Abstract
Hantavirus induced hemorrhagic fever with renal syndrome (HFRS) is an emerging viral zoonosis affecting up to 200,000 humans annually worldwide. This review article is focused on recent advances in the mechanism, epidemiology, diagnosis, and treatment of hantavirus induced HFRS. The importance of interactions between viral and host factors in the design of therapeutic strategies is discussed. Hantavirus induced HFRS is characterized by thrombocytopenia and proteinuria of varying severities. The mechanism of kidney injury appears immunopathological with characteristic deterioration of endothelial cell function and compromised barrier functions of the vasculature. Although multidisciplinary research efforts have provided insights about the loss of cellular contact in the endothelium leading to increased permeability, the details of the molecular mechanisms remain poorly understood. The epidemiology of hantavirus induced renal failure is associated with viral species and the geographical location of the natural host of the virus. The development of vaccine and antiviral therapeutics is necessary to avoid potentially severe outbreaks of this zoonotic illness in the future. The recent groundbreaking approach to the SARS-CoV-2 mRNA vaccine has revolutionized the general field of vaccinology and has provided new directions for the use of this promising platform for widespread vaccine development, including the development of hantavirus mRNA vaccine. The combinational therapies specifically targeted to inhibit hantavirus replication and vascular permeability in infected patients will likely improve the disease outcome.
Highlights
Viral hemorrhagic fever refers to a multisystem syndrome triggered by severe damage to the vascular system by the viruses from six distinct families: Filoviridae, Arenaviridae, Hantaviridae, Nairoviridae, Phenuiviridae, and Flaviviridae (Table 1)
The overwhelming immune response plays a major role in hantavirus disease (Figure 4), it is still difficult to draw a detailed mechanistic picture for the pathogenesis of hantavirus induced Acute Kidney Injury (AKI)
The loss of cellular contact in the endothelium may be due to disturbances in signaling pathways involving vascular endothelial growth factor, Ecadherin, and kallikrein-kinin system (Figure 4)
Summary
Viral hemorrhagic fever refers to a multisystem syndrome triggered by severe damage to the vascular system by the viruses from six distinct families: Filoviridae, Arenaviridae, Hantaviridae, Nairoviridae, Phenuiviridae, and Flaviviridae (Table 1). Hemorrhagic fever viruses (Table 1), the old-world hantaviruses are known to cause hemorrhagic fever with renal syndrome (HFRS), a group of clinically similar illnesses targeting the kidney. Old world hantaviruses infect the highly specialized and differentiated endothelial cells of the kidney, causing acute renal failure with tubular and glomerular involvement, which is referred to as hemorrhagic fever with renal syndrome (HFRS).
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