Abstract
INTRODUCTION: Coronaviruses are a large family of positive-stranded nonsegmented RNA viruses with genomes of 26-32 kilobases in length. Human coronaviruses are commonly associated with mild respiratory illness; however, the past three decades have seen the emergence of severe acute respiratory coronavirus (SARS-CoV), middle eastern respiratory coronavirus (MERS-CoV), and SARS-CoV-2 which is the etiologic agent for COVID-19. Severe forms of COVID-19 include acute respiratory distress syndrome (ARDS) associated with cytokine release syndrome that can culminate in multiorgan failure and death. Among the proinflammatory factors associated with severe COVID-19 are the chemokines CCL2, CCL3, CXCL8, and CXCL10. Infection of susceptible mice with murine coronaviruses, such as mouse hepatitis virus (MHV), elicits a similar chemokine response profile as observed in COVID-19 patients and these in vivo models have been informative and show that targeting chemokines reduces the severity of inflammation in target organs. AREAS COVERED: PubMed was used using keywords: Chemokines and coronaviruses; Chemokines and mouse hepatitis virus; Chemokines and COVID-19. Clinicaltrials.gov was used using keywords: COVID-19 and chemokines; COVID-19 and cytokines; COVID-19 and neutrophil. EXPERT OPINION: Chemokines and chemokine receptors are clinically relevant therapeutic targets for reducing coronavirus-induced inflammation.