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Middle East Respiratory Syndrome Coronavirus (MERS-CoV) RNA is the positive-sense, single-stranded genetic material of the MERS-CoV virus, a member of the Betacoronavirus genus (NCBI, 2023). The genome is approximately 30 kilobases in length and features a 5' cap and a 3' polyadenylated tail, allowing it to function directly as mRNA upon entry into the host cell (PubMed, PMID: 23012494). It encodes essential non-structural proteins (nsps) that form the replicase-transcriptase complex, as well as structural proteins such as the spike (S), envelope (E), membrane (M), and nucleocapsid (N) proteins (UniProt, 2024). During the viral life cycle, this RNA serves as the primary template for both the replication of the full-length genome and the transcription of subgenomic mRNAs. As a therapeutic target, MERS-CoV RNA replication is primarily inhibited by nucleoside analogs like remdesivir, which act as alternative substrates for the viral RNA-dependent RNA polymerase (RdRp), leading to delayed chain termination (PubMed, PMID: 32022325). Additionally, experimental strategies such as RNA interference (RNAi) and antisense oligonucleotides are designed to target and degrade specific sequences within the viral RNA to halt infection (PubMed, PMID: 25107318). The detection of MERS-CoV RNA via RT-qPCR in respiratory specimens remains the gold standard for clinical diagnosis and monitoring patient viral load (WHO, 2018).
Inhibition of viral RNA-dependent RNA polymerase (RdRp) resulting in premature RNA chain termination or lethal mutagenesis during the synthesis of the viral RNA strand (PubMed, PMID: 32022325).
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