interactions to confer resistance to disease, which are poorly understood. Here, we compare innate responses to different avian influenza viruses in ducks and chickens to reveal differences that point to potential mechanisms of disease resistance. Mallard ducks are permissive to LPAI replication in their intestinal tissues without overtly compromising their fitness. In contrast, the mallard response to HPAI infection reflects an immediate and robust induction of type I interferon and antiviral interferon stimulated genes, highlighting the importance of the RIG-I pathway. Ducks also appear to limit the duration of the response, particularly of pro-inflammatory cytokine expression. Chickens lack RIG-I, and some modulators of the signaling pathway and may be compromised in initiating an early interferon response, allowing more viral replication and consequent damage. We review current knowledge about innate response mediators to influenza infection in mallard ducks compared to chickens to gain insight into protective immune responses, and open questions for future research.

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Genome-wide gene expression pattern underlying differential host response to high or low pathogenic H5N1 avian influenza virus in ducks

Cited by 20 publications

References 49 publications

Whole transcriptome analysis reveals differential gene expression profile reflecting macrophage polarization in response to influenza A H5N1 virus infection

Whole transcriptome analysis reveals differential gene expression profile reflecting macrophage polarization in response to influenza A H5N1 virus infection

Pattern Recognition Receptor Signaling and Innate Responses to Influenza A Viruses in the Mallard Duck, Compared to Humans and Chickens

Innate Immune Responses to Avian Influenza Viruses in Ducks and Chickens

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