Special Issue "Innate Immune Sensing of Viruses and Viral Evasion"

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Antivirals & Vaccines".

Deadline for manuscript submissions: 15 June 2020.

Special Issue Editors

Dr. Renate König

Guest Editor
Paul-Ehrlich-Institut, Langen, Germany
Interests: virus–host interaction; innate immune responses
Dr. Carsten Münk

Guest Editor
Clinic for Gastroenterology, Hepatology, and Infectiology, Medical Faculty, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany
Interests: restriction factors; cytidine deaminases; gene evolution; animal models; non-primate lentiviruses; foamy retroviruses; uncoating

Special Issue Information

Dear Colleagues,

Innate immunity represents the first line of defense against viruses. The success of the immediate response relies on the recognition of invariant features encoded by viruses termed pathogen-associated molecular patterns (PAMPs) by specialized sensors called pattern recognition receptors (PRRs). The consequence of this surveillance network and the downstream pathway activation is the secretion of cytokines, type I interferons (IFNs), and the expression of interferon-stimulated genes. Viruses have evolved multiple ways to dampen the host IFN response by interfering, disrupting, or evading specific host regulators, both up- and downstream of IFN induction. Recent discoveries have shown that the sensing pathways are highly regulated by post-translational modifications and co-regulating proteins. Moreover, emerging evidence indicates that there exists crosstalk between the sensing pathways. Furthermore, unexpected pathways seem to play important roles in detecting and responding to viral infections. This Special Issue will cover recent discoveries in the regulation of innate immune pathways during viral infections, novel mechanisms of exploitation, or the manipulation of regulators of the pathways by viruses and novel cellular network complexes that play a role in sensing viruses.

Dr. Renate König
Dr. Carsten Münk
Guest Editors

Manuscript Submission Information

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Keywords

  • innate sensing
  • viral counteraction
  • pattern-recognition receptor complex
  • regulation of innate pathways
  • innate immune response
  • virus–host interaction

Published Papers (3 papers)

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Research

Open AccessArticle
Hepatitis B Virus DNA is a Substrate for the cGAS/STING Pathway but is not Sensed in Infected Hepatocytes
Viruses 2020, 12(6), 592; https://doi.org/10.3390/v12060592 (registering DOI) - 29 May 2020
Abstract
Hepatitis B virus (HBV) chronic infection is a critical risk factor for hepatocellular carcinoma. The innate immune response to HBV infection is a matter of debate. In particular, viral escape mechanisms are poorly understood. Our study reveals that HBV RNAs are not [...] Read more.
Hepatitis B virus (HBV) chronic infection is a critical risk factor for hepatocellular carcinoma. The innate immune response to HBV infection is a matter of debate. In particular, viral escape mechanisms are poorly understood. Our study reveals that HBV RNAs are not immunostimulatory in immunocompetent myeloid cells. In contrast, HBV DNA from viral particles and DNA replication intermediates are immunostimulatory and sensed by cyclic GMP-AMP Synthase (cGAS) and Stimulator of Interferon Genes (STING). We show that primary human hepatocytes express DNA sensors to reduced levels compared to myeloid cells. Nevertheless, hepatocytes can respond to HBV relaxed-circular DNA (rcDNA), when transfected in sufficient amounts, but not to HBV infection. Finally, our data suggest that HBV infection does not actively inhibit the DNA-sensing pathway. In conclusion, in infected hepatocytes, HBV passively evades recognition by cellular sensors of nucleic acids by (i) producing non-immunostimulatory RNAs, (ii) avoiding sensing of its DNAs by cGAS/STING without active inhibition of the pathway. Full article
(This article belongs to the Special Issue Innate Immune Sensing of Viruses and Viral Evasion)
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Open AccessArticle
IRF7 Is Required for the Second Phase Interferon Induction during Influenza Virus Infection in Human Lung Epithelia
Viruses 2020, 12(4), 377; https://doi.org/10.3390/v12040377 - 29 Mar 2020
Abstract
Influenza A virus (IAV) infection is a major cause of morbidity and mortality. Retinoic acid-inducible protein I (RIG-I) plays an important role in the recognition of IAV in most cell types, and leads to the activation of interferon (IFN). We investigated mechanisms of [...] Read more.
Influenza A virus (IAV) infection is a major cause of morbidity and mortality. Retinoic acid-inducible protein I (RIG-I) plays an important role in the recognition of IAV in most cell types, and leads to the activation of interferon (IFN). We investigated mechanisms of RIG-I and IFN induction by IAV in the BCi-NS1.1 immortalized human airway basal cell line and in the A549 human alveolar epithelial cell line. We found that the basal expression levels of RIG-I and regulatory transcription factor (IRF) 7 were very low in BCi-NS1.1 cells. IAV infection induced robust RIG-I and IRF7, not IRF3, expression. siRNA against IRF7 and mitochondrial antiviral-signaling protein (MAVS), but not IRF3, significantly inhibited RIG-I mRNA expression and IFN induction by IAV infection. Most importantly, even without virus infection, IFN-β alone induced RIG-I, and siRNA against IRF7 did not inhibit RIG-I induction by IFN-β. Similar results were found in the alveolar basal epithelial A549 cell line. RIG-I and IRF7 expression in humans is highly inducible and greatly amplified by IFN produced from virus infected cells. IFN induction can be separated into two phases, that initially induced by the virus with basal RIG-I (the first phase), and that induced by the subsequent virus with amplified RIG-I from the first phase IFN (the second phase). The de novo synthesis of IRF7 is required for the second phase IFN induction during influenza virus infection in human lung bronchial and alveolar epithelial cells. Full article
(This article belongs to the Special Issue Innate Immune Sensing of Viruses and Viral Evasion)
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Open AccessArticle
Feline Infectious Peritonitis Virus Nsp5 Inhibits Type I Interferon Production by Cleaving NEMO at Multiple Sites
Viruses 2020, 12(1), 43; https://doi.org/10.3390/v12010043 - 30 Dec 2019
Abstract
Feline infectious peritonitis (FIP), caused by virulent feline coronavirus, is the leading infectious cause of death in cats. The type I interferon (type I IFN)-mediated immune responses provide host protection from infectious diseases. Several coronaviruses have been reported to evolve diverse strategies to [...] Read more.
Feline infectious peritonitis (FIP), caused by virulent feline coronavirus, is the leading infectious cause of death in cats. The type I interferon (type I IFN)-mediated immune responses provide host protection from infectious diseases. Several coronaviruses have been reported to evolve diverse strategies to evade host IFN response. However, whether feline infectious peritonitis virus (FIPV) antagonizes the type I IFN signaling remains unclear. In this study, we demonstrated that FIPV strain DF2 infection not only failed to induce interferon-β (IFN-β) and interferon-stimulated gene (ISG) production, but also inhibited Sendai virus (SEV) or polyinosinic-polycytidylic acid (poly(I:C))-induced IFN-β production. Subsequently, we found that one of the non-structural proteins encoded by the FIPV genome, nsp5, interrupted type I IFN signaling in a protease-dependent manner by cleaving the nuclear factor κB (NF-κB) essential modulator (NEMO) at three sites—glutamine132 (Q132), Q205, and Q231. Further investigation revealed that the cleavage products of NEMO lost the ability to activate the IFN-β promoter. Mechanistically, the nsp5-mediated NEMO cleavage disrupted the recruitment of the TRAF family member-associated NF-κB activator (TANK) to NEMO, which reduced the phosphorylation of interferon regulatory factor 3 (IRF3), leading to the inhibition of type I IFN production. Our research provides new insights into the mechanism for FIPV to counteract host innate immune response. Full article
(This article belongs to the Special Issue Innate Immune Sensing of Viruses and Viral Evasion)
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