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Severe fever with thrombocytopenia syndrome virus (SFTSV) genomic RNA is the tripartite, negative-sense, single-stranded RNA genome of a tick-borne phlebovirus in the Phenuiviridae family (Yu et al., 2011, NEJM). The genome is organized into Large (L), Medium (M), and Small (S) segments, which encode the viral RNA-dependent RNA polymerase, glycoprotein precursor, and nucleocapsid/non-structural proteins, respectively (Li et al., 2014, Frontiers in Microbiology). This genomic RNA serves as the essential template for both transcription of viral mRNA and replication of the viral genome within the host cell cytoplasm. SFTSV is the causative agent of a severe infectious disease characterized by high fever, thrombocytopenia, and leukopenia, often progressing to multi-organ failure with high fatality rates (Liu et al., 2014, Emerging Infectious Diseases). Therapeutic strategies targeting the genomic RNA include the use of favipiravir, a nucleoside analog that inhibits the replication process by acting as a substrate for the viral polymerase (Tani et al., 2016, Scientific Reports). Additionally, experimental RNA interference (RNAi) approaches are being developed to specifically target and degrade SFTSV RNA sequences to suppress viral replication. Monitoring viral RNA levels in patient serum is a primary biomarker for diagnosing the infection and evaluating the efficacy of antiviral interventions. The high mutation rate of the viral RNA segments poses a significant challenge for long-term therapeutic efficacy and the development of broad-spectrum vaccines.
Inhibition of viral RNA synthesis through the action of nucleoside analogs on the viral RNA-dependent RNA polymerase (RdRp) or direct degradation of viral RNA segments via sequence-specific RNA interference (RNAi).
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