The Effect And Mechanism Of MicroRNA-17-5p In Influenza A Virus Infection

The influenza virus is an RNA virus that can cause respiratory infections and,in severe cases,even death.With a wide host range,these viruses are able to spread almost anywhere on Earth.Seasonal epidemics occur during the spring and winter of each year,and pandemics can also be triggered,posing a serious threat to public health security.Furthermore,the high mutation rate of influenza A viruses makes it challenging to develop effective vaccines and drugs.Therefore,there is an urgent need to find novel alternative targets to prevent and treat influenza infection.MicroRNA(miRNA)are small non-coding RNAs that participate in numerous biological processes.Virus infections can cause differential expression of miRNAs,which can be utilized by the host or virus to initiate the host’s immune response or the virus’s immune escape.Therefore,miRNAs represent a valuable source for studying the mechanisms underlying virus-host interactions and may provide new targets for the development of influenza vaccines and antiviral drugs.To verify the role of miRNA in influenza virus infection,qPCR,western blot,target gene overexpression and knockdown techniques and virus titer test were used in this study.The main results of the present research are as follows:1.To investigate the potential role of miR-17-5p in influenza virus infection,we utilized qPCR to examine the expression of miR-17-5p in A549 cells infected with H5N1 and H1N1 subtypes of IAV.The study revealed a significant increase in the expression level of miR-17-5p in A549 cells infected with H5N1 and H1N1 subtypes IAV 12 and 24 hours after IAV infection.This finding suggests that miR-175p may have a regulatory function in the process of IAV infection.Next,we transfected miR-17-5p mimic into A549 cells,and infected H5N1 and H1N1 24 hours after transfection.Virus culture supernatants were obtained 24 hours after infected,and used TCID50 to measure the virus titer of virus-containing supernatants.The results showed that virus titer was significantly increased after miR-17-5p mimic transfection compared with the control group.2.It is well known that miRNAs usually exert their effects by regulating the transcription of downstream target genes.Therefore,in this study,miRNA target gene prediction website,dual luciferase reporter gene experiment and western blot were used to verify the target gene of miR-17-5p.It was found that transfection of miR-17-5p mimic can inhibit the expression of TRIM37,while transfection of miR17-5p inhibitor can promote the expression of TRIM37,indicating that TRIM37 is indeed the target gene of miR-17-5p.3.To further investigate the mechanism by which miR-17-5p regulates IAV replication,we overexpressed or interference TRIM37 in A549 cells to examine its effect on viral replication.The results indicated that TRIM37 overexpression may inhibit IAV replication,while TRIM37 interference may promote IAV replication.In addition,TRIM37 also participates in the immune response of host cells and regulates the expression of cytokines such as IFN-α,TNF-α,IL-6 and IL-1β.In summary,this study proves that influenza virus infection can cause an increase in the expression of host miR-17-5p,and the expression of miR-17-5p can enhance the replication of IAV,and this inhibition is through miR-17-5p Regulated by targeting TRIM37.This study elucidated the relationship between miR-17-5p in the interaction between influenza virus and host,enriched the regulatory role of miRNA in influenza virus infection,and provided a reference for the study of host antiviral mechanism and the development of new antiviral drugs.