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Review
. 2020 Nov 25;21(23):8962.
doi: 10.3390/ijms21238962.

Role of microRNA and Oxidative Stress in Influenza A Virus Pathogenesis

Md Mamunul Haque  1 , Dhiraj P Murale  1 , Jun-Seok Lee  1   2
Affiliations
Review

Role of microRNA and Oxidative Stress in Influenza A Virus Pathogenesis

Md Mamunul Haque et al. Int J Mol Sci. .

Abstract

MicroRNAs (miRNAs) are non-coding RNAs that regulate diverse cellular pathways by controlling gene expression. Increasing evidence has revealed their critical involvement in influenza A virus (IAV) pathogenesis. Host-IAV interactions induce different levels of oxidative stress (OS) by disrupting the balance between reactive oxygen species (ROS) and antioxidant factors. It is thought that miRNA may regulate the expression of ROS; conversely, ROS can induce or suppress miRNA expression during IAV infection. Thus, miRNA and OS are the two key factors of IAV infection and pathogenesis. Accordingly, interactions between OS and miRNA during IAV infection might be a critical area for further research. In this review, we discuss the crosstalk between miRNAs and OS during IAV infection. Additionally, we highlight the potential of miRNAs as diagnostic markers and therapeutic targets for IAV infections. This knowledge will help us to study host-virus interactions with novel intervention strategies.

Keywords: influenza A virus; microRNA; oxidative stress.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The involvement of miRNAs that modulate host-mediated pathways. IAV infection alters the expression profiles of certain cellular miRNAs related to viral replication, pathogenesis, and antiviral responses. Certain miRNAs have important roles in inflammatory responses and apoptotic pathways as well.
Figure 2
Figure 2
Involvement of miRNAs in the pathogenesis of an influenza virus. The IAV invades the cell and is taken up by the endosome. Upon the rupture of the endosome, the virus releases its genetic material into the nucleus. In turn, transcription, translation, and replication processes are carried out, followed by the release of newly synthesized viral progenies. Several microRNAs regulate these pathways to inhibit or promote IAV pathogenesis.
Figure 3
Figure 3
Impact of oxidative stress upon IAV infection. The overproduction of ROS contributes to different pathological changes (i.e., virus replication and cellular inflammation) and leads to apoptosis. On the other hand, medium levels of ROS may induce antioxidant defense systems to control redox homeostasis and promote cell survival in the infected cells.
Figure 4
Figure 4
The different interactions among miRNA, OS, and IAV infection. Some specific miRNAs are aberrantly expressed by IAV infection and work as upstream regulators or downstream effectors in OS conditions (→ indicates activation, ⊥ indicates inhibition).
See this image and copyright information in PMC

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