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REVIEW article

Front. Cell. Infect. Microbiol.

Sec. Virus and Host

The Regulatory Roles of STAT3 Protein in the Pathogenesis of Viral Infections

Provisionally accepted
Rongrong  GuRongrong GuHaiyang  ZhangHaiyang ZhangErying  XuErying XuShasha  LiuShasha Liu*
  • Fujian Agriculture and Forestry University, Fuzhou, China

The final, formatted version of the article will be published soon.

Signal transducer and activator of transcription 3 (STAT3) serves as a critical regulatory molecule in a multitude of physiological processes, encompassing cell proliferation, differentiation, immune defense, and inflammatory responses. The interaction between STAT3 and viruses is highly intricate, with particular relevance to the viral life cycle. It is widely acknowledged that during viral infection, the phosphorylation of STAT3, which is triggered by upstream activators such as interleukin-6 (IL-6), can exert an effective inhibitory effect on viral invasion. However, accumulating evidence has demonstrated that viruses may exploit their interaction with STAT3 to evade host immune surveillance, thereby facilitating viral persistence. Furthermore, the excessive activation of STAT3 induced by viral infection directly promotes viral replication. The precise mechanism underlying the role of STAT3 in viral infection and pathogenicity remains to be further elucidated. In this review, we summarize recent findings regarding the critical roles of STAT3 in host-virus interactions. Additionally, we discuss the mechanisms of related molecules involved in the antiviral immune response.

Keywords: STAT3 protein, viral infection, interferon, Replication, immune response

Received: 16 Sep 2025; Accepted: 02 Dec 2025.

Copyright: © 2025 Gu, Zhang, Xu and Liu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Shasha Liu

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