About: The Role of Myeloid Cell Activation and Arginine Metabolism in the Pathogenesis of Virus-Induced Diseases

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An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	The Role of Myeloid Cell Activation and Arginine Metabolism in the Pathogenesis of Virus-Induced Diseases
Creator	Burrack, Kristina Morrison, Thomas
Source	Medline; PMC
abstract	When an antiviral immune response is generated, a balance must be reached between two opposing pathways: the production of proinflammatory and cytotoxic effectors that drive a robust antiviral immune response to control the infection and regulators that function to limit or blunt an excessive immune response to minimize immune-mediated pathology and repair tissue damage. Myeloid cells, including monocytes and macrophages, play an important role in this balance, particularly through the activities of the arginine-hydrolyzing enzymes nitric oxide synthase 2 (Nos2; iNOS) and arginase 1 (Arg1). Nitric oxide (NO) production by iNOS is an important proinflammatory mediator, whereas Arg1-expressing macrophages contribute to the resolution of inflammation and wound repair. In the context of viral infections, expression of these enzymes can result in a variety of outcomes for the host. NO has direct antiviral properties against some viruses, whereas during other virus infections NO can mediate immunopathology and/or inhibit the antiviral immune response to promote chronic infection. Arg1 activity not only has important wound healing functions but can also inhibit the antiviral immune response during some viral infections. Thus, depending on the specific virus and the tissue(s) involved, the activity of both of these arginine-hydrolyzing enzymes can either exacerbate or limit the severity of virus-induced disease. In this review, we will discuss a variety of viral infections, including HIV, SARS-CoV, LCMV, HCV, RSV, and others, where myeloid cells influence the control and clearance of the virus from the host, as well as the severity and resolution of tissue damage, via the activities of iNOS and/or Arg1. Clearly, monocyte/macrophage activation and arginine metabolism will continue to be important areas of investigation in the context of viral infections.
has issue date	2014-09-08(xsd:dateTime)
bibo:doi	10.3389/fimmu.2014.00428
bibo:pmid	25250029
has license	cc-by
sha1sum (hex)	94ba61be5805b1b0caef6716c00ed234be78b021
schema:url	https://doi.org/10.3389/fimmu.2014.00428
resource representing a document's title	The Role of Myeloid Cell Activation and Arginine Metabolism in the Pathogenesis of Virus-Induced Diseases
has PubMed Central identifier	PMC4157561
has PubMed identifier	25250029
schema:publication	Front Immunol
resource representing a document's body	covid:94ba61be5805b1b0caef6716c00ed234be78b021#body_text
is schema:about of	named entity 'ROLE' named entity 'metabolism' named entity 'ARGININE METABOLISM' named entity 'MYELOID CELL ACTIVATION' named entity 'INDUCED' named entity 'PATHOGENESIS' named entity 'VIRUS' named entity 'DISEASES' named entity 'iNOS' named entity 'intracellular' named entity 'B-cell' named entity 'CCR2' named entity 'lung tissue' named entity 'nitric oxide' named entity 'mice' named entity 'alveolar macrophages' named entity 'arginase' named entity 'mice' named entity 'cytokines' named entity 'anti-inflammatory' named entity 'transgenically' named entity 'immunodeficiency' named entity 'tumors' named entity 'NOS' named entity 'alveolar macrophages' named entity 'Immunology' named entity 'Monocyte' named entity 'genetic deletion' named entity 'nitric oxide' named entity 'viral titers' named entity 'influenza infection' named entity 'mice' named entity 'macrophages' named entity 'antiviral' named entity 'iNOS' named entity 'nitric oxide' named entity 'Infection' named entity 'F4/80' named entity 'myeloid cell' named entity 'SARS-CoV' named entity 'macrophages' named entity 'viral burden' named entity 'Antigen Presenting Cell' named entity 'herpes simplex virus' named entity 'liver disease' named entity 'phenotype' named entity 'pathophysiological' named entity 'CD3ζ' named entity 'similar manner' named entity 'Treg' named entity 'CD8 T cells' named entity 'footpad' named entity 'nitric oxide' named entity 'infection' named entity 'cell death' named entity 'mice' named entity 'mice' named entity 'Arg1' named entity 'lung' named entity 'demyelinating disease' named entity 'antiviral effect' named entity 'iNOS' named entity 'viruses' named entity 'iNOS' named entity 'lung' named entity 'arginase' named entity 'ligands' named entity 'CNS' named entity 'viral persistence' named entity 'mice' named entity 'iNOS' named entity 'Nos2' named entity 'NOS' named entity 'infection' named entity 'virally infected' named entity 'macrophages' named entity 'mice' named entity 'CCR2' named entity 'virus' named entity 'myeloid-derived suppressor cells'

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