scholarly journals Interplay between Hepatitis E Virus and Host Cell Pattern Recognition Receptors

2021 ◽  
Vol 22 (17) ◽  
pp. 9259
Author(s):  
Pradip Devhare ◽  
Mridula Madiyal ◽  
Chiranjay Mukhopadhyay ◽  
Shiran Shetty ◽  
Shamee Shastry
Keyword(s):  
Immune Response ◽  
Pattern Recognition ◽  
Host Cell ◽  
Innate Immune Response ◽  
Hepatitis E Virus ◽  
Hepatitis E ◽  
Pattern Recognition Receptors ◽  
Innate Immune ◽  
Renal Diseases ◽  
Cell Pattern

Hepatitis E virus (HEV) usually causes self-limiting acute hepatitis, but the disease can become chronic in immunocompromised individuals. HEV infection in pregnant women is reported to cause up to 30% mortality, especially in the third trimester. Additionally, extrahepatic manifestations like neuronal and renal diseases and pancreatitis are also reported during the course of HEV infection. The mechanism of HEV pathogenesis remains poorly understood. Innate immunity is the first line of defense triggered within minutes to hours after the first pathogenic insult. Growing evidence based on reverse genetics systems, in vitro cell culture models, and representative studies in animal models including non-human primates, has implicated the role of the host’s innate immune response during HEV infection. HEV persists in presence of interferons (IFNs) plausibly by evading cellular antiviral defense. This review summarizes our current understanding of recognizing HEV-associated molecular patterns by host cell Pattern Recognition Receptors (PRRs) in eliciting innate immune response during HEV infection as well as mechanisms of virus-mediated immune evasion.

scholarly journals Pattern Recognition Receptors and the Innate Immune Response to Viral Infection

Viruses ◽  
2011 ◽  
Vol 3 (6) ◽  
pp. 920-940 ◽  
Author(s):  
Mikayla R. Thompson ◽  
John J. Kaminski ◽  
Evelyn A. Kurt-Jones ◽  
Katherine A. Fitzgerald
Keyword(s):  
Immune Response ◽  
Pattern Recognition ◽  
Viral Infection ◽  
Innate Immune Response ◽  
Pattern Recognition Receptors ◽  
Innate Immune

scholarly journals Effect of hepatitis E virus infection on the human hepatic innate immune response in human liver chimeric mice

2017 ◽  
Vol 66 (1) ◽  
pp. S246
Author(s):  
I.M. Sayed ◽  
L. Verhoye ◽  
L. Cocquerel ◽  
F. Abravanel ◽  
L. Foquet ◽  
...  
Keyword(s):  
Immune Response ◽  
Virus Infection ◽  
Innate Immune Response ◽  
Human Liver ◽  
Hepatitis E Virus ◽  
Hepatitis E ◽  
Innate Immune ◽  
Chimeric Mice

P0554 : Hepatitis E virus infection induces an innate immune response in human chimeric mice

2015 ◽  
Vol 62 ◽  
pp. S522-S523
Author(s):  
L. Allweiss ◽  
S. Gass ◽  
T. Volz ◽  
K. Giersch ◽  
J. Kah ◽  
...  
Keyword(s):  
Immune Response ◽  
Virus Infection ◽  
Innate Immune Response ◽  
Hepatitis E Virus ◽  
Hepatitis E ◽  
Innate Immune ◽  
Chimeric Mice

scholarly journals Peptidomimetic 1-Benzyl-5-methyl-4-(n-octylamino)pyrimidin-2(1H)-one Showed Cardioprotection Effect in a Myocardial Ischemia (MI) Mouse Model

Proceedings ◽  
2019 ◽  
Vol 22 (1) ◽  
pp. 72
Author(s):  
Lena Trifonov ◽  
Vadim Nudelman ◽  
Michael Zhenin ◽  
Guy Cohen ◽  
Krzysztof Jozwiak ◽  
...  
Keyword(s):  
Immune Response ◽  
Pattern Recognition ◽  
Myocardial Ischemia ◽  
Mouse Model ◽  
Innate Immune Response ◽  
Pattern Recognition Receptor ◽  
Innate Immune ◽  
Microbial Pathogens ◽  
Toll Like Receptors ◽  
Recognition Receptor

TLR4, a member of the toll-like receptors (TLRs) family, serves as a pattern recognition receptor in the innate immune response to different microbial pathogens. [...]

scholarly journals How Many Mammalian Reovirus Proteins are involved in the Control of the Interferon Response?

Pathogens ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 83 ◽  
Author(s):  
Delphine Lanoie ◽  
Simon Boudreault ◽  
Martin Bisaillon ◽  
Guy Lemay
Keyword(s):  
Immune Response ◽  
Host Cell ◽  
Innate Immune Response ◽  
Resistance Mechanisms ◽  
Innate Immune ◽  
Interferon Response ◽  
Gene Products ◽  
Interferon Signaling ◽  
Host Cell Response ◽  
Response Network

As with most viruses, mammalian reovirus can be recognized and attacked by the host-cell interferon response network. Similarly, many viruses have developed resistance mechanisms to counteract the host-cell response at different points of this response. Reflecting the complexity of the interferon signaling pathways as well as the resulting antiviral response, viruses can—and often have—evolved many determinants to interfere with this innate immune response and allow viral replication. In the last few years, it has been evidenced that mammalian reovirus encodes many different determinants that are involved in regulating the induction of the interferon response or in interfering with the action of interferon-stimulated gene products. In this brief review, we present our current understanding of the different reovirus proteins known to be involved, introduce their postulated modes of action, and raise current questions that may lead to further investigations.

Nanoparticle impact on innate immune cell pattern-recognition receptors and inflammasomes activation

2017 ◽  
Vol 34 ◽  
pp. 3-24 ◽  
Author(s):  
Ana Luísa Silva ◽  
Carina Peres ◽  
João Conniot ◽  
Ana I. Matos ◽  
Liane Moura ◽  
...  
Keyword(s):  
Pattern Recognition ◽  
Immune Cell ◽  
Pattern Recognition Receptors ◽  
Innate Immune ◽  
Innate Immune Cell ◽  
Cell Pattern

scholarly journals Vpu-Deficient HIV Strains Stimulate Innate Immune Signaling Responses in Target Cells

2012 ◽  
Vol 86 (16) ◽  
pp. 8499-8506 ◽  
Author(s):  
Brian P. Doehle ◽  
Kristina Chang ◽  
Lamar Fleming ◽  
John McNevin ◽  
Florian Hladik ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Host Cell ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Target Cells ◽  
Major Public Health Problem ◽  
Type I ◽  
Innate Defense ◽  
Hiv 1

Acute virus infection induces a cell-intrinsic innate immune response comprising our first line of immunity to limit virus replication and spread, but viruses have developed strategies to overcome these defenses. HIV-1 is a major public health problem; however, the virus-host interactions that regulate innate immune defenses against HIV-1 are not fully defined. We have recently identified the viral protein Vpu to be a key determinant responsible for HIV-1 targeting and degradation of interferon regulatory factor 3 (IRF3), a central transcription factor driving host cell innate immunity. IRF3 plays a major role in pathogen recognition receptor (PRR) signaling of innate immunity to drive the expression of type I interferon (IFN) and interferon-stimulated genes (ISGs), including a variety of HIV restriction factors, that serve to limit viral replication directly and/or program adaptive immunity. Here we interrogate the cellular responses to target cell infection with Vpu-deficient HIV-1 strains. Remarkably, in the absence of Vpu, HIV-1 triggers a potent intracellular innate immune response that suppresses infection. Thus, HIV-1 can be recognized by PRRs within the host cell to trigger an innate immune response, and this response is unmasked only in the absence of Vpu. Vpu modulation of IRF3 therefore prevents virus induction of specific innate defense programs that could otherwise limit infection. These observations show that HIV-1 can indeed be recognized as a pathogen in infected cells and provide a novel and effective platform for defining the native innate immune programs of target cells of HIV-1 infection.

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