Saturday, 16 July 2022

Molecular Pathogenesis of Ebola Viral Hemorrhagic Disease: An Update | Chapter 8 | Emerging Trends in Disease and Health Research Vol. 9

Although it is uncommon, Ebola viral hemorrhagic illness is a severe thrombo-hemorrhagic condition that can develop in Ebola viral sepsis. The patient passes away as a result of a poorly understood coagulopathy, severe inflammation, multi-organ failure syndrome, and bleeding. However, new research on the COVID-19 pandemic has demonstrated that viral sepsis, including the Ebola virus, results in endothelial damage via complement activation that fosters inflammation and microthrombogenesis, resulting in endotheliopathy-associated vascular microthrombotic illness (EA-VMTD). It frequently manifests in the lungs of COVID-19 infection and the liver of Ebola infection (i.e., acute hepatic necrosis) (i.e., acute respiratory distress syndrome). A unique aetiology based on the "two-activation hypothesis of the endothelium" was presented to address clinical and haematological characteristics. Following endothelial release of ULVWF/FVIII and platelet recruitment, viral sepsis induces microthrombosis via the ultra large on Willebrand factor (ULVWF) mechanism of hemostasis in vivo. Endothelial damage encourages endothelial cell release of biomolecules, which leads to a variety of clinical syndromes include severe inflammation, consumptive thrombocytopenia, microangiopathic hemolytic anaemia, and multiorgan failure syndrome. While activation of the microthrombotic route results in diffuse VMTD in Ebola viral sepsis, activation of the inflammatory pathway results in severe inflammation. Hepatic coagulopathy brought on by acute hepatic necrosis, which causes "microthrombo-hemorrhagic syndrome" (previously incorrectly referred to as "disseminated intravascular coagulation") associated with thrombotic thrombocytopenic purpura (TTP)-like syndrome, further complicates the pathogenesis of the Ebola viral disease. "EA-VMTD with hepatic coagulopathy" is the right diagnostic name for the viral thrombo-hemorrhagic syndrome.


Author (s) Details:

Jae C. Chang,
Department of Medicine, University of California Irvine School of Medicine Irvine, California, USA.

Please see the link here:
https://stm.bookpi.org/ETDHR-V9/article/view/7446

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