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Researchers at UC San Diego and UC Riverside have mapped previously unknown interactions between SARS-CoV-2's RNA genome and key viral proteins, uncovering new drug targets. By disrupting these interactions using modified nucleic acid sequences, the team significantly reduced viral replication in both animal and human lung cells. The findings could pave the way for treatments that are harder for coronaviruses to evolve around — and may even work across multiple coronavirus strains.
Scientists at UC San Diego and UC Riverside have identified new targets for antiviral drugs against coronaviruses, including SARS-CoV-2, by mapping previously unknown interactions between the virus's RNA genome and key proteins involved in replication. Published in Nature Communications, the study used a technique called enhanced cross-linking and immunoprecipitation (eCLIP) to survey the entire viral genome — not just regions previously thought to be important — revealing unexpected binding sites for three proteins: NSP8, NSP12, and the nucleocapsid (N) protein.
The team then used locked nucleic acids (LNAs) — short, modified sequences designed to block specific RNA regions — to disrupt these interactions, which significantly reduced viral replication in both animal and human lung cells. Because some of the targeted RNA sequences and proteins are conserved across multiple coronaviruses, these findings could support the development of broad-spectrum treatments less prone to drug resistance.
Key Takeaways:
Why it matters: As coronaviruses continue to evolve rapidly, treatments that target fundamental and conserved viral processes — rather than variant-specific features — could be more durable and effective, and better prepare us for future outbreaks.
