Abstract
Annually, over 10,000 cases of hemorrhagic fever with renal syndrome (HFRS) are diagnosed in Europe. Puumala hantavirus (PUUV) causes most of the European HFRS cases. PUUV causes usually a relatively mild disease, which is rarely fatal. However, the severity of the infection varies greatly, and factors affecting the severity are mostly unrevealed. Host genes are known to have an effect. The typical clinical features in PUUV infection include acute kidney injury, thrombocytopenia, and increased vascular permeability. The primary target of hantavirus is the endothelium of the vessels of different organs. Although PUUV does not cause direct cytopathology of the endothelial cells, remarkable changes in both the barrier function of the endothelium and the function of the infected endothelial cells occur. Host immune or inflammatory mechanisms are probably important in the development of the capillary leakage. Several immunoinflammatory biomarkers have been studied in the context of assessing the severity of HFRS caused by PUUV. Most of them are not used in clinical practice, but the increasing knowledge about the biomarkers has elucidated the pathogenesis of PUUV infection.
Highlights
Hantaviruses are enveloped viruses with a trisegmented viral RNA genome [1]
Puumala virus (PUUV) infection is typically associated with increased vascular permeability, acute kidney injury (AKI), and thrombocytopenia [6,7,8,9,10]
We summarize the current knowledge about different biomarkers in PUUV hantavirus infection
Summary
Hantaviruses are enveloped viruses with a trisegmented viral RNA genome [1]. The segments called small, medium, and large encode the nucleocapsid protein N, the two glycoproteins Gn and Gc, and the RNA polymerase, respectively [1]. PUUV, carried by the bank vole (Myodes glareolus), causes most of the European HFRS cases [4] The majority of these infections are reported in Finland, which has the highest incidence globally of a diagnosed hantavirus disease, with 1000–3000 serological diagnoses each year [4,5]. PUUV infection is typically associated with increased vascular permeability, acute kidney injury (AKI), and thrombocytopenia [6,7,8,9,10]. In PUUV-infected patients, IL-6 production is increased, and high plasma levels are associated with a more severe clinical disease [28,31,32,33,34,35]. IL-6 appears as a useful biomarker when assessing the severity of PUUV hantavirus infection
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