Effect of Influenza-A Virus Infection On Inflammatory gene Expression Profiles Of Leukocyte

Abstract Objectives: Influenza A virus is a major cause of respiratory infections with high rates of morbidity and mortality worldwide. An understanding of how InfluenzaA virus (IAV) modulates host cellular responses is critically important to explore the molecular mechanisms of viral-host interaction. The aims of this study are; to detect changes in the mRNA expression in a panel of inflammatory genes in the leukocyte concentrate Buffy coat of IAV infected patients after 48 hrs of infection. Also to determine the relation between the inflammatory gene expression and asthma in IAV patients. Methods: Blood from 90 hospital admitted patients suffering from flu within the first 48 hrs of infection was tested for IgM- influenzaA virus. Only eight patients were positive. Leukocytes from the IAV positive patients were tested for a panel of 84 inflammatory genes using real time-PCR array technology. Results: Only 14 inflammatory genes (IL1B, IL8, IL10, IL13, CCL2, CCL5, CCL7, CXCL1, CXCL10/IP-10, CX3CR1, C5, TNF, ABCF1, and BCL6) shown a significant upregulation fold ranging between between 1.01 and 121.35 fold in all the eight patients with a 100% frequency. The upregulation of IL8, IL 10, IL13, C5, CCL7, CCL5/RANTES, CXCL1 and CCL18mRNA transcription with high significance might suggest that the asthma complication during IAV infection is due to the stimulation of immune response. Six inflammatory genes (CEBPB, CCR1, IL1R1, MIF, CXCL11 and IL9R) shown a decrease in the mRNAexpression with fold ranged between -250.99 and -1.11 compared to control cells after recovery but with variable frequencies indicating a time dependent response. Conclusion: Our results revealed several alterations of many Leukocyte`s inflammatory gene expressions induced by influenza A virus. Eight of the over expressed genes are involved in asthma complication. All samples are mostly infected with related subtypes of influenza A viruses. These results may help for further analysis of influenza A virus role on host–pathogen interaction