Abstract
Viral hemorrhagic diseases are a group of systemic viral infections with worldwide distribution and are significant causes of global mortality and morbidity. The hallmarks of viral hemorrhagic fevers are plasma leakage, thrombocytopenia, coagulopathy and hemorrhagic manifestations. The molecular mechanisms leading to plasma leakage in viral hemorrhagic fevers are not well understood. A common theme has emerged in which a complex interplay between pathogens, host immune response, and endothelial cells leads to the activation of endothelial cells and perturbation of barrier integrity. In this article, two clinically distinct viral hemorrhagic fevers caused by dengue viruses and hantaviruses are discussed to highlight their similarities and differences that may provide insights into the pathogenesis and therapeutic approach.
Highlights
Four families of viruses are known to cause viral hemorrhagic diseases (VHFs): Flaviviridae, Bunyaviridae, Arenaviridae and Filoviridae
Distinct vascular beds are affected in dengue hemorrhagic fever (DHF) and hantavirus pulmonary syndrome (HPS), leading to different clinical manifestations, these two VHFs share certain clinical features and pathophysiologic processes
The complex interplay between the viruses, the immune systems and the endothelial cells determines the activation of endothelial cells and the functional consequences (Fig. 1)
Summary
Four families of viruses are known to cause viral hemorrhagic diseases (VHFs): Flaviviridae, Bunyaviridae, Arenaviridae and Filoviridae. Pathogenic hantaviruses have developed multiple mechanisms to evade the early host innate immune response and inhibit the induction of type 1 IFN in infected cells, allowing efficient viral replication and spread.
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