Researchers at Houston Methodist kept mice from getting the flu by removing a gene that regulates their immune system. According to a study recently published in Nature Immunology (online Oct. 3), mice missing the gene Trim29 eliminated human influenza virus within 48 hours, protecting them from infection.

“Influenza is the leading cause of death from infections worldwide. An effective treatment is vital, especially for children, the elderly and patients with compromised immune systems,” said Zhiqiang Zhang, Ph.D., the paper’s lead author and assistant member of transplant immunology at Houston Methodist Research Institute. “Mice lacking Trim29 kept them from a full blown infection and completely cleared them of the virus. This finding points the way to a potential flu treatment.”

Immune cells around the lungs are the first line of defense against infections. The gene Trim29, or Tripartite Interaction Motif 29, controls activation of lung immune cells after viral infections. Zhang’s team infected mice without the gene with the H1N1 flu virus and compared their survival and amount of virus to normal mice. Mice lacking Trim29 survived with no detectable infection or virus.
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Co-authors of the study included Junji Xing, Ph.D., Bin Yuan, Ph.D., Zhuo Wang, Ph.D., Li Jia, Ph.D., Rui Jin, Ph.D. and Xian Chang Li, M.D. and Ph.D. (Houston Methodist Research Institute); Leiyun Weng, Ph.D., Hongbo Lu, M.D., and Yong-Jun Liu, M.D. and Ph.D. (Medimmune, Inc., USA).

The research was supported in part by the Wellcome Trust Sanger Institute Mouse Genetics Project and the National Institutes of Health.

To speak with Zhiqiang Zhang, Ph.D., contact Patricia Akinfenwa, Houston Methodist, at 281.740.1402 or pakinfenwa@houstonmethodist.org. For more information about Houston Methodist, visit houstonmethodist.org. Follow us on Twitter and Facebook.

For more information: Identification of a role for TRIM29 in the control of innate immunity in the respiratory tract. Nature Immunology DOI: 10.1038/ni.3580. (Online October 3, 2016) J. Xing, L. Weng, B. Yuan, Z. Wang, L. Jia, R. Jin, H. Lu, X. C. Li, Y. Liu and Z. Zhang.