The potential role of scavenger receptor B type I (SR‐BI) in SARS‐CoV‐2 infection

Abstract Scavenger receptor type B I (SR‐BI), the major receptor for high‐density lipoprotein (HDL) mediates the delivery of cholesterol ester and cholesterol from HDL to the cell membrane. SR‐BI is implicated as a receptor for entry of severe acute respiratory syndrome coronavirus type 2 (SARS‐CoV‐...

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Main Authors: Luay Alkazmi, Hayder M. Al‐kuraishy, Ali I. Al‐Gareeb, Athanasios Alexiou, Marios Papadakis, Hebatallah M. Saad, Gaber El‐Saber Batiha
Format: Article
Language:English
Published: Wiley 2023-04-01
Series:Immunity, Inflammation and Disease
Subjects:
Online Access:https://doi.org/10.1002/iid3.786
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author Luay Alkazmi
Hayder M. Al‐kuraishy
Ali I. Al‐Gareeb
Athanasios Alexiou
Marios Papadakis
Hebatallah M. Saad
Gaber El‐Saber Batiha
author_facet Luay Alkazmi
Hayder M. Al‐kuraishy
Ali I. Al‐Gareeb
Athanasios Alexiou
Marios Papadakis
Hebatallah M. Saad
Gaber El‐Saber Batiha
author_sort Luay Alkazmi
collection DOAJ
description Abstract Scavenger receptor type B I (SR‐BI), the major receptor for high‐density lipoprotein (HDL) mediates the delivery of cholesterol ester and cholesterol from HDL to the cell membrane. SR‐BI is implicated as a receptor for entry of severe acute respiratory syndrome coronavirus type 2 (SARS‐CoV‐2). SR‐BI is colocalized with the angiotensin‐converting enzyme 2 (ACE2) increasing the binding and affinity of SARS‐CoV‐2 to ACE2 with subsequent viral internalization. SR‐BI regulates lymphocyte proliferation and the release of pro‐inflammatory cytokines from activated macrophages and lymphocytes. SR‐BI is reduced during COVID‐19 due to consumption by SARS‐CoV‐2 infection. COVID‐19‐associated inflammatory changes and high angiotensin II (AngII) might be possible causes of repression of SR‐BI in SARS‐CoV‐2 infection. In conclusion, the downregulation of SR‐BI in COVID‐19 could be due to direct invasion by SARS‐CoV‐2 or through upregulation of pro‐inflammatory cytokines, inflammatory signaling pathways, and high circulating AngII. Reduction of SR‐BI in COVID‐19 look like ACE2 may provoke COVID‐19 severity through exaggeration of the immune response. Further studies are invoked to clarify the potential role of SR‐BI in the pathogenesis of COVID‐19 that could be protective rather than detrimental.
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spelling doaj.art-232e4671340247728a4ea776199e3f432025-02-25T20:57:39ZengWileyImmunity, Inflammation and Disease2050-45272023-04-01114n/an/a10.1002/iid3.786The potential role of scavenger receptor B type I (SR‐BI) in SARS‐CoV‐2 infectionLuay Alkazmi0Hayder M. Al‐kuraishy1Ali I. Al‐Gareeb2Athanasios Alexiou3Marios Papadakis4Hebatallah M. Saad5Gaber El‐Saber Batiha6Biology Department, Faculty of Applied Sciences Umm Al‐Qura University Makkah Saudi ArabiaDepartment of Clinical Pharmacology and Medicine College of Medicine ALmustansiriyia University Baghdad IraqDepartment of Clinical Pharmacology and Medicine College of Medicine ALmustansiriyia University Baghdad IraqDepartment of Science and Engineering Novel Global Community Educational Foundation Hebersham New South Wales AustraliaDepartment of Surgery II University Hospital Witten‐Herdecke University of Witten‐Herdecke Wuppertal GermanyDepartment of Pathology Faculty of Veterinary Medicine Matrouh University Matrouh EgyptDepartment of Pharmacology and Therapeutics Faculty of Veterinary Medicine Damanhour University Damanhour EgyptAbstract Scavenger receptor type B I (SR‐BI), the major receptor for high‐density lipoprotein (HDL) mediates the delivery of cholesterol ester and cholesterol from HDL to the cell membrane. SR‐BI is implicated as a receptor for entry of severe acute respiratory syndrome coronavirus type 2 (SARS‐CoV‐2). SR‐BI is colocalized with the angiotensin‐converting enzyme 2 (ACE2) increasing the binding and affinity of SARS‐CoV‐2 to ACE2 with subsequent viral internalization. SR‐BI regulates lymphocyte proliferation and the release of pro‐inflammatory cytokines from activated macrophages and lymphocytes. SR‐BI is reduced during COVID‐19 due to consumption by SARS‐CoV‐2 infection. COVID‐19‐associated inflammatory changes and high angiotensin II (AngII) might be possible causes of repression of SR‐BI in SARS‐CoV‐2 infection. In conclusion, the downregulation of SR‐BI in COVID‐19 could be due to direct invasion by SARS‐CoV‐2 or through upregulation of pro‐inflammatory cytokines, inflammatory signaling pathways, and high circulating AngII. Reduction of SR‐BI in COVID‐19 look like ACE2 may provoke COVID‐19 severity through exaggeration of the immune response. Further studies are invoked to clarify the potential role of SR‐BI in the pathogenesis of COVID‐19 that could be protective rather than detrimental.https://doi.org/10.1002/iid3.786COVID‐19pro‐inflammatory cytokinesscavenger receptor type B I
spellingShingle Luay Alkazmi
Hayder M. Al‐kuraishy
Ali I. Al‐Gareeb
Athanasios Alexiou
Marios Papadakis
Hebatallah M. Saad
Gaber El‐Saber Batiha
The potential role of scavenger receptor B type I (SR‐BI) in SARS‐CoV‐2 infection
Immunity, Inflammation and Disease
COVID‐19
pro‐inflammatory cytokines
scavenger receptor type B I
title The potential role of scavenger receptor B type I (SR‐BI) in SARS‐CoV‐2 infection
title_full The potential role of scavenger receptor B type I (SR‐BI) in SARS‐CoV‐2 infection
title_fullStr The potential role of scavenger receptor B type I (SR‐BI) in SARS‐CoV‐2 infection
title_full_unstemmed The potential role of scavenger receptor B type I (SR‐BI) in SARS‐CoV‐2 infection
title_short The potential role of scavenger receptor B type I (SR‐BI) in SARS‐CoV‐2 infection
title_sort potential role of scavenger receptor b type i sr bi in sars cov 2 infection
topic COVID‐19
pro‐inflammatory cytokines
scavenger receptor type B I
url https://doi.org/10.1002/iid3.786
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