Abstract
One major symptom found in COVID-19 patients is the low levels of differentiated T-cells found especially in hospitalized patients. Furthermore, these patients suffer from T-cell exhaustion. NFkB plays a large role in the differentiation and survival of T-cells so this research analyzes how the SARS-CoV-2 virus could impact NFkB activation. Viroporins are incredibly important to viruses because of their ability to insert ion channels into the cell. As overactivation of the IKK complex leads to T-cell failure, this research focuses on the viroporins that activate PKCtheta to understand if the addition of the viroporin ion channel changes the activation of NFkB. This research adapts an existing computational model that models transcription factors including NFkB. To do this, the model was changed to add a calcium, potassium, and sodium ion channel and analyzed the immune response separately. This research found that the virus can add a sodium channel which can effectively slow down the activation of NFkB leading to a smaller immune response. This serves a potential mechanism for the survival of the SARS-CoV-2 virus longer in a host cell.
How to Cite:
, V. & , S.,
(2022) “Incorporating COVID-19 Ion Channel Adaptations to Understand Immune Response ”,
Journal of Student-Scientists' Research 4.
doi: https://doi.org/10.13021/jssr2022.3427
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