Middle East respiratory syndrome coronavirus replication (MERS-CoV replication)

Middle East respiratory syndrome coronavirus (MERS-CoV) replication is the complex intracellular process by which the virus duplicates its positive-sense single-stranded RNA genome and produces viral proteins. This cycle is primarily driven by the replicase-transcriptase complex (RTC), which is composed of multiple non-structural proteins (nsps) such as the RNA-directed RNA polymerase (RdRp/nsp12), helicase (nsp13), and proteases (3CLpro and PLpro) (de Wit et al., 2016). These enzymes are responsible for synthesizing full-length genomic RNA and a nested set of subgenomic mRNAs, as well as processing large polyproteins into individual functional units (Hilgenfeld, 2014). Because these viral components are essential for infection and differ significantly from host cell proteins, they are prime targets for therapeutic intervention. Antiviral drugs like remdesivir target the RdRp to inhibit RNA synthesis, while various experimental inhibitors target the viral proteases to prevent the assembly of the replication machinery (Gordon et al., 2020).

Other names

MERS-CoV viral replicationMERS-CoV life cycleMERS-CoV replicase-transcriptase complexMERS-CoV RTC

Inhibition of the RNA-directed RNA polymerase (RdRp) to cause premature RNA chain termination, or inhibition of viral proteases (3CLpro/PLpro) to block the cleavage of viral polyproteins into functional non-structural proteins.