Future perspective: biologic agents in patients with severe COVID-19.

The SARS-CoV-2 is a β-CoV, which is enveloped by non-segmented positive-stranded RNA virüs. When β-CoV infects the respiratory tract, it can cause mild and/or severe acute respiratory syndrome (SARS) with consequent release of cytokines/mediators, including interleukin (IL)-1β, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8 (CXCL8), IL-10, IP10, IL-12, IL-13, IL-17, IL-33, IL-25, IL-37, IL-38, GCSF, GM-CSF, HGF, IP-10, MCP-1, MIP-1α (also known as CCL3), IFN-γ, IFN-α, TRAIL, MCSF, and TNF-α. Our hypothesis of writing this article can be summarized as; if the monoclonal antibody (mAb) administered by us does not inhibit the immune response for the β-CoV and inhibits uncontrolled-adaptive/hyperimmune responses (also called cytokine storm) on endothelium level, then it may cause severe coronavirus disease 2019 (COVID-19). Anakinra is a human IL-1 receptor antagonist. By inhibiting IL-1α/IL-1β competitively from binding to the IL-1 type-I receptor, anakinra, neutralizes the activity that pertains to these key mediators of autoinflammatory and/or immune processes. Tocilizumab is a blocker of IL-6R that can effectively block IL-6 signal transduction pathway. Omalizumab that binds to the CH3 domain is near to the binding site for the high-affinity IgE Fc receptors type-I of human IgE. Myocardial, lung and hepatorenal injury in patients with COVID-19 could be due to cytokine storm, hypoxic injury, or/and direct endothelial/vascular injury. We propose combination of mAbs with remdesivir and/or favipiravir in severe COVID-19 cases, such as septic shock, acute respiratory deficiency syndrome, and/or multiple organ failure. Finally, we highlight the therapeutic mAbs that target patients with severe COVID-19.