Two myeloid differentiation factor 88 (MyD88) isoforms identified in ducks

Cheng, Yuqiang; Wang, Hengan; Yan, Yaxian; Ding, Chan; Sun, Jianhe

doi:10.1016/j.dci.2015.03.015

Cited by 12 publications

(3 citation statements)

References 44 publications

(48 reference statements)

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“…MyD88 may also be an important factor in initiating damaging cytokine storms in the host, since there was a significant reduction in proinflammatory cytokines and activated macrophages and neutrophils in the lungs of MyD88 −/− mice, but not TRIF −/− mice, following IAV infection (Teijaro et al, 2014). Ducks have two isoforms of the myd88 gene that have been characterized, named DuMyD88-X1 and DuMyD88-X2 (Cheng et al, 2015b). DuMyD88-X2 is a truncated version that encodes a premature stop codon and produces a protein with an interruption in the TIR signaling domain.…”

Section: Myd88mentioning

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: Myd88mentioning

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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“…Signalling downstream of TLR7 involves MyD88 and TRAF6 recruitment to the myddosome described above (Fitzgerald and Kagan 2020). Duck MyD88 showed 88% similarity to chicken MyD88 (Cheng et al 2015b). Overexpression induced activation of NF-κB and IL-6.…”

Section: Tlr7mentioning

confidence: 90%

Evolution of RNA sensing receptors in birds

Magor

2022

Immunogenetics

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Birds are important hosts for many RNA viruses, including influenza A virus, Newcastle disease virus, West Nile virus and coronaviruses. Innate defense against RNA viruses in birds involves detection of viral RNA by pattern recognition receptors. Several receptors of different classes are involved, such as endosomal toll-like receptors and cytoplasmic retinoic acid-inducible gene I-like receptors, and their downstream adaptor proteins. The function of these receptors and their antagonism by viruses is well established in mammals; however, this has received less attention in birds. These receptors have been characterized in a few bird species, and the completion of avian genomes will permit study of their evolution. For each receptor, functional work has established ligand specificity and activation by viral infection. Engagement of adaptors, regulation by modulators and the supramolecular organization of proteins required for activation are incompletely understood in both mammals and birds. These receptors bind conserved nucleic acid agonists such as single-or double-stranded RNA and generally show purifying selection, particularly the ligand binding regions. However, in birds, these receptors and adaptors differ between species, and between individuals, suggesting that they are under selection for diversification over time. Avian receptors and signalling pathways, like their mammalian counterparts, are targets for antagonism by a variety of viruses, intent on escape from innate immune responses.

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“…To date, at least 13 TLRs have been identified in mammals. Although TLR9 is absent and TLR8 is disrupted by a retroviral-like insertion element in avian species, other TLR orthologs have been described in avian species ( Cheng et al, 2015 ). Additionally, two uncommon avian TLRs, TLR15 and TLR21, have been also identified ( Keestra et al, 2010 ; Ramasamy et al, 2012 ).…”

Section: Introductionmentioning

confidence: 99%

Induction of Avian β-Defensin 2 Is Possibly Mediated by the p38 MAPK Signal Pathway in Chicken Embryo Fibroblasts After Newcastle Disease Virus Infection

et al. 2018

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The study was conducted to evaluate whether avian β-defensins (AvBDs) could be induced by Newcastle disease virus (NDV) infection, and to investigate the potential signaling pathway of AvBD2 induction in response to NDV infection as well. First, mRNA expression of AvBDs (1–14) was evaluated in the chicken embryo fibroblasts (CEFs) infected with NDV strain F48E9 at 6, 12, 24, 36, and 48 h post-inoculation (hpi), respectively. The results demonstrated a significant induction of AvBD2 in CEFs elicited by the NDV strain. Then, we expressed and purified the AvBD2 proteins in both eukaryotic cells and prokaryotic cells. Of the two recombinant AvBD2 proteins, only the protein expressed in eukaryotic cells showed directly antiviral activity against NDV strain F48E9 in vitro. Ligands of toll-like receptors (TLRs) were chosen as alternatives to NDV to further study signaling pathway of AvBD2 induction here, due to insufficient upregulation of AvBD2 expression elicited by NDV. We found that the mRNA expression of AvBD2 was highly upregulated by Pam3CSK4, FLA-ST, and ODN-M362. Then, four inhibitors of signaling pathway, including inhibitors of JNK, ERK1/2, p38 MAPK, and NF-κB, were used in this study. Of the four inhibitors, only inhibition of the p38 MAPK signaling pathway significantly reduced AvBD2 expression after stimulation with Pam3CSK4, FLA-ST and ODN-M362, respectively. Taken together, these results revealed that AvBD2 play a pivotal role in host innate immunity response to NDV infection. The mRNA expression of AvBD2 might be regulated in a p38 MAPK-dependent manner.

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Two myeloid differentiation factor 88 (MyD88) isoforms identified in ducks

Cited by 12 publications

References 44 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

Evolution of RNA sensing receptors in birds

Induction of Avian β-Defensin 2 Is Possibly Mediated by the p38 MAPK Signal Pathway in Chicken Embryo Fibroblasts After Newcastle Disease Virus Infection

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