Making Short Work

Like prey animals evolve camouflage over time to evade their predators, viruses evolve tricks to bypass cells’ antiviral tactics. Since it first emerged in humans as a lethal lockdown-prompting menace, SARS-CoV-2 has accrued many mutations, but the functional consequence of these mutations is not fully understood. A study has found that certain variants, such as Omicron, produce a shortened version of the core structural protein, N (blue in the infected cells pictured, preventing yellow defensive stress granules forming). This diminutive alternative binds to viral genetic material (double-stranded RNA, a red flag for infection) and blunts key immune responses, helping the virus dodge the cell’s defences and silence the alarm. Viruses with more of the truncated protein grew better in both human cells and in mice. Understanding how SARS-CoV-2 uses this truncated protein to evade immune defences highlights a potential target for therapies to counter future variants.

Written by Anthony Lewis

Anthony Lewis

Writer

Ant was the web editor in the early days of BPoD, and has since worked with the UK’s top science organisations as a writer and multimedia producer. He now splits his time between freelance work and managing multimedia at The Lancet.

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• Image on Bluesky from work by Rory P. Mulloy and colleagues, Corcoran Lab
• Microbiology, Immunology and Infectious Diseases Department, Snyder Institute for Chronic Diseases, Charbonneau Cancer Research Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada
• Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)
• Research published in PLOS Biology, December 2025