Inflammatory pathways and potential therapies for COVID-19: A mini review

Abstract

The public health crisis of the novel coronavirus disease (COVID-19) is alarming since January 2020. COVID-19 genome (SARS-CoV-2) is related to other highly pathogenic coronaviruses SARS-CoV (severe acute respiratory syndrome coronavirus) and MERS-CoV (Middle East respiratory syndrome coronavirus). Amino acid substitutions in some of SARS-CoV-2 proteins resulted in mutations proposing more virulent and contagious properties for this novel virus. Coronavirus penetrates the host cell via endocytosis and once infected, immune responses are triggered to fight against the pathogen. Innate immune response activates major transcription factors to secrete proinflammatory cytokines and type 1 interferon response (T1INF) to induce antiviral immunity. While adaptive immunity initiates cascade of B-cells antibody mediated and T-cells cellular mediate immunities, several mechanisms are raised by SARS-CoV-2 to evade host immune response. Consequently, a surge of proinflammatory cytokines, known as cytokine storm (CS) are released. Failure to manage CS results in several pathological complications as acute respiratory distress syndrome (ARDS). Although researches have not discovered an effective treatment against SARS-CoV-2, recent therapeutic approaches recommending the use of anti-inflammatories in combination with antivirals and some repurposed drugs for COVID-19 patients. Future medications should be designed to target essential hallmarks in the CS to improve clinical outcomes.