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ORIGINAL RESEARCH article
Front. Microbiol.
Sec. Infectious Agents and Disease
Volume 16 - 2025 | doi: 10.3389/fmicb.2025.1591473
This article is part of the Research Topic Research Advances and Challenges in Emerging and Re-Emerging Viral Diseases View all 18 articles
The Economical Role of RIOK3 in Modulating the Jak1/STAT1 Pathway and Antiviral Immunity Against Respiratory Syncytial Virus (RSV) Infection in Macrophages: Implications for Therapeutic Potential
Provisionally accepted- 1 Department of Colorectal Surgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Jiangsu Province, China
- 2 Key Laboratory of Cancer Prevention and Intervention, Ministry of Education, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
- 3 Department of Endocrinology, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Jiangsu Province, China
- 4 Department of General Medicine and Geriatrics, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang Province, China
- 5 Department of Orthopedic Surgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
- 6 Institute of Orthopaedics, School of Medicine, Zhejiang University, Hangzhou, Jiangsu Province, China
Respiratory Syncytial Virus (RSV) is a leading cause of lower respiratory tract infections, particularly in vulnerable populations such as infants, the elderly, and immunocompromised individuals. RSV infection can result in mortality rates as high as 20%, attributable not only to viral replication but also to an excessive host immune response. Current therapeutic options are limited, partly due to gaps in understanding the host immune response, especially the role of macrophages and their signaling pathways. This study investigates the role of RIOK3, an unconventional kinase, in modulating the Jak1/STAT1 pathway during RSV infection in macrophages and its impact on viral replication and interferon production. Using both in vitro and in vivo models, including primary bone marrow-derived macrophages (BMM) from control and RIOK3 knockout (KO) mice, we demonstrate that RIOK3 is a critical regulator of the Jak1/STAT1 pathway in macrophages during RSV infection. The absence of RIOK3 enhances viral replication and disrupts the balance of type I interferons. Targeting RIOK3 may represent a promising strategy to enhance antiviral immunity and mitigate RSV-induced inflammation, thus warranting further investigation for therapeutic potential.
Keywords: RSV, macrophage, RIOK3, Jak1/STAT pathway, type I interferon
Received: 14 Mar 2025; Accepted: 07 Apr 2025.
Copyright: © 2025 Sun, Liang, Qian and Hu. 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:
Pengfei Hu, Department of Orthopedic Surgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
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