tetano
Editor, Senior Moderator
FASEB J
. 2026 Jan 15;40(1):e71396.
doi: 10.1096/fj.202502542R. Roles of Cellular Noncoding RNAs in Productive Infection of Influenza A Virus
Ying Zeng[SUP] 1 2 [/SUP], Tianqi Wang[SUP] 1 2 [/SUP], Aijia Sun[SUP] 1 [/SUP], Chuan Xia[SUP] 1 [/SUP]
Affiliations
Influenza A virus (IAV) causes annual epidemics and occasional pandemics, remaining a threat to public health and economy worldwide. It has been established that many cellular noncoding RNAs (ncRNAs) are differentially expressed during IAV infection. These ncRNAs vigorously modulate the productive infection of the virus through diverse mechanisms, such as directly affecting the virus life cycle, altering the cellular signaling pathways, or regulating the host's innate immune response to viral infection. Some of the ncRNAs are deemed to be essential for IAV replication, while others, conversely, show a negative impact on the virus. Nevertheless, the mode of actions behind these regulatory effects has not been extensively elucidated. In this review, we summarize the roles of cellular differentially expressed ncRNAs in modulating IAV infection, highlighting the molecular mechanisms of the ncRNA-virus interactions, providing a framework for inventing novel ncRNA targeted therapeutics to control influenza.
Keywords: cellular signaling pathway; influenza A virus; innate immunity; noncoding RNA; virus life cycle; virus–host interaction.
. 2026 Jan 15;40(1):e71396.
doi: 10.1096/fj.202502542R. Roles of Cellular Noncoding RNAs in Productive Infection of Influenza A Virus
Ying Zeng[SUP] 1 2 [/SUP], Tianqi Wang[SUP] 1 2 [/SUP], Aijia Sun[SUP] 1 [/SUP], Chuan Xia[SUP] 1 [/SUP]
Affiliations
- PMID: 41460636
- DOI: 10.1096/fj.202502542R
Influenza A virus (IAV) causes annual epidemics and occasional pandemics, remaining a threat to public health and economy worldwide. It has been established that many cellular noncoding RNAs (ncRNAs) are differentially expressed during IAV infection. These ncRNAs vigorously modulate the productive infection of the virus through diverse mechanisms, such as directly affecting the virus life cycle, altering the cellular signaling pathways, or regulating the host's innate immune response to viral infection. Some of the ncRNAs are deemed to be essential for IAV replication, while others, conversely, show a negative impact on the virus. Nevertheless, the mode of actions behind these regulatory effects has not been extensively elucidated. In this review, we summarize the roles of cellular differentially expressed ncRNAs in modulating IAV infection, highlighting the molecular mechanisms of the ncRNA-virus interactions, providing a framework for inventing novel ncRNA targeted therapeutics to control influenza.
Keywords: cellular signaling pathway; influenza A virus; innate immunity; noncoding RNA; virus life cycle; virus–host interaction.