Faculty Opinions recommendation of A type I-secreted, sulfated peptide triggers XA21-mediated innate immunity.

Viral respiratory infections are recognized risk factors for the loss of control of allergic asthma and the induction of exacerbations, both in adults and children. Severe asthma is more susceptible to virus-induced asthma exacerbations, especially in the presence of high IgE levels. In the course of immune responses to viruses, an initial activation of innate immunity typically occurs and the production of type I and III interferons is essential in the control of viral spread. However, the Th2 inflammatory environment still appears to be protective against viral infections in general and in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections as well. As for now, literature data, although extremely limited and preliminary, show that severe asthma patients treated with biologics don’t have an increased risk of SARS-CoV-2 infection or progression to severe forms compared to the non-asthmatic population. Omalizumab, an anti-IgE monoclonal antibody, exerts a profound cellular effect, which can stabilize the effector cells, and is becoming much more efficient from the point of view of innate immunity in contrasting respiratory viral infections. In addition to the antiviral effect, clinical efficacy and safety of this biological allow a great improvement in the management of asthma.

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Role of Alternative Splicing in Regulating Host Response to Viral Infection

Cells ◽

10.3390/cells10071720 ◽

2021 ◽

Vol 10 (7) ◽

pp. 1720

Author(s):

Kuo-Chieh Liao ◽

Mariano A. Garcia-Blanco

Keyword(s):

Innate Immunity ◽

Alternative Splicing ◽

Immune Responses ◽

Viral Infection ◽

Rna Splicing ◽

Type I ◽

Host Immune Responses ◽

Transcriptional Regulatory Mechanisms ◽

Host Virus Interactions

The importance of transcriptional regulation of host genes in innate immunity against viral infection has been widely recognized. More recently, post-transcriptional regulatory mechanisms have gained appreciation as an additional and important layer of regulation to fine-tune host immune responses. Here, we review the functional significance of alternative splicing in innate immune responses to viral infection. We describe how several central components of the Type I and III interferon pathways encode spliced isoforms to regulate IFN activation and function. Additionally, the functional roles of splicing factors and modulators in antiviral immunity are discussed. Lastly, we discuss how cell death pathways are regulated by alternative splicing as well as the potential role of this regulation on host immunity and viral infection. Altogether, these studies highlight the importance of RNA splicing in regulating host–virus interactions and suggest a role in downregulating antiviral innate immunity; this may be critical to prevent pathological inflammation.

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Virus-associated activation of innate immunity induces rapid disruption of Peyer’s patches in mice

Blood ◽

10.1182/blood-2013-01-479311 ◽

2013 ◽

Vol 122 (15) ◽

pp. 2591-2599 ◽

Cited By ~ 2

Author(s):

Simon Heidegger ◽

David Anz ◽

Nicolas Stephan ◽

Bernadette Bohn ◽

Tina Herbst ◽

...

Keyword(s):

Innate Immunity ◽

Virus Infection ◽

Lymph Nodes ◽

Immune Activation ◽

Innate Immune ◽

Peyer's Patches ◽

Peyer’S Patches ◽

Type I ◽

Peripheral Lymph ◽

Key Points

Key Points Systemic virus infection leads to rapid disruption of the Peyer’s patches but not of peripheral lymph nodes. Virus-associated innate immune activation and type I IFN release blocks trafficking of B cells to Peyer’s patches.

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Tumor Necrosis Factor-α-Induced Protein 8-Like 2 Negatively Regulates Innate Immunity Against RNA Virus by Targeting RIG-I in Macrophages

Frontiers in Immunology ◽

10.3389/fimmu.2021.642715 ◽

2021 ◽

Vol 12 ◽

Author(s):

Ziqi Zou ◽

Mengyao Li ◽

Yunlian Zhou ◽

Jiaying Li ◽

Ting Pan ◽

...

Keyword(s):

Innate Immunity ◽

Retinoic Acid ◽

Viral Infection ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Rna Virus ◽

Type I ◽

Factor Α ◽

Necrosis Factor ◽

Inducible Gene

A systematic and flexible immunoregulatory network is required to ensure the proper outcome of antiviral immune signaling and maintain homeostasis during viral infection. Tumor necrosis factor-α-induced protein 8-like 2 (TIPE2), a novel immunoregulatory protein, has been extensively studied in inflammatory response, apoptosis, and cancer. However, the function of TIPE2 in antiviral innate immunity is poorly clarified. In this study, we reported that the expression of TIPE2 declined at the early period and then climbed up in macrophages under RNA virus stimulation. Knockout of TIPE2 in the macrophages enhanced the antiviral capacity and facilitated type I interferon (IFN) signaling after RNA viral infection both in vitro and in vivo. Consistently, overexpression of TIPE2 inhibited the production of type I IFNs and pro-inflammatory cytokines, and thus promoted the viral infection. Moreover, TIPE2 restrained the activation of TBK1 and IRF3 in the retinoic acid inducible gene-I (RIG-I)-like receptors (RLR) signaling pathway by directly interacting with retinoic acid inducible gene-I (RIG-I). Taken together, our results suggested that TIPE2 suppresses the type I IFN response induced by RNA virus by targeting RIG-I and blocking the activation of downstream signaling. These findings will provide new insights to reveal the immunological function of TIPE2 and may help to develop new strategies for the clinical treatment of RNA viral infections.

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Inducible microRNA-155 Feedback Promotes Type I IFN Signaling in Antiviral Innate Immunity by Targeting Suppressor of Cytokine Signaling 1

The Journal of Immunology ◽

10.4049/jimmunol.1000491 ◽

2010 ◽

Vol 185 (10) ◽

pp. 6226-6233 ◽

Cited By ~ 277

Author(s):

Pin Wang ◽

Jin Hou ◽

Li Lin ◽

Chunmei Wang ◽

Xingguang Liu ◽

...

Keyword(s):

Innate Immunity ◽

Cytokine Signaling ◽

Type I ◽

Type I Ifn ◽

Suppressor Of Cytokine Signaling ◽

Antiviral Innate Immunity

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DHAV-1 Blocks the Signaling Pathway Upstream of Type I Interferon by Inhibiting the Interferon Regulatory Factor 7 Protein

Frontiers in Microbiology ◽

10.3389/fmicb.2021.700434 ◽

2021 ◽

Vol 12 ◽

Author(s):

Yalan Lai ◽

Xiaoyan Xia ◽

Anchun Cheng ◽

Mingshu Wang ◽

Xumin Ou ◽

...

Keyword(s):

Immune Response ◽

Innate Immunity ◽

Viral Protein ◽

Interferon Regulatory Factor ◽

Host Cells ◽

Luciferase Reporter ◽

Type I ◽

Dependent Manner ◽

Regulatory Factor ◽

Interferon Regulatory Factor 7

Duck hepatitis A virus (DHAV), which mainly infects 1- to 4-week-old ducklings, has a fatality rate of 95% and poses a huge economic threat to the duck industry. However, the mechanism by which DHAV-1 regulates the immune response of host cells is rarely reported. This study examined whether DHAV-1 contains a viral protein that can regulate the innate immunity of host cells and its specific regulatory mechanism, further exploring the mechanism by which DHAV-1 resists the host immune response. In the study, the dual-luciferase reporter gene system was used to screen the viral protein that regulates the host innate immunity and the target of this viral protein. The results indicate that the DHAV-1 3C protein inhibits the pathway upstream of interferon (IFN)-β by targeting the interferon regulatory factor 7 (IRF7) protein. In addition, we found that the 3C protein inhibits the nuclear translocation of the IRF7 protein. Further experiments showed that the 3C protein interacts with the IRF7 protein through its N-terminus and that the 3C protein degrades the IRF7 protein in a caspase 3-dependent manner, thereby inhibiting the IFN-β-mediated antiviral response to promote the replication of DHAV-1. The results of this study are expected to serve as a reference for elucidating the mechanisms of DHAV-1 infection and pathogenicity.

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RNA sensors as a mechanism of innate immune evasion among SARS-CoV2, HIV and Nipah viruses

Current Protein and Peptide Science ◽

10.2174/1389203722666210322142725 ◽

2021 ◽

Vol 22 ◽

Author(s):

Dalia Cicily Kattiparambil Dixon ◽

Chameli Ratan ◽

Bhagyalakshmi Nair ◽

Sabitha Mangalath ◽

Rachy Abraham ◽

...

Keyword(s):

Immune Response ◽

Innate Immunity ◽

Innate Immune Response ◽

Vaccine Development ◽

Innate Immune ◽

Interferon Response ◽

Host Immune System ◽

Type I ◽

Adaptive Responses ◽

Rna Sensors

: Innate immunity is the first line of defence elicited by the host immune system to fight against invading pathogens such as viruses and bacteria. From this elementary immune response, the more complex antigen-specific adaptive responses are recruited to provide a long-lasting memory against the pathogens. Innate immunity gets activated when the host cell utilizes a diverse set of receptors known as pattern recognition receptors (PRR) to recognize the viruses that have penetrated the host and respond with cellular processes like complement system, phagocytosis, cytokine release and inflammation and destruction of NK cells. Viral RNA or DNA or viral intermediate products are recognized by receptors like toll-like receptors(TLRs), nucleotide oligomerization domain(NOD)-like receptors (NLRs) and retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) thereby, inducing type I interferon response (IFN) and other proinflammatory cytokines in infected cells or other immune cells. But certain viruses can evade the host innate immune response to replicate efficiently, triggering the spread of the viral infection. The present review describes the similarity in the mechanism chosen by viruses from different families -HIV, SARS-CoV2 and Nipah viruses to evade the innate immune response and how efficiently they establish the infection in the host. The review also addresses the stages of developments of various vaccines against these viral diseases and the challenges encountered by the researchers during vaccine development.

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Interplay between Intrinsic and Innate Immunity during HIV Infection

Cells ◽

10.3390/cells8080922 ◽

2019 ◽

Vol 8 (8) ◽

pp. 922 ◽

Cited By ~ 9

Author(s):

Louis Bergantz ◽

Frédéric Subra ◽

Eric Deprez ◽

Olivier Delelis ◽

Clémence Richetta

Keyword(s):

Innate Immunity ◽

Immune Responses ◽

Hiv Infection ◽

Type I ◽

Restriction Factors ◽

Intrinsic Immunity ◽

First Line ◽

Hiv Replication ◽

Interferon Stimulated Genes ◽

Immunodeficiency Virus

Restriction factors are antiviral components of intrinsic immunity which constitute a first line of defense by blocking different steps of the human immunodeficiency virus (HIV) replication cycle. In immune cells, HIV infection is also sensed by several pattern recognition receptors (PRRs), leading to type I interferon (IFN-I) and inflammatory cytokines production that upregulate antiviral interferon-stimulated genes (ISGs). Several studies suggest a link between these two types of immunity. Indeed, restriction factors, that are generally interferon-inducible, are able to modulate immune responses. This review highlights recent knowledge of the interplay between restriction factors and immunity inducing antiviral defenses. Counteraction of this intrinsic and innate immunity by HIV viral proteins will also be discussed.

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