Mechanisms and potential therapeutic targets of hyperinflammatory responses in SARS-CoV-2.

Abstract

Coronavirus infection is now the leading cause of death globally. Despite the several bedsides- to- bench investigations carried out by researchers all over the world to identify the best prophylactic and therapeutic options for this deadly virus, no novel vaccine or treatment drug has been developed. Accumulating evidence suggests that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is associated with hyper inflammation characterized by excessive release of pro-inflammatory cytokines known as a cytokine storm. The hallmark of this unregulated inflammatory response includes viral sepsis, pneumonitis shock, coagulopathy, and acute respiratory distress syndrome (ARDS) which is the major cause of death in COVID-19 patients. In the midst of cytokine storm and coagulopathy, anti-viral agents alone will not provide the much-needed therapeutic effect. Hence, the need to combine anti-inflammatory agents such as interferons, angiotensinogen converting enzyme 2 (ACE-2) inhibitors, interleukin 6 (IL-6), and Janus kinase (JAK) family inhibitors, anticoagulants and other agents involved in inflammation resolution. This review critically presented a comprehensive overview of SAR-CoV-2, unveiled the mechanisms of the inflammatory response in SARS-CoV-2 and also highlighted possible specific prophylactic and therapeutic interventions that will circumvent inflammatory induced deaths in COVID-19 patients. Keywords: COVID-19; SARS-CoV-2; cytokine storm; coagulopathy and anti-inflammatory.