Abstract
Coronavirus 2019 (COVID-19) is an infection caused by the newly discovered severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The innate system is the first line of defense against pathogens and diverse infectious agents. It has been suggested to play a key role in the development of the cytokine storm and promoting other severe forms of chronic inflammation. Toll-like receptors (TLRs) are crucial for the innate immune response to pathogens. TLR8 is expressed on myeloid cells and phagocytes, where it acts as an endosomal sensor of RNA degradation. The present study aimed to investigate whether the severity of COVID-19 symptoms could be associated with certain genetic variations of TLR8. We collected blood samples from 45 participants who had moderate to severe respiratory symptoms and a positive COVID-19 PCR test result within 3-5 days of sample collection. Genomic DNA was extracted from the blood samples, then exon 2 of the TLR8 gene was amplified with polymerase chain reaction (PCR), and PCR products were utilized for sequencing. DNA sequencing showed an average of 99.63% sequence homology in TLR8 across all samples. Base-pair homology analysis revealed variations in TLR8 at two positions: X:12937804 (rs5744080) and X:12937513 (rs2159377). The results revealed that these two mutations had no detrimental effect on symptoms in the target population. Our results show that specific SNPs did not affect the final receptor function of TLR8. This finding also indicates that the innate immune response, once activated, does not depend on the innate immune receptor's level of affinity for identifying their respective glycoprotein structures on the SARS-CoV-2 virus.