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Hantaan orthohantavirus (HTNV) is a negative-sense, single-stranded RNA virus belonging to the Hantaviridae family and is the prototypical cause of Hemorrhagic Fever with Renal Syndrome (HFRS) [2, 15]. Primarily transmitted to humans via aerosolized excreta from infected rodents, such as the striped field mouse (Apodemus agrarius), HTNV predominantly targets microvascular endothelial cells in the kidneys and other organs [13, 19]. The viral genome encodes three essential structural proteins: the nucleocapsid (N) protein, which is involved in genome packaging and immune evasion; the glycoproteins (Gn and Gc), which facilitate viral attachment and entry via host cell integrins; and the RNA-dependent RNA polymerase (L protein), which mediates viral replication [10, 14]. While there are currently no FDA-approved specific treatments, drugs like ribavirin and favipiravir are used off-label or in clinical trials to inhibit viral replication by targeting the L protein [2, 7, 11]. Therapeutic development also focuses on entry inhibitors and monoclonal antibodies to neutralize the virus and prevent the severe vascular leakage and acute kidney injury characteristic of HFRS [5, 18].
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