Open Access

Downregulation of microRNA‑221 facilitates H1N1 influenza A virus replication through suppression of type‑IFN response by targeting the SOCS1/NF‑κB pathway

  • Authors:
    • Nali Zhang
    • Yuan Ma
    • Yuheng Tian
    • Yafei Zhou
    • Yuhua Tang
    • Shaobo Hu
  • View Affiliations

  • Published online on: May 6, 2021     https://doi.org/10.3892/mmr.2021.12136
  • Article Number: 497
  • Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Accumulating data has indicated that host microRNAs (miRNAs/miRs) play essential roles in innate immune responses to viral infection; however, the roles and the underlying mechanisms of miRNAs in influenza A virus (IAV) replication remain unclear. The present study examined on the effects of miRNAs on hemagglutinin (H)1 neuraminidase (N)1 replication and antiviral innate immunity. Using a microarray assay, the expression profiles of miRNA molecules in IAV‑infected A549 cells were analyzed. The results indicated that miR‑221 was significantly downregulated in IAV‑infected A549 cells. It was also observed that IAV infection decreased the expression levels of miR‑221 in A549 cells in a dose‑ and time‑dependent manner. Functionally, upregulation of miR‑221 repressed IAV replication, whereas knockdown of miR‑221 had an opposite effect. Subsequently, it was demonstrated that miR‑221 overexpression could enhance IAV‑triggered IFN‑α and IFN‑β production and IFN‑stimulated gene expression levels, while miR‑221‑knockdown had the opposite effect. Target prediction and dual luciferase assays indicated that suppressor of cytokine signaling 1 (SOCS1) was a direct target of miR‑221 in A549 cells. Furthermore, knockdown of SOCS1 efficiently abrogated the influences caused by miR‑221 inhibition on IAV replication and the type‑I IFN response. It was also found that the miR‑221 positively regulated NF‑κB activation in IAV‑infected A549 cells. Taken together, these data suggested that miR‑221‑downregulation promotes IAV replication by suppressing type‑I IFN response through targeting SOCS1/NF‑κB pathway. These findings suggest that miR‑221 may serve as a novel potential therapeutic target for IAV treatment.
View Figures
View References

Related Articles

Journal Cover

July-2021
Volume 24 Issue 1

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Zhang N, Ma Y, Tian Y, Zhou Y, Tang Y and Hu S: Downregulation of microRNA‑221 facilitates H1N1 influenza A virus replication through suppression of type‑IFN response by targeting the SOCS1/NF‑κB pathway. Mol Med Rep 24: 497, 2021.
APA
Zhang, N., Ma, Y., Tian, Y., Zhou, Y., Tang, Y., & Hu, S. (2021). Downregulation of microRNA‑221 facilitates H1N1 influenza A virus replication through suppression of type‑IFN response by targeting the SOCS1/NF‑κB pathway. Molecular Medicine Reports, 24, 497. https://doi.org/10.3892/mmr.2021.12136
MLA
Zhang, N., Ma, Y., Tian, Y., Zhou, Y., Tang, Y., Hu, S."Downregulation of microRNA‑221 facilitates H1N1 influenza A virus replication through suppression of type‑IFN response by targeting the SOCS1/NF‑κB pathway". Molecular Medicine Reports 24.1 (2021): 497.
Chicago
Zhang, N., Ma, Y., Tian, Y., Zhou, Y., Tang, Y., Hu, S."Downregulation of microRNA‑221 facilitates H1N1 influenza A virus replication through suppression of type‑IFN response by targeting the SOCS1/NF‑κB pathway". Molecular Medicine Reports 24, no. 1 (2021): 497. https://doi.org/10.3892/mmr.2021.12136