Chemokines and chemokine receptors during COVID-19 infection

Abstract

Chemokines are crucial inflammatory mediators needed during an immune response to clear pathogens. However, their excessive release is the main cause of hyperinflammation. In the recent COVID-19 outbreak, chemokines may be the direct cause of acute respiratory disease syndrome, a major complication leading to death in about 40% of severe cases. Several clinical investigations revealed that chemokines are directly involved in the different stages of SARS-CoV-2 infection. Here, we review the role of chemokines and their receptors in COVID-19 pathogenesis to better understand the disease immunopathology which may aid in developing possible therapeutic targets for the infection.

Keywords: AECs, airway epithelial cells; AP-1, Activator Protein 1; ARDS; ARDS, acute respiratory disease syndrome; BALF, bronchial alveolar lavage fluid; CAP, community acquired pneumonia; COVID-19; CRS, cytokine releasing syndrome; Chemokine Receptors; Chemokines; DCs, dendritic cells; ECM, extracellular matrix; GAGs, glycosaminoglycans; HIV, human immunodeficiency virus; HRSV, human respiratory syncytial virus; IFN, interferon; IMM, inflammatory monocytes and macrophages; IP-10, IFN-γ-inducible protein 10; IRF, interferon regulatory factor; Immunity; MERS-CoV, Middle East respiratory syndrome coronavirus; NETs, neutrophil extracellular traps; NF-κB, Nuclear Factor kappa-light-chain-enhancer of activated B cells; NK cells, natural killer cells; PBMCs, peripheral blood mononuclear cells; PRR, pattern recognition receptors; RSV, rous sarcoma virus; SARS-CoV, severe acute respiratory syndrome coronavirus; SARS-CoV-2; TLR, toll like receptor; TRIF, TIR-domain-containing adapter-inducing interferon-β.