Cytoplasm and Beyond: Dynamic Innate Immune Sensing of Influenza A Virus by RIG-I

Liu, Guanqun; Zhou, Yan

doi:10.1128/jvi.02299-18

Cited by 16 publications

(14 citation statements)

References 68 publications

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“…Lack of CARDs essentially makes LGP2 signaling incompetent and it is believed to have a role in the regulation of RIG-I and MDA5. RLR family members are primarily cytosolic except for RIG-I, a small fraction of which localizes to the nucleus as well and is reported to sense nuclear replicating IAV [ 66 , 67 ]. Although both RIG-I and MDA5 recognize viral dsRNA, RIG-I specifically recognizes short dsRNA of ~10 to 19 bp, whereas MDA5 recognizes relatively longer viral dsRNA [ 68 , 69 , 70 ].…”

Section: Retinoic Acid-inducible Gene I (Rig-i)mentioning

confidence: 99%

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Innate Immune Sensing of Influenza A Virus

Malik

Zhou

2020

Viruses

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Influenza virus infection triggers host innate immune response by stimulating various pattern recognition receptors (PRRs). Activation of these PRRs leads to the activation of a plethora of signaling pathways, resulting in the production of interferon (IFN) and proinflammatory cytokines, followed by the expression of interferon-stimulated genes (ISGs), the recruitment of innate immune cells, or the activation of programmed cell death. All these antiviral approaches collectively restrict viral replication inside the host. However, influenza virus also engages in multiple mechanisms to subvert the innate immune responses. In this review, we discuss the role of PRRs such as Toll-like receptors (TLRs), Retinoic acid-inducible gene I (RIG-I), NOD-, LRR-, pyrin domain-containing protein 3 (NLRP3), and Z-DNA binding protein 1 (ZBP1) in sensing and restricting influenza viral infection. Further, we also discuss the mechanisms influenza virus utilizes, especially the role of viral non-structure proteins NS1, PB1-F2, and PA-X, to evade the host innate immune responses.

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Section: Retinoic Acid-inducible Gene I (Rig-i)mentioning

confidence: 99%

“…Interestingly, the RNAs synthesized in NP-free reconstitutuion are immunostimulatory for RIG-I pathway, leading to IFN production [ 98 ]. Given the single strandedness of aberrant and svRNAs, their RIG-I activating potential might lie in their ability to form intermolecular duplexes with vRNA or cRNA [ 67 ].…”

Section: Retinoic Acid-inducible Gene I (Rig-i)mentioning

confidence: 99%

Innate Immune Sensing of Influenza A Virus

Malik

Zhou

2020

Viruses

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“…This may be particularly relevant for influenza detection, since influenza replicates in the nucleus. A recent review considers how dsRNA and viral transcriptional intermediates bearing 5 ′ -pppRNA made in the nucleus are detected by RIG-I in the cytoplasm of infected cells (Liu and Zhou, 2019). It is not known whether RIG-I is capable of nuclear detection in lower vertebrates.…”

Section: Rig-imentioning

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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“…In pulmonary epithelial cells, pathogen-associated molecular patterns (PAMPs) of IAV are sensed by pattern recognition receptors (PRRs). PRRs include retinoic acid-inducible gene I (RIG-I), which senses viral RNA (Liu & Zhou, 2019), and toll-like receptors (TLRs) which detect viral proteins on the cell surface or on endosomes (Pothlichet et al, 2013). IAV can also induce endoplasmatic reticulum F I G U R E 3 Ultrastructure of lung alveolar tissue from influenza A PR8 H1N1-infected mice 8 days post-infection by transmission electron microscopy.…”

Section: The Role Of the Endotheli Um In Iav-induced Pneumoniamentioning

confidence: 99%

Endothelial–platelet interactions in influenza‐induced pneumonia: A potential therapeutic target

Rommel

Milde

Eberle

et al. 2019

Anat Histol Embryol

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Every year, influenza viruses spread around the world, infecting the respiratory systems of countless humans and animals, causing illness and even death. Severe influenza infection is associated with pulmonary epithelial damage and endothelial dysfunction leading to acute lung injury (ALI). There is evidence that an aggressive cytokine storm and cell damage in lung capillaries as well as endothelial/platelet interactions contribute to vascular leakage, pro‐thrombotic milieu and infiltration of immune effector cells. To date, treatments for ALI caused by influenza are limited to antiviral drugs, active ventilation or further symptomatic treatments. In this review, we summarize the mechanisms of influenza‐mediated pathogenesis, permissive animal models and histopathological changes of lung tissue in both mice and men and compare it with histological and electron microscopic data from our own group. We highlight the molecular and cellular interactions between pulmonary endothelium and platelets in homeostasis and influenza‐induced pathogenesis. Finally, we discuss novel therapeutic targets on platelets/endothelial interaction to reduce or resolve ALI.

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Cytoplasm and Beyond: Dynamic Innate Immune Sensing of Influenza A Virus by RIG-I

Cited by 16 publications

References 68 publications

Innate Immune Sensing of Influenza A Virus

Innate Immune Sensing of Influenza A Virus

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

Endothelial–platelet interactions in influenza‐induced pneumonia: A potential therapeutic target

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