Contribution of cytokines to pathology and protection in virus infection

Wack, Andreas; Openshaw, Peter; O’Garra, Anne

doi:10.1016/j.coviro.2011.05.015

Cited by 24 publications

(21 citation statements)

References 124 publications

(130 reference statements)

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“…However, since a significant proportion of the underlying mechanisms of IAV-bacterial interactions have been studied in the context of acute coinfection [9], we sought to address the influence of M. tuberculosis /IAV coinfection on mycobacterial control in the lungs. Mice were infected via aerosol with M. tuberculosis and then challenged sequentially via the intranasal route with 2 different IAV subtypes, one (Cal/09) on day 1 and another (X31) on day 14 after M. tuberculosis infection.…”

Section: Resultsmentioning

confidence: 99%

“…Based on the published effects of IAV on acute bacterial infections such as S. pneumonia , several mechanisms could be responsible for this observed increase in bacterial levels in M. tuberculosis /IAV-coinfected mice, including the production of type I IFN. The induction of type I IFN during intracellular bacterial infections, such as those due to Listeria monocytogenes , is associated with suppression of the innate immune response and loss of resistance to infection [9]. With these studies in mind, we investigated the role of type I IFN in promoting mycobacterial growth in concurrent M. tuberculosis /IAV-coinfected mice.…”

Section: Resultsmentioning

confidence: 99%

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Influenza A Virus Impairs Control of Mycobacterium tuberculosis Coinfection Through a Type I Interferon Receptor–Dependent Pathway

Redford

Mayer‐Barber

McNab

et al. 2013

The Journal of Infectious Diseases

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130

113

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Influenza followed by severe acute bacterial pneumonia is a major cause of mortality worldwide. Several mechanisms account for this enhanced susceptibility, including increased production of type I interferon (IFN). In individuals infected with Mycobacterium tuberculosis, the influence of acute viral infections on tuberculosis progression is unclear. We show that prior exposure of mice to influenza A virus, followed by M. tuberculosis infection, leads to enhanced mycobacterial growth and decreased survival. Following M. tuberculosis/influenza virus coinfection, mycobacterial growth is enhanced by a type I IFN signaling pathway. Our findings highlight the detrimental influence influenza virus infection can have before or during M. tuberculosis infection.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Influenza A Virus Impairs Control of Mycobacterium tuberculosis Coinfection Through a Type I Interferon Receptor–Dependent Pathway

Redford

Mayer‐Barber

McNab

et al. 2013

The Journal of Infectious Diseases

Self Cite

130

113

View full text Add to dashboard Cite

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“…In response to viral infection, the NFkappaB transcription factor can be activated and induce the production of numerous cytokines and chemokines by different cell types including macrophages, dendritic cells or epithelial cells [22]. Some viruses produce their own interleukins, chemokine regulators, or IgG Fc receptor-like proteins [23] which either inhibit the immune response or attract lymphoid cells (in the case of lymphotrophic viruses).…”

Section: Resultsmentioning

confidence: 99%

An Integrated Ontology Resource to Explore and Study Host-Virus Relationships

et al. 2014

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Our growing knowledge of viruses reveals how these pathogens manage to evade innate host defenses. A global scheme emerges in which many viruses usurp key cellular defense mechanisms and often inhibit the same components of antiviral signaling. To accurately describe these processes, we have generated a comprehensive dictionary for eukaryotic host-virus interactions. This controlled vocabulary has been detailed in 57 ViralZone resource web pages which contain a global description of all molecular processes. In order to annotate viral gene products with this vocabulary, an ontology has been built in a hierarchy of UniProt Knowledgebase (UniProtKB) keyword terms and corresponding Gene Ontology (GO) terms have been developed in parallel. The results are 65 UniProtKB keywords related to 57 GO terms, which have been used in 14,390 manual annotations; 908,723 automatic annotations and propagated to an estimation of 922,941 GO annotations. ViralZone pages, UniProtKB keywords and GO terms provide complementary tools to users, and the three resources have been linked to each other through host-virus vocabulary.

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“…Many viruses of public health significance may cause disease by triggering an immunopathology in which the damage is produced by the host inflammatory response elicited by the virus [20]. …”

Section: Discussionmentioning

confidence: 99%

Antiviral Action of Synthetic Stigmasterol Derivatives on Herpes Simplex Virus Replication in Nervous CellsIn Vitro

Petrera

Níttolo

Alché

2014

BioMed Research International

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Polyfunctionalized stigmasterol derivatives, (22S,23S)-22,23-dihydroxystigmast-4-en-3-one (compound 1) and (22S,23S)-3β-bromo-5α,22,23-trihydroxystigmastan-6-one (compound 2), inhibit herpes simplex virus type 1 (HSV-1) replication and spreading in human epithelial cells derived from ocular tissues. Both compounds reduce the incidence and severity of lesions in a murine model of herpetic stromal keratitis when administered in different treatment modalities. Since encephalitis caused by HSV-1 is another immunopathology of viral origin, we evaluate here the antiviral effect of both compounds on HSV-1 infected nervous cell lines as well as their anti-inflammatory action. We found that both stigmasterol derivatives presented low cytotoxicity in the three nervous cell lines assayed. Regarding the antiviral activity, in all cases both compounds prevented HSV-1 multiplication when added after infection, as well as virus propagation. Additionally, both compounds were able to hinder interleukin-6 and Interferon-gamma secretion induced by HSV-1 infection in Neuro-2a cells. We conclude that compounds 1 and 2 have exerted a dual antiviral and anti-inflammatory effect in HSV-1 infected nervous cell lines, which makes them interesting molecules to be further studied.

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Contribution of cytokines to pathology and protection in virus infection

Cited by 24 publications

References 124 publications

Influenza A Virus Impairs Control of Mycobacterium tuberculosis Coinfection Through a Type I Interferon Receptor–Dependent Pathway

Influenza A Virus Impairs Control of Mycobacterium tuberculosis Coinfection Through a Type I Interferon Receptor–Dependent Pathway

An Integrated Ontology Resource to Explore and Study Host-Virus Relationships

Antiviral Action of Synthetic Stigmasterol Derivatives on Herpes Simplex Virus Replication in Nervous CellsIn Vitro

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