Presence of double stranded regions of viral RNA in infected cells

Koliais, S. I.

doi:10.1007/bf01971785

Cited by 4 publications

(3 citation statements)

References 13 publications

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“…A key signal for the presence of viral infection is dsRNA, which is present as the genomic fragment (rotavirus, reovirus, and bluetongue virus) or as replicative intermediates (rhinovirus, influenza virus, dengue virus, and rubella virus; refs. 1–4). Previous work by our laboratory and others showed that dsRNA was a potent inducer of inflammatory cytokines and chemokines in many different cell types (5–7, 9–13, 45).…”

Section: Discussionmentioning

confidence: 99%

“…Formation of double-stranded RNA (dsRNA) is a common signal that is recognized by infected cells for the presence of a viral infection. DsRNA (Ͼ100 bp) is not present within normally growing cells but is almost universally present as a genomic fragment, as a replicative intermediate, or as a stem and loop structure during viral infections (1)(2)(3)(4). Experimental evidence suggests that recognition of dsRNA, either intracellularly or extracellularly, is an early and potent regulatory signal for the activation of innate and adaptive immune responses (5)(6)(7)(8)(9)(10)(11)(12).…”

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confidence: 99%

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Scavenger receptor class‐A is a novel cell surface receptor for double‐stranded RNA

et al. 2007

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Double-stranded RNA (dsRNA) is a potent signal to the host immune system for the presence of an ongoing viral infection. The presence of dsRNA, intracellularly or extracellularly, leads to the induction of innate inflammatory cytokines in many cell types including epithelial cells. However, the cell surface receptor for recognition of extracellular dsRNA is not yet determined. Here, we report that extracellular dsRNA is recognized and internalized by scavenger receptor class-A (SR-A). Treatment of human epithelial cells with specific antagonists of SR-A or with an anti-SR-A antibody significantly inhibited dsRNA induction of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-8, and regulated on activation normal T-cell expressed and secreted (RANTES). Furthermore, intranasal dsRNA treatment of SR-A-deficient (SR-A(-/-)) mice showed a significant decrease in the expression of inflammatory cytokines and a corresponding decrease in the accumulation of polymorphonuclear leukocytes (PMNs) in lungs. These data provide direct evidence that SR-A is a novel cell surface receptor for dsRNA, and therefore, SR-A may play a role in antiviral immune responses.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Scavenger receptor class‐A is a novel cell surface receptor for double‐stranded RNA

et al. 2007

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“…Our results from rhinovirus infections showed that serotypes 14 and 16 were both able to induce expression of germ line ε. Cells infected with members of the Picornaviridae, including rhinovirus, are known to contain dsRNA, and PKR has been shown to be activated in cells infected with members of this family (9,16,31,32).…”

Section: Fig 3 Viral Infections Of Ramos Cells Induce Germ Line ε Ementioning

confidence: 99%

Activation of Antiviral Protein Kinase Leads to Immunoglobulin E Class Switching in Human B Cells

Rager

Langland

Jacobs

et al. 1998

J Virol

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An epidemiologic association between viral infections and the onset of asthma and allergy has been documented. Also, evidence from animal and human studies has suggested an increase in antigen-specific immunoglobulin E (IgE) production during viral infections, and elevated levels of IgE are characteristic of human asthma and allergy. Here, we provide molecular evidence for the roles of viral infection and of activation of the antiviral protein kinase (PKR) (double-stranded-RNA [dsRNA]-activated protein kinase) in the induction of IgE class switching. The presence of dsRNA, a known component of viral infection and an activator of PKR, induced IgE class switching as detected by the expression of germ line ɛ in the human Ramos B-cell line. Furthermore, dsRNA treatment of Ramos cells resulted in the activation of PKR and in vivo activation of the NF-κB complex. Interestingly, infection of Ramos cells with rhinovirus (common cold virus) serotypes 14 and 16 resulted in the induction of germ line ɛ expression. To further evaluate the role of PKR in the viral induction of IgE class switching, we infected Ramos cells with two different vaccinia virus (cowpox virus) strains. Infection with wild-type vaccinia virus failed to induce germ line ɛ expression; however, a deletion mutant of vaccinia virus (VP1080) lacking the PKR-inhibitory polypeptide E3L induced the expression of germ line ɛ. Collectively, the results of our study define a common molecular mechanism underlying the role of viral infections in IgE class switching and subsequent induction of IgE-mediated disorders such as allergy and asthma.

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Bluetongue Virus and Double-Stranded RNA Increase Human Vascular Permeability: Role of p38 MAPK

et al. 2006

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Endothelial cell (EC) involvement in viral hemorrhagic fevers has been clearly established. However, virally activated mechanisms leading to endothelial activation and dysfunction are not well understood. Several different potential mechanisms such as direct viral infection, alterations in procoagulant/anticoagulant balance, and increased cytokine production have been suggested. We utilized a model of EC barrier dysfunction and vascular endothelial leakage to explore the effect of bluetongue virus (BTV), a hemorrhagic fever virus of ruminants, on human lung endothelial cell barrier properties. Infection of human lung EC with BTV induced a significant and dose-dependent decrease in trans-endothelial electrical resistance (TER). Furthermore, decreases in TER occurred in conjunction with cytoskeletal rearrangement, suggesting a direct mechanism for viral infection-mediated endothelial barrier disruption. Interestingly, double-stranded RNA (dsRNA) mimicked the effects of BTV on endothelial barrier properties. Both BTV- and dsRNA-induced endothelial barrier dysfunction was blocked by treatment with a pharmacological inhibitor of p38 MAPK. The induction of vascular permeability by dsRNA treatment or BTV infection was concomitent with induction of inflammatory cytokines. Taken together, our data suggest that the presence of dsRNA during viral infections and subsequent activation of p38 MAPK is a potential molecular pathway for viral induction of hemorrhagic fevers. Collectively, our data suggest that inhibition of p38 MAPK may be a possible therapeutic approach to alter viral-induced acute hemorrhagic diseases.

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Presence of double stranded regions of viral RNA in infected cells

Cited by 4 publications

References 13 publications

Scavenger receptor class‐A is a novel cell surface receptor for double‐stranded RNA

Scavenger receptor class‐A is a novel cell surface receptor for double‐stranded RNA

Activation of Antiviral Protein Kinase Leads to Immunoglobulin E Class Switching in Human B Cells

Bluetongue Virus and Double-Stranded RNA Increase Human Vascular Permeability: Role of p38 MAPK

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