Citation: Qiong Mo, Yun-Jia Ning. ACSL3 at the UPR crossroads: Tactician of anti-influenza defense, target of influenza offense .VIROLOGICA SINICA, 2026, 41(5) : 1265-1267.  http://dx.doi.org/10.1016/j.virs.2026.09.002

ACSL3 at the UPR crossroads: Tactician of anti-influenza defense, target of influenza offense

  • Corresponding author: Yun-Jia Ning, nyj@wh.iov.cn
  • Received Date: 02 July 2026
    Accepted Date: 31 August 2026
    Available online: 04 September 2026
  • Highlights
    1 A new dimension of the host-IAV arms race is revealed, centered on ACSL3 at the UPR crossroads.
    2 Key questions remain regarding ACSL3-UPR sensor interfaces and ACSL3 induction/degradation mechanisms.
    3 Addressing the questions will advance ACSL3-IAV interplay insights and may inform host-targeted therapy.

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    8. Martin-Sancho, L., Tripathi, S., Rodriguez-Frandsen, A., Pache, L., Sanchez-Aparicio, M., Mcgregor, M.J., Haas, K.M., Swaney, D.L., Nguyen, T.T., Mamede, J.I., et al., 2021. Restriction factor compendium for influenza A virus reveals a mechanism for evasion of autophagy. Nat Microbiol, 6, 1319-1333.

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    10. Poppelreuther, M., Rudolph, B., Du, C., Grossmann, R., Becker, M., Thiele, C., Ehehalt, R., Fullekrug, J., 2012. The N-terminal region of acyl-CoA synthetase 3 is essential for both the localization on lipid droplets and the function in fatty acid uptake. J Lipid Res, 53, 888-900.

    11. Sae-Fung, A., Vinayavekhin, N., Fadeel, B., Jitkaew, S., 2024. ACSL3 is an unfavorable prognostic marker in cholangiocarcinoma patients and confers ferroptosis resistance in cholangiocarcinoma cells. NPJ Precis Oncol, 8, 284.

    12. Yao, H., Ye, J., 2008. Long Chain Acyl-CoA Synthetase 3-mediated Phosphatidylcholine Synthesis Is Required for Assembly of Very Low Density Lipoproteins in Human Hepatoma Huh7 Cells *. Journal of Biological Chemistry, 283, 849-854.

    13. Zhang, B., Han, L., Cui, C., Huang, J., Zhu, Q., Lei, C., Xu, S., 2026. Influenza a virus NS2 suppresses NFKB/NF-κB signaling to facilitate viral replication by mediating the autophagic-degradation of IKBKG/NEMO. Autophagy, 10.1080/15548627.2026.2676801.

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    ACSL3 at the UPR crossroads: Tactician of anti-influenza defense, target of influenza offense

      Corresponding author: Yun-Jia Ning, nyj@wh.iov.cn
    • a. Department of Infectious Diseases, The Affiliated People's Hospital of Ningbo University, Ningbo 315020, China;
    • b. State Key Laboratory of Virology and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China;
    • c. University of Chinese Academy of Sciences, Beijing 101408, China;
    • d. Hubei Jiangxia Laboratory, Wuhan 430200, China

    Abstract: Highlights
    1 A new dimension of the host-IAV arms race is revealed, centered on ACSL3 at the UPR crossroads.
    2 Key questions remain regarding ACSL3-UPR sensor interfaces and ACSL3 induction/degradation mechanisms.
    3 Addressing the questions will advance ACSL3-IAV interplay insights and may inform host-targeted therapy.

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