RING-Domain E3 Ligase-Mediated Host–Virus Interactions: Orchestrating Immune Responses by the Host and Antagonizing Immune Defense by Viruses

Despite annual vaccination, influenza B viruses (IBV) cause significant disease with substantial health and socio-economic impacts. Novel vaccination strategies inducing broadly protective and long-lasting immunity across IBV lineages are needed. However, as immune responses toward IBV are largely understudied, host–virus interactions and protective immune mechanisms need to be defined to rationally design such vaccines. Here, we summarize recent advances in our understanding of immunological mechanisms underpinning protection from IBV. We discuss how innate antiviral host factors inhibit IBV replication and the ways by which IBV escapes such restriction. We review the specificity of broadly cross-reactive antibodies and universal T cells, and the mechanisms by which they mediate protection. We highlight important knowledge gaps needing to be addressed to design improved IBV vaccines.

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Host-virus interactions: Lessons from the model organismDrosophila melanogaster

10.1603/ice.2016.92693 ◽

2016 ◽

Author(s):

Jean-Luc Imler

Keyword(s):

Host Virus Interactions ◽

Virus Interactions

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The molecular footprints of COVID-19

Turkish Journal of Biochemistry ◽

10.1515/tjb-2020-0255 ◽

2020 ◽

Vol 45 (3) ◽

pp. 241-248

Author(s):

Engin Yilmaz ◽

Yakut Akyön ◽

Muhittin Serdar

Keyword(s):

Reaction Time ◽

Changing Environment ◽

The Third ◽

The Past ◽

The People ◽

The World ◽

The Future ◽

Host Virus Interactions ◽

Virus Interactions

AbstractCOVID-19 is the third spread of animal coronavirus over the past two decades, resulting in a major epidemic in humans after SARS and MERS. COVID-19 is responsible of the biggest biological earthquake in the world. In the global fight against COVID-19 some serious mistakes have been done like, the countries’ misguided attempts to protect their economies, lack of international co-operation. These mistakes that the people had done in previous deadly outbreaks. The result has been a greater economic devastation and the collapse of national and international trust for all. In this constantly changing environment, if we have a better understanding of the host-virus interactions than we can be more prepared to the future deadly outbreaks. When encountered with a disease which the causative is unknown, the reaction time and the precautions that should be taken matters a great deal. In this review we aimed to reveal the molecular footprints of COVID-19 scientifically and to get an understanding of the pandemia. This review might be a highlight to the possible outbreaks.

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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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Human stem cell models to study host–virus interactions in the central nervous system

Nature Reviews Immunology ◽

10.1038/s41577-020-00474-y ◽

2021 ◽

Author(s):

Oliver Harschnitz ◽

Lorenz Studer

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Stem Cell ◽

Human Stem Cell ◽

Cell Models ◽

The Central Nervous System ◽

Host Virus Interactions ◽

Virus Interactions ◽

Stem Cell Models

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Poxviral Strategies to Overcome Host Cell Apoptosis

Pathogens ◽

10.3390/pathogens10010006 ◽

2020 ◽

Vol 10 (1) ◽

pp. 6

Author(s):

Chathura D. Suraweera ◽

Mark G. Hinds ◽

Marc Kvansakul

Keyword(s):

Viral Infections ◽

B Cell Lymphoma ◽

Intrinsic Apoptosis ◽

Host Cell Apoptosis ◽

Successful Infection ◽

Infected Cells ◽

Host Virus Interactions ◽

Almost All ◽

Virus Interactions ◽

Multicellular Organisms

Apoptosis is a form of cellular suicide initiated either via extracellular (extrinsic apoptosis) or intracellular (intrinsic apoptosis) cues. This form of programmed cell death plays a crucial role in development and tissue homeostasis in multicellular organisms and its dysregulation is an underlying cause for many diseases. Intrinsic apoptosis is regulated by members of the evolutionarily conserved B-cell lymphoma-2 (Bcl-2) family, a family that consists of pro- and anti-apoptotic members. Bcl-2 genes have also been assimilated by numerous viruses including pox viruses, in particular the sub-family of chordopoxviridae, a group of viruses known to infect almost all vertebrates. The viral Bcl-2 proteins are virulence factors and aid the evasion of host immune defenses by mimicking the activity of their cellular counterparts. Viral Bcl-2 genes have proved essential for the survival of virus infected cells and structural studies have shown that though they often share very little sequence identity with their cellular counterparts, they have near-identical 3D structures. However, their mechanisms of action are varied. In this review, we examine the structural biology, molecular interactions, and detailed mechanism of action of poxvirus encoded apoptosis inhibitors and how they impact on host–virus interactions to ultimately enable successful infection and propagation of viral infections.

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Role of Mitochondria in Viral Infections

Life ◽

10.3390/life11030232 ◽

2021 ◽

Vol 11 (3) ◽

pp. 232

Author(s):

Srikanth Elesela ◽

Nicholas W. Lukacs

Keyword(s):

Viral Infections ◽

Mitochondrial Dynamics ◽

The Body ◽

Viral Diseases ◽

Multiple Organs ◽

Innate Immune Signaling ◽

Mitochondrial Functions ◽

Host Virus Interactions ◽

Virus Interactions

Viral diseases account for an increasing proportion of deaths worldwide. Viruses maneuver host cell machinery in an attempt to subvert the intracellular environment favorable for their replication. The mitochondrial network is highly susceptible to physiological and environmental insults, including viral infections. Viruses affect mitochondrial functions and impact mitochondrial metabolism, and innate immune signaling. Resurgence of host-virus interactions in recent literature emphasizes the key role of mitochondria and host metabolism on viral life processes. Mitochondrial dysfunction leads to damage of mitochondria that generate toxic compounds, importantly mitochondrial DNA, inducing systemic toxicity, leading to damage of multiple organs in the body. Mitochondrial dynamics and mitophagy are essential for the maintenance of mitochondrial quality control and homeostasis. Therefore, metabolic antagonists may be essential to gain a better understanding of viral diseases and develop effective antiviral therapeutics. This review briefly discusses how viruses exploit mitochondrial dynamics for virus proliferation and induce associated diseases.

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Gamma Interferon Produced by Antigen-Specific CD4+ T Cells Regulates the Mucosal Immune Responses to Citrobacter rodentium Infection

Infection and Immunity ◽

10.1128/iai.01343-09 ◽

2010 ◽

Vol 78 (6) ◽

pp. 2653-2666 ◽

Cited By ~ 45

Author(s):

Hideyuki Shiomi ◽

Atsuhiro Masuda ◽

Shin Nishiumi ◽

Masayuki Nishida ◽

Tetsuya Takagawa ◽

...

Keyword(s):

T Cells ◽

Immune Responses ◽

Gamma Interferon ◽

Immune Defense ◽

Interleukin 4 ◽

Mucosal Inflammation ◽

Citrobacter Rodentium ◽

Macrophage Phagocytosis ◽

Ifn Γ ◽

Deficient Mice

ABSTRACT Citrobacter rodentium, a murine model pathogen for enteropathogenic Escherichia coli, colonizes the surface of intestinal epithelial cells and causes mucosal inflammation. This bacterium is an ideal model for investigating pathogen-host immune interactions in the gut. It is well known that gene transcripts for Th1 cytokines are highly induced in colonic tissue from mice infected with C. rodentium. However, it remains to be seen whether the Th1 or Th2 cytokines produced by antigen-specific CD4+ T cells provide effective regulation of the host immune defense against C. rodentium infection. To investigate the antigen-specific immune responses, C. rodentium expressing ovalbumin (OVA-C. rodentium), a model antigen, was generated and used to define antigen-specific responses under gamma interferon (IFN-γ)-deficient or interleukin-4 (IL-4)-deficient conditions in vivo. The activation of antigen-specific CD4+ T cells and macrophage phagocytosis were evaluated in the presence of IFN-γ or IL-4 in vitro. IFN-γ-deficient mice exhibited a loss of body weight and a higher bacterial concentration in feces during OVA-C. rodentium infection than C57BL/6 (wild type) or IL-4-deficient mice. This occurred through the decreased efficiency of macrophage phagocytosis and the activation of antigen-specific CD4+ T cells. Furthermore, a deficiency in antigen-specific CD4+ T-cell-expressed IFN-γ led to a higher susceptibility to mucosal and gut-derived systemic OVA-C. rodentium infection. These results show that the IFN-γ produced by antigen-specific CD4+ T cells plays an important role in the defense against C. rodentium.

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