Highly pathogenic avian influenza H5N1 clade 2.3.2.1 and clade 2.3.4 viruses do not induce a clade-specific phenotype in mallard ducks

Ducatez, Mariette; Sonnberg, Stephanie; Crumpton, Jeri Carol; Rubrum, Adam; Phommachanh, Phouvong; Douangngeun, Bounlom; Peiris, Malik; Guan, Yi; Webster, Robert G.; Webby, Richard J.

doi:10.1099/jgv.0.000806

Cited by 12 publications

(15 citation statements)

References 84 publications

(8 reference statements)

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“…While ducks can control most strains of IAV, some HPAI strains cause significant disease and mortality in ducks, especially those belonging to the H5 subgroup and clade 2.3.2.1 (Sturm-Ramirez et al, 2004;Bingham et al, 2009;Hagag et al, 2015;Haider et al, 2017). It is difficult to generalize, however, because in challenge experiments using viruses belonging to this clade, ducks demonstrated differences in mortality ranging from 100% lethal to no mortality (Kang et al, 2013;Ducatez et al, 2017). Most strikingly, two viruses from the 2.3.2.1 clade that differed by only 30 amino acids showed complete differences in mortality in mallards, with one virus being 100% lethal while the other causing no mortality (Hu et al, 2013).…”

Section: Introductionmentioning

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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Section: Introductionmentioning

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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“…A limitation of our study was that only one representative virus from each clade was included in the transmission experiments. Within-clade variation in transmission and virulence is likely and has been reported previously in transmission experiments [30]. In addition, the two clade 1 viruses were both isolated from cases of A/H5N1 infection in humans, whereas the clade 2.3.2.1c virus was isolated from a poultry outbreak associated with the death of approximately 4500 ducks [42].…”

Section: Discussionmentioning

confidence: 84%

“…Global data appear to support this hypothesis, with there being few reports of clade 2.3.2.1c virus infections in humans, despite widespread poultry circulation in China, Indonesia, Vietnam, and West Africa [25][26][27][28][29]. The frequent detection of clade 2.3.2.1 viruses in wild birds and their rapid global dissemination [24,30] may indicate that these viruses are more "avian-like," affecting their ability to infect humans. Further studies are needed to investigate the in vivo characteristics of these viruses and the possible genetic mechanisms associated with their host specificity.…”

Section: Discussionmentioning

confidence: 99%

Transmission experiments support clade-level differences in the transmission and pathogenicity of Cambodian influenza A/H5N1 viruses

Horwood

Fabrizio

Horm

et al. 2020

Emerging Microbes & Infections

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Influenza A/H5N1 has circulated in Asia since 2003 and is now enzootic in many countries in that region. In Cambodia, the virus has circulated since 2004 and has intermittently infected humans. During this period, we have noted differences in the rate of infections in humans, potentially associated with the circulation of different viral clades. In particular, a reassortant clade 1.1.2 virus emerged in early 2013 and was associated with a dramatic increase in infections of humans (34 cases) until it was replaced by a clade 2.3.2.1c virus in early 2014. In contrast, only one infection of a human has been reported in the 6 years since the clade 2.3.2.1c virus became the dominant circulating virus. We selected three viruses to represent the main viral clades that have circulated in Cambodia (clade 1.1.2, clade 1.1.2 reassortant, and clade 2.3.2.1c), and we conducted experiments to assess the virulence and transmissibility of these viruses in avian (chicken, duck) and mammalian (ferret) models. Our results suggest that the clade 2.3.2.1c virus is more "avian-like," with high virulence in both ducks and chickens, but there is no evidence of aerosol transmission of the virus from ducks to ferrets. In contrast, the two clade 1 viruses were less virulent in experimentally infected and contact ducks. However, evidence of chicken-to-ferret aerosol transmission was observed for both clade 1 viruses. The transmission experiments provide insights into clade-level differences that might explain the variation in A/H5N1 infections of humans observed in Cambodia and other settings.

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“…Age-dependent susceptibility in ducks against HP H5N6 avian influenza virus is not yet known though there were reports on age-dependent susceptibility of ducks against the HP H5N1 avian influenza virus [ 33 , 34 , 35 ]. To assess the age-dependent mortality, we intranasally (i.n.)…”

Section: Resultsmentioning

confidence: 99%

Age-Dependent Lethality in Ducks Caused by Highly Pathogenic H5N6 Avian Influenza Virus

Jang

Seo

2020

Viruses

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Ducks show notably higher resistance to highly pathogenic avian influenza viruses as compared to chickens. Here, we studied the age-dependent susceptibility in ducks to the infections caused by highly pathogenic avian influenza viruses. We intranasally infected ducks aged 1, 2, 4, and 8 weeks with highly pathogenic H5N6 avian influenza viruses isolated in South Korea in 2016. All the 1-and 2-week-old ducks died after infection, 20% of 3-week-old ducks died, and from the ducks aged 4 and 8 weeks, all of them survived. We performed microarray analysis and quantitative real-time PCR using total RNA isolated from the lungs of infected 2- and 4-week-old ducks to determine the mechanism underlying the age-dependent susceptibility to highly pathogenic avian influenza virus. Limited genes were found to be differentially expressed between the lungs of 2- and 4-week-old ducks. Cell damage-related genes, such as CIDEA and ND2, and the immune response-related gene NR4A3 were notably induced in the lungs of infected 2-week-old ducks compared to those in the lungs of infected 4-week-old ducks.

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Highly pathogenic avian influenza H5N1 clade 2.3.2.1 and clade 2.3.4 viruses do not induce a clade-specific phenotype in mallard ducks

Cited by 12 publications

References 84 publications

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

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

Transmission experiments support clade-level differences in the transmission and pathogenicity of Cambodian influenza A/H5N1 viruses

Age-Dependent Lethality in Ducks Caused by Highly Pathogenic H5N6 Avian Influenza Virus

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