Fig. 1.
Schematic representation of SARS-CoV-2 infection, its replication, host cell activation and potential points to be considered for targeting the viral infection. The first step requires agents interfering with viral entry and its replication. Thus, during viral entry, SARS-CoV-2 mAbs may be useful (1). HCQ acts by altering the lysosomal activity (2), while remdesivir inhibitis RNA polymerase (3). The second step focuses on targeting host cell activation. In this setting, colchicine acts by inhibiting NLRP3 inflammasome and caspace-1 (4). Anakinra is an IL-1 receptor antagonist (5), while TCZ and SAR are IL-6 receptor antagonists (6). BARI and TOFA inhibit JAKs (7). Finally, DX acts by inhibiting cytokine receptor signaling, gene transcription, cell differentiation, proliferation and survival (7), (8). SARS-CoV-2: severe acute respiratory syndrome coronavirus-2; ACE2: angiotensin converting enzyme 2; IL-6R: interleukin-6 receptor; Cytokine R: cytokine receptor; TLR: toll-like receptor; IL-1R: interleukin-1 receptor; NLR: nod-like receptor; JAK: Janus Kinase; STAT: signal transducer and activator of transcription; IRAK: interleukin-1 receptor-associated kinase; STATP: signal transducer and activator transcription phosphorylation; NFkB: nuclear factor kB; AP-1: activated protein-1; NLRP3: nod-like receptor protein-3; Pro-IL-β: pro interleukin-1β; TNFα: tumor necrosis factor α; IL-6: interleukin-6; IL-1β: interleukin-1β.