Early Immune Signaling Among Different Genera Of Influenza Viruses
Three genera of Influenza can cause illness in humans. However, the effects of these viruses differ within the human population. Influenza A is known to cause both pandemics and seasonal epidemics while Influenza B only causes seasonal epidemics. In contrast, Influenza C reportedly causes milder symptoms compared to Influenza A and B. We hypothesized that virus-specific differences in the immune response may account for these different clinical illnesses. When a virus enters a cell, viral products are sensed and lead to the production of antiviral molecules called interferons. These interferons in turn cause the activation of interferon-stimulated genes which produce proteins that block the life cycle of the virus. Studies of other viruses have shown that the ability to produce interferons correlates with disease severity. While it’s been reported that Influenza B induces an earlier interferon response than Influenza A, the timing and magnitude of interferon gene expression have yet to be fully explored and compared between the viruses. This project aims to investigate the innate immune response to influenza viruses by comparing the interferon response to Influenza A to that of Influenza B. We hypothesize that Influenza B, a less pathogenic influenza virus, will have an earlier and more robust interferon response than Influenza A. Quantitative PCR was utilized to compare the mRNA expression of Influenza viruses and two interferon-stimulated genes in cells infected with either Influenza A or Influenza B virus. It was found that Influenza B virus expression is seen earlier and at higher levels than Influenza A, but only one interferon-stimulated gene showed the expected expression earlier and to higher levels in Influenza B-infected cells. However, distinct patterns of expression emerged. This preliminary data will be used to determine optimal time points for comparison of the viruses to then inform a broader RNAseq study that can look at many more genes. By understanding the time course of infection, exogenous interferon products could be given to sick patients to improve outcomes.