The effect of environmental pollution on immune evasion checkpoints of SARS-CoV-2


ENGİN A. B. , ENGİN E. D. , ENGİN A.

ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY, vol.81, 2021 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Review
  • Volume: 81
  • Publication Date: 2021
  • Doi Number: 10.1016/j.etap.2020.103520
  • Journal Name: ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, CAB Abstracts, Chemical Abstracts Core, EMBASE, Environment Index, Greenfile, MEDLINE, Pollution Abstracts, Veterinary Science Database
  • Keywords: Aryl hydrocarbon receptor, Environmental pollution, Indoleamine 2,3-dioxygenase, Severe acute respiratory syndrome coronavirus 2, Angiotensin-converting enzyme 2, Interferons, ARYL-HYDROCARBON RECEPTOR, POLYCYCLIC AROMATIC-HYDROCARBONS, SUBCELLULAR-LOCALIZATION, AH RECEPTOR, IN-VITRO, ACTIVATION, KYNURENINE, TRYPTOPHAN, INDUCTION, SEVERITY
  • Gazi University Affiliated: Yes

Abstract

Many diverse strategies allow and facilitate severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to evade antiviral innate immune mechanisms. Although the type I interferon (IFN) system has a critical role in restricting the dissemination of viral infection, suppression of IFN receptor signals by SARS-CoV-2 constitutes a checkpoint that plays an important role in the immune escape of the virus. Environmental pollution not only facilitates SARS-CoV-2 infection but also increases infection-associated fatality risk, which arises due to Systemic Aryl hydrocarbon Receptor (AhR) Activation Syndrome. The intracellular accumulation of endogenous kynurenic acid due to overexpression of the indoleamine 2,3-dioxygenase (IDO) by AhR activation induces AhRinterleukin-6 (IL-6)-signal transducers and activators of the transcription 3 (STAT3) signaling pathway. The AhR-IDO1-Kynurenine pathway is an important checkpoint, which leads to fatal consequences in SARS-CoV-2 infection and immune evasion in the context of Treg/Th17 imbalance and cytokine storm.