Patients with chronic illness are particularly at risk of developing these complications when suffering from (seasonal) influenza, like the observed increased risk for developing cardiovascular disease during or shortly after influenza virus infection. Although most seasonal influenza virus infections are self-limiting, they do cause a considerable burden of disease that may be aggravated by complications of the infection. While avian influenza A viruses cause sporadic zoonotic infections in humans, that do not spread efficiently among humans, these infections may result in respiratory disease manifestations that range from mild to fatal, which among other variables largely depends on the virulence of the virus involved. Symptoms depend largely, however, on the health and immune status of the infected individual and the pathogenicity of the specific virus involved.
Symptoms vary from mild respiratory complaints to fatal respiratory distress due to multiple organ failur. Seasonal influenza is caused by influenza A or B viruses which infect 5-15% of the human population every year. There are three manifestations of influenza in humans: seasonal, avian and pandemic influenza. Alterations largely correlated with the severity of the respective influenza virus infections. This 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. At tissue level, fibrin staining showed intracapillary fibrin deposition especially in HPAI-H5N1 virus infected ferrets. Mean thrombin-antithrombin complex levels increased in both pandemic and HPAI-H5N1 virus infected ferrets. Von Willebrand factor activity levels increased early in infection suggesting endothelial cell activation. D-dimer concentrations increased in all 3 influenza groups with the highest concentrations in the pandemic influenza group. Specifically on day 4 post infection, a four second rise in both PT and aPTT was observed. ResultsĪfter 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. Therefore, we decided to study the influence of infection with human influenza virus isolates on coagulation in the well-established ferret influenza model. However, these studies often made use of animal models only susceptible to adapted influenza viruses (mouse adapted influenza strains) or remained inconclusive. The hypothesis that influenza infection has procoagulant effects on humans has been investigated by experimental animal models.
Epidemiological studies relate influenza infection with vascular diseases like myocardial infarction.
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