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Severity Biomarkers in Puumala Hantavirus Infection

期刊

VIRUSES-BASEL
卷 14, 期 1, 页码 -

出版社

MDPI
DOI: 10.3390/v14010045

关键词

hantavirus; hemorrhagic fever with renal syndrome; Puumala virus; biomarker

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资金

  1. Tampere University Hospital
  2. Sigrid Juselius Foundation
  3. Magnus Ehrnrooth Foundation
  4. Tampere Tuberculosis Foundation

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In Europe, over 10,000 cases of hemorrhagic fever with renal syndrome (HFRS) are reported annually, with Puumala hantavirus (PUUV) being the main causative agent. PUUV usually causes a mild disease with low fatality rates, but the factors influencing disease severity are largely unknown. Host genes have been found to have an effect. Typical clinical features of PUUV infection include acute kidney injury, thrombocytopenia, and increased vascular permeability. Although PUUV does not directly cause cytopathology of the endothelial cells, significant changes in both the barrier function of the endothelium and the infected endothelial cells occur. Host immune or inflammatory mechanisms are likely important in the development of capillary leakage. Several immunoinflammatory biomarkers have been studied to assess the severity of PUUV-induced HFRS. Most of them are not currently used in clinical practice, but the increasing knowledge about these biomarkers has helped to elucidate the pathogenesis of PUUV infection.
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.

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