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Insights into Innate Immune Response Against SARS-CoV-2 Infection Cover

Insights into Innate Immune Response Against SARS-CoV-2 Infection

Open Access
|Jul 2021

Abstract

The innate immune system is mandatory for the activation of antiviral host defense and eradication of the infection. In this regard, dendritic cells, natural killer cells, macrophages, neutrophils representing the cellular component, and cytokines, interferons, complement or Toll-Like Receptors, representing the mediators of unspecific response act together for both activation of the adaptive immune response and viral clearance. Of great importance is the proper functioning of the innate immune response from the very beginning. For instance, in the early stages of viral infection, the defective interferon response leads to uncontrolled viral replication and pathogen evasion, while hypersecretion during the later stages of infection generates hyperinflammation. This cascade activation of systemic inflammation culminates with cytokine storm syndrome and hypercoagulability state, due to a close interconnection between them. Thus an unbalanced reaction, either under- or over- stimulation of the innate immune system will lead to an uncoordinated response and unfavorable disease outcomes. Since both cellular and humoral factors are involved in the time-course of the innate immune response, in this review we aimed to address their gradual involvement in the antiviral response with emphasis on key steps in SARS-CoV-2 infection.

DOI: https://doi.org/10.2478/rrlm-2021-0022 | Journal eISSN: 2284-5623 | Journal ISSN: 1841-6624
Language: English
Page range: 255 - 269
Submitted on: Jun 14, 2021
Accepted on: Jul 10, 2021
Published on: Jul 31, 2021
Published by: Romanian Association of Laboratory Medicine
In partnership with: Paradigm Publishing Services
Publication frequency: 4 issues per year

© 2021 Adina Huțanu, Anca Meda Georgescu, Akos Vince Andrejkovits, William Au, Minodora Dobreanu, published by Romanian Association of Laboratory Medicine
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.