A comparative analysis of miRNA expression in human lung epithelial cells during infection with influenza virus and RNAse treatment

Abstract

The influenza virus is capable of causing an acute respiratory infection that affects 5 to 20% of the human population annually. The spread of the influenza virus epidemic occurs within a short period of time due to its high contagiousness. In addition, the annual circulation of the virus among livestock and waterfowl increases for new strains a risk of zoonotic transmission to human populations with unestablished yet immunity. In addition, several high virulence pandemic strains have emerged in the past, and the threat of a new pandemic strain is constantly present. The identification of the physiological and molecular aspects related to influenza A can help developing therapeutic approaches to lower side effects associated with the disease caused by this virus. The RNA profile in human cells changes after exposure to influenza virus. Currently, scientists have been increasingly paying attention to study of microRNAs capable of regulating gene expression. Thus, microRNAs may play a critical role in a wide range of biological processes and have been previously shown to be important effectors in multilayered host-pathogen interplay. The study of the quantitative and qualitative miRNA composition is an important tool for diagnosing and treating various diseases at an early stage. The aim of this work is to analyze the microRNA profile for investigating an effect of influenza A (H1N1) virus on human lung epithelial adenocarcinoma cells. The microRNA fraction was isolated by using phenol-chloroform extraction and analyzed with high-throughput sequencing on the SOLiD 550xl wildfire platform using bioinformatic methods. The study examined 129 mature microRNAs from uninfected cells treated with Bacillus pumilus RNAse as well as cells infected with the influenza A (H1N1) virus. It was found that uninfected cells treated with RNase contained 2-fold more different microRNAs that can participate in suppressing carcinogenesis. The peak expression in influenza virus-infected cells is observed for miR-6884-5p. For cells treated with RNase, the peak expression is observed for miR-3923 that was higher by 400-fold than in cells infected with the influenza virus. We hypothesize that intact viruses or their intracellular components are able to alter cellular metabolism by skewing it to decreased resistance to carcinogenesis processes.