TRIF Is a Critical Survival Factor in Viral Cardiomyopathy

Riad, Alexander; Westermann, Dirk; Zietsch, Christin; Savvatis, Konstantinos; Becher, Peter Moritz; Bereswill, Stefan; Heimesaat, Markus M.; Lettau, Olga; Laßner, Dirk; Dörner, Andrea; Poller, Wolfgang; Busch, M.; Felix, Stephan B.; Schultheiß, Heinz Peter; Tschöpe, Carsten

doi:10.4049/jimmunol.1002029

Cited by 75 publications

(85 citation statements)

References 44 publications

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“…The concordant results demonstrated that CiTRIF can inhibit the replication of GCRV in vitro. TRIF(À/À) mice infected with coxsackievirus group B serotype 3 (CVB3) lead to severe heart failure and 100% mortality (Riad et al, 2011). TRIF overexpression mice are less susceptible to encephalomyocarditis virus (EMCV) infection, have a significantly lower viral load in the heart .…”

Section: Discussionmentioning

confidence: 99%

Identification and functional characterizations of a novel TRIF gene from grass carp (Ctenopharyngodon idella)

Yang

et al. 2013

Developmental & Comparative Immunology

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Section: Discussionmentioning

confidence: 99%

Identification and functional characterizations of a novel TRIF gene from grass carp (Ctenopharyngodon idella)

Yang

et al. 2013

Developmental & Comparative Immunology

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“…47 Mouse studies have shown that a deficiency of either TLR3 or its adaptor, TRIF, is associated with an increase in levels of virus and mortality after CVB3 or CVB4 infection. [48][49][50] Interestingly, type I IFNs (IFN-a and IFN-b), but not type II IFN (IFN-g), are required for the innate immune response to CVB3. 51 IFN-a and IFN-b are expressed at low levels by various cells but are induced in virally infected cells, such as CFs and cardiomyocytes in the heart.…”

Section: Par1 Modulation Of Tlr3 and Tlr4 Signaling In Cfsmentioning

confidence: 99%

Multiple roles of the coagulation protease cascade during virus infection

Antoniak

Mackman

2014

Blood

192

205

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The coagulation cascade is activated during viral infections. This response may be part of the host defense system to limit spread of the pathogen. However, excessive activation of the coagulation cascade can be deleterious. In fact, inhibition of the tissue factor/factor VIIa complex reduced mortality in a monkey model of Ebola hemorrhagic fever. Other studies showed that incorporation of tissue factor into the envelope of herpes simplex virus increases infection of endothelial cells and mice. Furthermore, binding of factor X to adenovirus serotype 5 enhances infection of hepatocytes but also increases the activation of the innate immune response to the virus. Coagulation proteases activate protease-activated receptors (PARs). Interestingly, we and others found that PAR1 and PAR2 modulate the immune response to viral infection. For instance, PAR1 positively regulates TLR3-dependent expression of the antiviral protein interferon β, whereas PAR2 negatively regulates expression during coxsackievirus group B infection. These studies indicate that the coagulation cascade plays multiple roles during viral infections.

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“…For example, in the experimental setting of viral myocarditis, this disease is strongly associated with increased cardiac content of collagens. 21,22 This is also the case in experimental ischemic cardiomyopathy. 23 In nonischemic cardiomyopathy, midwall myocardial fibrosis has been shown to be a major component of pathological remodeling, and to be a predictor of adverse outcome.…”

Section: Stiffness Of Cfbs Derived From Rv and LV Tissue Samplesmentioning

confidence: 99%

Stiffness of Left Ventricular Cardiac Fibroblasts Is Associated With Ventricular Dilation in Patients With Recent-Onset Nonischemic and Nonvalvular Cardiomyopathy

Glaubitz¹,

Block²,

Witte

et al. 2014

Circ J

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Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp (LV) dilation. 1 This subgroup (ie, those with dilated cardiomyopathy: DCM) constitutes the third most common type of heart failure and is the most frequent indication for heart transplantation. 2 Etiological aspects of LV dilation in DCM are under intense current investigation. 3-5 Among other factors, imbalance in the cardiac extracellular matrix (ECM) is believed to be a key pathogenic factor of ventricular chamber dilation in heart failure. This includes increased accumulation of collagens, disturbance in ECM-regulating factors such as metalloecent-onset cardiomyopathy (ROCM), described as nonischemic and nonvalvular ventricular dysfunction with cardiac symptoms of less than 6 months' duration, is a relevant cause of heart failure and includes increased morbidity and mortality. 1 Patients with ROCM show great variation in the clinical course, which ranges from sufficient myocardial recovery to end-stage heart failure and increased mortality. Background: Ventricular dilation is known as a pivotal predictor in recent-onset cardiomyopathy (ROCM), but its pathophysiology is not fully understood. In the present study we investigated whether single-cell stiffness of right and left ventricular-derived fibroblasts has an effect on cardiac phenotype in patients with ROCM.

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TRIF Is a Critical Survival Factor in Viral Cardiomyopathy

Cited by 75 publications

References 44 publications

Identification and functional characterizations of a novel TRIF gene from grass carp (Ctenopharyngodon idella)

Identification and functional characterizations of a novel TRIF gene from grass carp (Ctenopharyngodon idella)

Multiple roles of the coagulation protease cascade during virus infection

Stiffness of Left Ventricular Cardiac Fibroblasts Is Associated With Ventricular Dilation in Patients With Recent-Onset Nonischemic and Nonvalvular Cardiomyopathy

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