Review: Viral infections and mechanisms of thrombosis and bleeding

Goeijenbier, Marco; Wissen, Matthijs Van; Weg, C. van de; Jong, Eefje; Gerdes, Victor E. A.; Meijers, Joost C. M.; Brandjes, D. P. M.; Gorp, Eric C. M. Van

doi:10.1002/jmv.23354

Cited by 264 publications

(291 citation statements)

References 205 publications

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“…These findings are in line with earlier epidemiological, clinical, animal and in vitro data [6,8,13-15,20,22-24]. Ferrets have been shown to be an adequate model to study the coagulation cascade [25-27] with PT and APTT normal values varying from 11.6-12.7 and 18.9-22.3 seconds respectively.…”

Section: Discussionsupporting

confidence: 89%

Activation of coagulation and tissue fibrin deposition in experimental influenza in ferrets

et al. 2014

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BackgroundEpidemiological studies relate influenza infection with vascular diseases like myocardial infarction. The hypothesis that influenza infection has procoagulant effects on humans has been investigated by experimental animal models. However, these studies often made use of animal models only susceptible to adapted influenza viruses (mouse adapted influenza strains) or remained inconclusive. Therefore, we decided to study the influence of infection with human influenza virus isolates on coagulation in the well-established ferret influenza model.ResultsAfter infection with either a seasonal-, pandemic- or highly pathogenic avian influenza (HPAI-H5N1) virus strain infected animals showed alterations in hemostasis compared to the control animals. Specifically on day 4 post infection, a four second rise in both PT and aPTT was observed. D-dimer concentrations increased in all 3 influenza groups with the highest concentrations in the pandemic influenza group. Von Willebrand factor activity levels increased early in infection suggesting endothelial cell activation. Mean thrombin-antithrombin complex levels increased in both pandemic and HPAI-H5N1 virus infected ferrets. At tissue level, fibrin staining showed intracapillary fibrin deposition especially in HPAI-H5N1 virus infected ferrets.ConclusionThis study showed hemostatic alterations both at the circulatory and at the tissue level upon infection with different influenza viruses in an animal model closely mimicking human influenza virus infection. Alterations largely correlated with the severity of the respective influenza virus infections.

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Section: Discussionsupporting

confidence: 89%

Activation of coagulation and tissue fibrin deposition in experimental influenza in ferrets

et al. 2014

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“…Influenza A virus (IAV) infection is a common cause of respiratory tract infection worldwide resulting in considerable mortality every year, especially in the elderly . Viral infections in general are often associated with activation of the coagulation system as part of the innate immune response . In mouse models of lethal IAV subtype H1N1 infection, there is both pulmonary activation and systemic activation of coagulation .…”

Section: Introductionmentioning

confidence: 99%

Tissue factor deficiency increases alveolar hemorrhage and death in influenza A virus‐infected mice

Antoniak

Tatsumi

Hisada

et al. 2016

Journal of Thrombosis and Haemostasis

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Background Influenza A virus (IAV) infection is a common respiratory tract infection that causes considerable morbidity and mortality worldwide. Objective To investigate the effect of a genetic deficiency of tissue factor (TF) in a mouse model of influenza A infection. Methods Wild-type mice, low tissue factor (LTF) mice and mice with the TF gene deleted in different cell types were infected with a mouse-adapted A/Puerto Rico/8/34 H1N1 strain of IAV. TF expression was measured in the lungs, and bronchoalveolar lavage fluid (BALF) was collected to measure extracellular vesicle TF, activation of coagulation, alveolar hemorrhage and inflammation. Results IAV infection of wild-type mice increased lung TF expression, activation of coagulation and inflammation in the BALF, but also led to alveolar hemorrhage. LTF mice and mice with a selective deficiency of TF in lung epithelial cells had low basal levels of TF and failed to increase TF expression after infection; these two strains of mice had more alveolar hemorrhage and death compared with controls. In contrast, deletion of TF in either myeloid cells or endothelial cells and hematopoietic cells did not increase alveolar hemorrhage or death after IAV infection. These results indicate that TF expression in the lung, particularly in epithelial cells, is required to maintain alveolar hemostasis after IAV infection. Conclusion Our study indicates that TF-dependent activation of coagulation is required to limit alveolar hemorrhage and death after influenza A infection.

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“…However, IFN-α administration reduced platelet reactivity and ventricular thrombus formation during CVB3 myocarditis [21,41]. Furthermore, proinflammatory cytokines produced during viral infections may increase TF expression in endothelial cells and monocytes [4,35,42]. …”

Section: Activation Of Coagulation In Viral Infectionsmentioning

confidence: 99%

Coagulation, Protease-Activated Receptors, and Viral Myocarditis

Antoniak

Mackman

2013

J. of Cardiovasc. Trans. Res.

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The coagulation protease cascade plays an essential role in hemostasis. In addition, a clot contributes to host defense by limiting the spread of pathogens. Coagulation proteases induce intracellular signaling by cleavage of cell surface receptors called protease-activated receptors (PARs). These receptors allow cells to sense changes in the extracellular environment, such as infection. Viruses activate the coagulation cascade by inducing tissue factor expression and by disrupting the endothelium. Virus infection of the heart can cause myocarditis, cardiac remodeling and heart failure. Recent studies using a mouse model have shown that tissue factor, thrombin and PAR-1 signaling all positively regulate the innate immune during viral myocarditis. In contrast, PAR-2 signaling was found to inhibit interferon-β expression and the innate immune response. These observations suggest that anticoagulants may impair the innate immune response to viral infection and that inhibition of PAR-2 may be a new target to reduce viral myocarditis..

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Review: Viral infections and mechanisms of thrombosis and bleeding

Cited by 264 publications

References 205 publications

Activation of coagulation and tissue fibrin deposition in experimental influenza in ferrets

Activation of coagulation and tissue fibrin deposition in experimental influenza in ferrets

Tissue factor deficiency increases alveolar hemorrhage and death in influenza A virus‐infected mice

Coagulation, Protease-Activated Receptors, and Viral Myocarditis

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