Abstract
Puumala hantavirus (PUUV) causes a hemorrhagic fever with renal syndrome (HFRS), also called nephropathia epidemica (NE), which is mainly endemic in Europe and Russia. The clinical features include a low platelet count, altered coagulation, endothelial activation, and acute kidney injury (AKI). Multiple connections between coagulation pathways and inflammatory mediators, as well as complement and kallikrein–kinin systems, have been reported. The bleeding symptoms are usually mild. PUUV-infected patients also have an increased risk for disseminated intravascular coagulation (DIC) and thrombosis.
Highlights
We summarize the current knowledge about the alterations in the coagulation and complement systems that are associated with thrombocytopenia and clinical disease during acute Puumala hantavirus (PUUV) infection
Proinflammatory cytokines are produced in macrophages or dendritic cells as a response to the recognition of hantaviruses, which cause a change from the anti- to the pro-adhesive phenotype of endothelial cells
The the ECactivity barrier function, resulting in increased blood flow into tissues. Another factor produced by infected endothelial cells (EC), tissue of the opsonization plasminogen activator (tPA) is inhibited by plasminogen activator inhibitor (PAI)-1 that is upregulated in the more severe hemorrhagic fever with renal syndrome (HFRS) cases plasminogen activator solubilizes blood and thereby contributes to EC permeability
Summary
Hantaviruses can cause HFRS in Europe and Asia and hantavirus cardiopulmonary syndrome (HCPS) in America [1,2]. PUUV infection, called nephropathia epidemica (NE), is typically associated with thrombocytopenia, increased capillary permeability causing vascular leakage, and acute kidney injury (AKI). The mortality of NE is low and has been reported to vary from 0.1% in Finland to up to 0.4% in Sweden [6,7] Both hemorrhage and thrombosis have been associated with acute PUUV infection [8,9]. We summarize the current knowledge about the alterations in the coagulation and complement systems that are associated with thrombocytopenia and clinical disease during acute PUUV infection.
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