AI Article Synopsis
- Hantavirus, particularly Hantaan virus (HTNV), causes hemorrhagic fever with renal syndrome (HFRS), characterized by severe symptoms like low platelet counts and kidney issues.
- Current understanding of HFRS pathogenesis is limited, with immune dysfunction and damage to blood vessel linings thought to be key factors in disease development.
- The review explores various molecules involved in the immune response and vascular regulation, suggesting they could serve as indicators for monitoring HTNV infection and its related complications.
Article Abstract
Hantavirus, which causes hemorrhagic fever with renal syndrome (HFRS) is almost prevalent worldwide. While Hantaan virus (HTNV) causes the most severe form of HFRS with typical clinical manifestations of thrombocytopenia, increased vascular permeability, and acute kidney injury. Although the knowledge of the pathogenesis of HFRS is still limited, immune dysfunction and pathological damage caused by disorders of immune regulation are proposed to play a vital role in the development of the disorder, and the endothelium is considered to be the primary target of hantaviruses. Here, we reviewed the production and function of multiple molecules, mainly focusing on their role in immune response, endothelium, vascular permeability regulation, and platelet and coagulation activation which are closely related to the pathogenesis of HTNV infection. meanwhile, the relationship between these molecules and characteristics of HTNV infection including the hospital duration, immune dysfunction, thrombocytopenia, leukocytosis, and acute kidney injury are also presented, to provide a novel insight into the potential role of these molecules as monitoring markers for HTNV infection.
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| http://dx.doi.org/10.1016/j.cyto.2023.156340 | DOI Listing |
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