Role of IFN and Complements System: Innate Immunity in SARS-CoV-2

Abstract

The critical role of the innate immune system has been confirmed in driving local and systemic inflammation and the cytokine release storm in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This dysregulated immune response is focused on interferon (IFN) and complement activation, which are crucial for the development of metabolic inflammation, local lung tissue damage, and systemic multi-organ failure. IFNs control viral infections by inducing expression of IFN-stimulated genes (ISGs) that restrict distinct steps of viral replication. Therefore, in this review article, we propose the mechanism of SARS-CoV-2-associated acute respiratory disease syndrome, and assess treatment options by considering IFNs and by targeting IFN-antagonist SARS-CoV-2 virulent gene products. Furthermore, we elaborate on the mechanism of the amplified complement-mediated inflammatory cytokine storm, and propose an antiviral and immunotherapeutic strategy against coronavirus disease 2019 (COVID-19).

Keywords:

• SARS-CoV-2
• innate immune system
• cytokines
• complement
• IFNs
• virulent

Acknowledgments

We would like to forward our gratitude to the authors of the articles that we used to generate this review report.

Abbreviations

C, complement; Nsp, non-structural protein; ORF, open reading frame; IL-6, interleukin-6; MERS, Middle East respiratory syndrome; SARS, severe acute respiratory syndrome; COVID-19, coronavirus disease 2019.

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Disclosure

The authors declare that they have no any competing interest.