Inducible GBP5 Mediates the Antiviral Response via Interferon-Related Pathways during Influenza A Virus Infection

Jian Feng, Zhongying Cao, Li Wang, Yushun Wan, Nanfang Peng, Qing Wang, Xueyuan Chen, Yaqin Zhou, Ying Zhu

Research output: Contribution to journalArticlepeer-review

43 Scopus citations


Guanylate binding protein (GBP) 5 belongs to the GBP family, which is involved in important cellular processes, including signal transduction, translation, vesicle trafficking, and exocytosis. Structurally, GBPs display a high degree of homology and share highly conserved GTP-binding or hydrolysis domains. GBP5 was reported to be a critical cellular factor in inflammasome assembly. However, little is known about its role in the host antiviral innate immune response. In this study, we found that GBP5 expression was significantly elevated in influenza patients and influenza A virus-infected A549 human lung epithelial cells. The overexpression of GBP5 inhibited virus replication by enhancing the expression of virus-induced interferon (IFN) and IFN-related effectors. Knockdown of GBP5 had the opposite effect. Moreover, GBP5 enhanced endogenous IFN expression by interacting with the NF-κB-essential modulator complex and stimulating NF-κB signaling. Additionally, the expression of proinflammatory factors, such as IL-6, IL-8, tumor necrosis factor-α, cyclooxygenase-2, and inducible nitric oxide synthase, was also activated by GBP5. Taken together, our results reveal that GBP5 inhibited virus replication through the activation of IFN signaling and proinflammatory factors.

Original languageEnglish (US)
Pages (from-to)419-435
Number of pages17
JournalJournal of Innate Immunity
Issue number4
StatePublished - Jul 1 2017

Bibliographical note

Funding Information:
This work was supported by research grants from the National Natural Science Foundation of China (31570870 and 81461130019), the Major State Basic Research Development Program of China (2013CB911102), Chinese 111 project (B06018). The funding agencies had no role in study design, data collection, or analysis, decision to publish, or preparation of the manuscript.

Publisher Copyright:
© 2017 S. Karger AG, Basel.


  • Cyclooxygenase-2
  • Guanylate binding protein 5
  • Influenza A virus
  • Interferon signaling
  • NF-B-essential modulator


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