Molecular mechanisms and signaling pathways involved in immunopathological events of COVID-19

Abstract

Introduction: COVID-19, a novel coronavirus that causes severe acute respiratory syndrome (SARS-CoV-2), is currently regarded as the most serious viral disease. During corona infection, viruses bind to host proteins and employ a variety of cellular pathways for their own purposes. Cell signaling is important for the regulation of cellular function. SARS-CoV-2 infection alters multiple signal transduction pathways that are critical for cell survival. The virus causes a severe and prolonged period of hypercytokinemia with misusing of these signaling cascades. Hyperactivation of the host immune system after infection with SARS-CoV-2 is the main cause of death in COVID-19 patients. Thus, to develop effective therapeutic approaches, it is necessary to first understand the problem and the underlying molecular pathways implicated in host immunological function/dysfunction. A number of intracellular signaling cascades have been implicated in infected cell pathways, including MAPK pathway, NF-Kappa B pathway, JAK-STAT signaling pathway, PI3K/AKT/mTOR pathway and TLRI signaling cascades. Here, we have presented the molecular insights on the potential mechanisms involved in immunopathological events of COVID-19.