Identification of the mechanism of innate immune response against SARS-CoV-2

The globe is currently experiencing a situation that is similar to the Spanish flu pandemic of 1918: Coronavirus Disease 2019 (COVID-19), which is brought on by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been producing a pandemic since March 2020. The exact pathogenesis of SARS-CoV-2 and the innate immune system induced by the virus remain poorly understood. However, using rapid genome sequencing will help researchers elucidate the structure and function of the virus, which could lead to a better understanding of SARS-CoV-2. In response to viral infection, cells of the innate immune system produce antiviral cytokines, which are crucial in preventing viral reinfection and reducing viral replication and pathogenesis. Angiotensin-converting enzyme 2 (ACE2) membrane protein overexpression in airway epithelial cells has been found to be mediated by the antiviral cytokines INF-γ and TNF-α. The spike protein is essential for endogenous immunity and a major element in setting off a cytokine storm since it is the main binding protein of SARS-CoV-2. In this study, the differential gene expression of the cell experimental group was examined using RNA sequencing technology, and the results were compared to those from clinical sample analysis. Toll-like receptors (TLRs) play a crucial role in the innate immune system, which uses them to identify various viral proteins and release type I interferons and pro-inflammatory cytokines to combat infection. In our study, when comparing to the elderly patient group with the healthy control group, we found that TLR2, TLR5, TLR7/8 are activated, which activate the NF-κB pathway via the downstream MyD88 complex, leading to the release of inflammatory factors, but IRF3/7 cannot be activated, resulting in failed activation of type I interferons. Our study also showed that cytokine detection in the in vitro cell studies confirmed the increased expression of IL-2, IL-6, INF-γ, and TNF-α. Clinical COVID-19 patients had higher levels of IL-2, IL-6, INF-γ, and TNF-α expression while having fewer lymphocytes, which may play a significant role in cytokine storm. The inflammatory response can be balanced and the recovery of severe patients is aided by cytokine storm-blocking medications. It is important to find new prediction molecules or proteins for severe COVID-19 disease.