Abstract
In recent years, airway remodelling and tissue hypersensitization have been discovered to be key components in the development of asthma. No cure is known, only temporary medical and practical alleviations and the prospect of the body adapting to handle it better. It is the subject of ongoing research, yet its exact genotype is elusive, overlapping with many other diseases. Determining its genetic basis provides more opportunities for therapeutic intervention, which could eventually lead to halting and even reversing the physiological effects of asthma.
Could STAT2 and OAS genes (OAS1, OAS2, OAS3) be involved in the asthmatic inflammatory response? This study compares their differential expressions in response to HRV16 infection between asthmatic and non-asthmatic bronchiolar airway tissues; then by examining the literature to understand their functions and piece together any emergent theories.
Similar ratios of statistically significant upregulation were observed across all genes, suggesting an upstream cause rather than polymorphisms. All four genes play major roles in the antiviral immune response; OAS proteins defend against an array of viruses, but appear to be an axis to instigating apoptosis.
Regulation of these genes, controlling 2-5A production, and increasing SOCS presence (managing OAS-induced cytokine) are all potential therapeutic targets for alleviating asthma symptoms, reducing or preventing immune overreaction & inflammation, and retarding or reversing tissue sensitization & airway remodelling.
An alternative antiviral effect of OAS has been discovered previously, independent of RNaseL. Bypassing the magnified destructive effects of RNase in asthmatics by utilizing this pathway may be a desirable treatment.
STAT2 and OAS genes are known components of the antiviral response, but haven't yet been associated with asthma. This study demonstrates increased expression in the asthmatic antiviral response, but further research is required to determine the cause. The therapeutic potentials revealed may be beneficial contributions to the field of asthma treatment.
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