This collaboration enables efficient activation of MDA5 on shorter RNA molecules, broadening the range of RNA lengths capable of inducing an antiviral response.

Funding came from the Japan Agency for Medical Research and Development and the Japan Society for the Promotion of Science, with authors declaring no competing interests.

The work was carried out by teams led by Kazuki Kato and Osamu Nureki at Science Tokyo and The University of Tokyo, with the findings published in Molecular Cell on February 19, 2026 (online January 19, 2026).

Key implications include deeper mechanistic insight into how innate immunity detects diverse viral RNA lengths and potential strategies to boost antiviral responses or modulate inflammation for RNA-based vaccines.

The research offers a precise molecular picture of early antiviral recognition with potential applications in designing safer mRNA vaccines and delivery systems.

The Molecular Cell article (Volume 86, Issue 4) posted online January 19, 2026 and print published February 19, 2026, reports the discoveries from Science Tokyo and The University of Tokyo.

Lead researchers from the Institute of Science Tokyo and collaborators, under Associate Professor Kazuki Kato, present the study in Molecular Cell with a February 19, 2026 publication date.

The study provides a detailed molecular model of early innate immune recognition, highlighting LGP2–MDA5 cooperation and its implications for safer, more effective RNA-based therapies and vaccines.

LGP2 and MDA5 work together to detect viral RNA: LGP2 binds RNA ends and crawls along dsRNA to recruit MDA5, assembling filaments that trigger antiviral signaling.

Cryo-EM and high-speed atomic force microscopy reveal how RNA sensing translates into signaling, detailing structural and dynamic steps in the process.