scholarly journals Innate Immune Response and Immune Evasion in Viral Infections

2022 ◽  
Vol 3 (1) ◽  
pp. 1-19
Author(s):  
Hasan Karakuş
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Immune Evasion ◽  
Viral Infections ◽  
Innate Immune

scholarly journals Viral Infection: An Evolving Insight into the Signal Transduction Pathways Responsible for the Innate Immune Response

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Girish J. Kotwal ◽  
Steven Hatch ◽  
William L. Marshall
Keyword(s):  
Signal Transduction ◽  
Immune Response ◽  
Innate Immunity ◽  
Viral Infection ◽  
Innate Immune Response ◽  
Immune Evasion ◽  
Viral Infections ◽  
Innate Immune ◽  
Innate Immune Evasion ◽  
Insight Into

The innate immune response is initiated by the interaction of stereotypical pathogen components with genetically conserved receptors for extracytosolic pathogen-associated molecular patterns (PAMPs) or intracytosolic nucleic acids. In multicellular organisms, this interaction typically clusters signal transduction molecules and leads to their activations, thereby initiating signals that activate innate immune effector mechanisms to protect the host. In some cases programmed cell death—a fundamental form of innate immunity—is initiated in response to genotoxic or biochemical stress that is associated with viral infection. In this paper we will summarize innate immune mechanisms that are relevant to viral pathogenesis and outline the continuing evolution of viral mechanisms that suppress the innate immunity in mammalian hosts. These mechanisms of viral innate immune evasion provide significant insight into the pathways of the antiviral innate immune response of many organisms. Examples of relevant mammalian innate immune defenses host defenses include signaling to interferon and cytokine response pathways as well as signaling to the inflammasome. Understanding which viral innate immune evasion mechanisms are linked to pathogenesis may translate into therapies and vaccines that are truly effective in eliminating the morbidity and mortality associated with viral infections in individuals.

scholarly journals Vaccinia virus immune evasion: mechanisms, virulence and immunogenicity

2013 ◽  
Vol 94 (11) ◽  
pp. 2367-2392 ◽  
Author(s):  
Geoffrey L. Smith ◽  
Camilla T. O. Benfield ◽  
Carlos Maluquer de Motes ◽  
Michela Mazzon ◽  
Stuart W. J. Ember ◽  
...  
Keyword(s):  
Immune Response ◽  
Vaccinia Virus ◽  
Innate Immune Response ◽  
Immune Evasion ◽  
Mammalian Cells ◽  
Innate Immune ◽  
Gene Encoding ◽  
Cytokines And Chemokines ◽  
Host Innate Immune Response ◽  
New Hosts

Virus infection of mammalian cells is sensed by pattern recognition receptors and leads to an innate immune response that restricts virus replication and induces adaptive immunity. In response, viruses have evolved many countermeasures that enable them to replicate and be transmitted to new hosts, despite the host innate immune response. Poxviruses, such as vaccinia virus (VACV), have large DNA genomes and encode many proteins that are dedicated to host immune evasion. Some of these proteins are secreted from the infected cell, where they bind and neutralize complement factors, interferons, cytokines and chemokines. Other VACV proteins function inside cells to inhibit apoptosis or signalling pathways that lead to the production of interferons and pro-inflammatory cytokines and chemokines. In this review, these VACV immunomodulatory proteins are described and the potential to create more immunogenic VACV strains by manipulation of the gene encoding these proteins is discussed.

scholarly journals Enterococcus faecalis Capsular Polysaccharide Serotypes C and D and Their Contributions to Host Innate Immune Evasion

2009 ◽  
Vol 77 (12) ◽  
pp. 5551-5557 ◽  
Author(s):  
Lance R. Thurlow ◽  
Vinai Chittezham Thomas ◽  
Sherry D. Fleming ◽  
Lynn E. Hancock
Keyword(s):  
Immune Response ◽  
Enterococcus Faecalis ◽  
Innate Immune Response ◽  
Immune Evasion ◽  
Capsular Polysaccharide ◽  
Lipoteichoic Acid ◽  
Innate Immune ◽  
Necrosis Factor Alpha ◽  
Host Innate Immune Response ◽  
Innate Immune Evasion

ABSTRACT It has become increasingly difficult to treat infections caused by Enterococcus faecalis due to its high levels of intrinsic and acquired antibiotic resistance. However, few studies have explored the mechanisms that E. faecalis employs to circumvent the host innate immune response and establish infection. Capsular polysaccharides are important virulence factors that are associated with innate immune evasion. We demonstrate, using cultured macrophages (RAW 264.7), that capsule-producing E. faecalis strains of either serotype C or D are more resistant to complement-mediated opsonophagocytosis than unencapsulated strains. We show that differences in opsonophagocytosis are not due to variations in C3 deposition but are due to the ability of capsule to mask bound C3 from detection on the surface of E. faecalis. Similarly, E. faecalis capsule masks lipoteichoic acid from detection, which correlates with decreased tumor necrosis factor alpha production by cultured macrophages in the presence of encapsulated strains compared to that in the presence of unencapsulated strains. Our studies confirm the important role of the capsule as a virulence factor of E. faecalis and provide several mechanisms by which the presence of the capsule influences evasion of the innate immune response and suggest that the capsule could be a potential target for developing alternative therapies to treat E. faecalis infections.

Inflammation and Innate Immune Response Against Viral Infections in Marine Fish

2010 ◽  
Vol 16 (38) ◽  
pp. 4175-4184 ◽  
Author(s):  
B. Novoa ◽  
S. Mackenzie ◽  
A. Figueras
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Marine Fish ◽  
Viral Infections ◽  
Innate Immune

scholarly journals Autophagy receptors as viral targets

2021 ◽  
Vol 26 (1) ◽  
Author(s):  
Päivi Ylä-Anttila
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Innate Immune Response ◽  
Recent Progress ◽  
Viral Infections ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Host Interaction ◽  
Autophagic Degradation ◽  
Autophagy Inhibition

AbstractActivation of autophagy is part of the innate immune response during viral infections. Autophagy involves the sequestration of endogenous or foreign components from the cytosol within double-membraned vesicles and the delivery of their content to the lysosomes for degradation. As part of innate immune responses, this autophagic elimination of foreign components is selective and requires specialized cargo receptors that function as links between a tagged foreign component and the autophagic machinery. Pathogens have evolved ways to evade their autophagic degradation to promote their replication, and recent research has shown autophagic receptors to be an important and perhaps previously overlooked target of viral autophagy inhibition. This is a brief summary of the recent progress in knowledge of virus-host interaction in the context of autophagy receptors.

scholarly journals TRIMming Type I Interferon-Mediated Innate Immune Response in Antiviral and Antitumor Defense

Viruses ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 279
Author(s):  
Ling Wang ◽  
Shunbin Ning
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Stress Responses ◽  
Viral Infections ◽  
Immune Escape ◽  
E3 Ligase ◽  
Innate Immune ◽  
Type I ◽  
Antiviral Immune Response ◽  
Wide Range

The tripartite motif (TRIM) family comprises at least 80 members in humans, with most having ubiquitin or SUMO E3 ligase activity conferred by their N-terminal RING domain. TRIMs regulate a wide range of processes in ubiquitination- or sumoylation-dependent manners in most cases, and fewer as adaptors. Their roles in the regulation of viral infections, autophagy, cell cycle progression, DNA damage and other stress responses, and carcinogenesis are being increasingly appreciated, and their E3 ligase activities are attractive targets for developing specific immunotherapeutic strategies for immune diseases and cancers. Given their importance in antiviral immune response, viruses have evolved sophisticated immune escape strategies to subvert TRIM-mediated mechanisms. In this review, we focus on their regulation of IFN-I-mediated innate immune response, which plays key roles in antiviral and antitumor defense.

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