SARS-CoV-2 replication

SARS-CoV-2 replication in human lung cells is the multi-stage biological process by which the virus infects and multiplies within the respiratory epithelium (V'kovski et al., 2021). The cycle initiates when the viral Spike protein binds to the host Angiotensin-Converting Enzyme 2 (ACE2) receptor, often facilitated by the host protease TMPRSS2 (Hoffmann et al., 2020). Following entry, the viral positive-sense RNA genome is released into the cytoplasm and translated into polyproteins, which are cleaved by viral proteases (3CLpro and PLpro) to form the replication-transcription complex (Jin et al., 2020). This complex, centered around the RNA-dependent RNA polymerase (RdRp), facilitates the synthesis of new genomic and subgenomic RNAs (Hillen et al., 2020). Progeny virions are then assembled in the endoplasmic reticulum-Golgi intermediate compartment and released via exocytosis to infect adjacent cells (Ghosh et al., 2020). This replication process is the primary driver of COVID-19 pathogenesis, and therapeutic strategies focus on inhibiting specific viral enzymes like RdRp or 3CLpro to halt viral production and reduce disease severity (NIH, 2023).

Other names

SARS-CoV-2 life cycleViral replication in lung tissueCOVID-19 viral replicationSARS-CoV-2 propagation

Antiviral agents disrupt the replication cycle by inhibiting specific viral proteins, such as the RNA-dependent RNA polymerase (RdRp) to terminate RNA chain synthesis or the main protease (Mpro/3CLpro) to prevent the processing of viral polyproteins (NIH, 2023).