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SARS-CoV-2 viral RNA is a single-stranded, positive-sense RNA molecule approximately 29.9 kb in length that serves as both the genomic material and the messenger RNA for the coronavirus SARS-CoV-2, which causes COVID-19[1][5][7]. The genome contains a 5′ cap and a 3′ poly(A) tail and encodes 13 or more open reading frames for structural, nonstructural, and accessory proteins[5]. The RNA features complex secondary and tertiary structures, including stem-loops and long-range interactions, which regulate viral replication, transcription, translation, and evasion of the host immune response[1][3][6][7]. The genome acts as the template for synthesis of both new viral genomes and subgenomic RNAs during infection, making it a key molecular hub and a validated antiviral drug target. Drugs such as remdesivir and molnupiravir specifically act on viral RNA synthesis by inhibiting the RNA-dependent RNA polymerase or introducing mutations during replication[4]. Quantification of viral RNA in patient samples is widely used for diagnosis and management of COVID-19. The adaptability of the RNA genome poses challenges for therapy due to the risk of resistance and mutation[1][5].
Inhibitors of viral RNA-dependent RNA polymerase (e.g., remdesivir: nucleotide analog acts as a chain terminator); Induction of lethal mutagenesis (e.g., molnupiravir); Direct cleavage/degradation of viral RNA (e.g., siRNA, antisense oligonucleotides)
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