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SARS-CoV-2, Viral Interference and the Type I/III IFN Antiviral Innate...
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SARS-CoV-2, Viral Interference and the Type I/III IFN Antiviral Innate Immune Response

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (31 October 2021) | Viewed by 13454

Special Issue Editor

Prof. Marc Servant

E-Mail Website
Guest Editor
1. Faculty of Pharmacy, Université de Montréal, Montréal, QC H3C3J7, Canada
2. Réseau Québécois de Recherche sur les Médicaments (RQRM), Montréal, QC H3T1C5, Canada
Interests: molecular pharmacology; innate immune response; inflammatory response; integration of cellular signals (signal transduction)

Special Issue Information

Dear Colleagues,

The current pandemic involving SARS-CoV-2, a positive-sense single-stranded RNA virus that was recently showed to target components of the RIG-I like receptor (RLR) and the JAK/STAT pathways, has revealed a defect in the innate type I/III IFN antiviral responses in infected patients that is associated with robust virus replication and severe complications, i.e., inflammation and a “cytokine storm”, notably via the accumulation of monocytes, resulting in lung immunopathology, vascular leakage, and suboptimal T cell response. Thus, viral interference affecting the type I/III IFN antiviral response is likely a culprit here. However, this does not explain why older patients (and sometimes even young individuals) do not mount a proper and efficient innate type I/III IFN antiviral response as compared to others. Whereas autoantibodies against IFNa as well as IRF7 and TLR3 variants represent candidates to consider, other mechanisms are likely involved in the complex interplay that exist between the host and this novel coronavirus. This Special Issue will cover the biology of SARS-CoV viruses and their intrinsic ability to antagonize type I/III IFN responses. It will also review our current understanding of the severe complications associated with SARS-CoV-2 infection and address how precision medicine approaches (also known as high definition medicine) could help in diagnosis, prevention, and treatment. 

Prof. Marc Servant
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers (3 papers)

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11 pages, 1322 KiB  
Communication
SARS-CoV-2 Entry: At the Crossroads of CD147 and ACE2
by Claudio Fenizia, Silvia Galbiati, Claudia Vanetti, Riccardo Vago, Mario Clerici, Carlo Tacchetti and Tiziana Daniele
Cells 2021, 10(6), 1434; https://doi.org/10.3390/cells10061434 - 08 Jun 2021
Cited by 58 | Viewed by 5882
Abstract
In late 2019, the betacoronavirus SARS-CoV-2 was identified as the viral agent responsible for the coronavirus disease 2019 (COVID-19) pandemic. Coronaviruses Spike proteins are responsible for their ability to interact with host membrane receptors and different proteins have been identified as SARS-CoV-2 interactors, [...] Read more.
In late 2019, the betacoronavirus SARS-CoV-2 was identified as the viral agent responsible for the coronavirus disease 2019 (COVID-19) pandemic. Coronaviruses Spike proteins are responsible for their ability to interact with host membrane receptors and different proteins have been identified as SARS-CoV-2 interactors, among which Angiotensin-converting enzyme 2 (ACE2), and Basigin2/EMMPRIN/CD147 (CD147). CD147 plays an important role in human immunodeficiency virus type 1, hepatitis C virus, hepatitis B virus, Kaposi’s sarcoma-associated herpesvirus, and severe acute respiratory syndrome coronavirus infections. In particular, SARS-CoV recognizes the CD147 receptor expressed on the surface of host cells by its nucleocapsid protein binding to cyclophilin A (CyPA), a ligand for CD147. However, the involvement of CD147 in SARS-CoV-2 infection is still debated. Interference with both the function (blocking antibody) and the expression (knock down) of CD147 showed that this receptor partakes in SARS-CoV-2 infection and provided additional clues on the underlying mechanism: CD147 binding to CyPA does not play a role; CD147 regulates ACE2 levels and both receptors are affected by virus infection. Altogether, these findings suggest that CD147 is involved in SARS-CoV-2 tropism and represents a possible therapeutic target to challenge COVID-19. Full article
(This article belongs to the Special Issue SARS-CoV-2, Viral Interference and the Type I/III IFN Antiviral Innate Immune Response)
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20 pages, 1200 KiB  
Article
Innate and Adaptive Immune Genes Associated with MERS-CoV Infection in Dromedaries
by Sara Lado, Jean P. Elbers, Martin Plasil, Tom Loney, Pia Weidinger, Jeremy V. Camp, Jolanta Kolodziejek, Jan Futas, Dafalla A. Kannan, Pablo Orozco-terWengel, Petr Horin, Norbert Nowotny and Pamela A. Burger
Cells 2021, 10(6), 1291; https://doi.org/10.3390/cells10061291 - 23 May 2021
Cited by 6 | Viewed by 4124
Abstract
The recent SARS-CoV-2 pandemic has refocused attention to the betacoronaviruses, only eight years after the emergence of another zoonotic betacoronavirus, the Middle East respiratory syndrome coronavirus (MERS-CoV). While the wild source of SARS-CoV-2 may be disputed, for MERS-CoV, dromedaries are considered [...] Read more.
The recent SARS-CoV-2 pandemic has refocused attention to the betacoronaviruses, only eight years after the emergence of another zoonotic betacoronavirus, the Middle East respiratory syndrome coronavirus (MERS-CoV). While the wild source of SARS-CoV-2 may be disputed, for MERS-CoV, dromedaries are considered as source of zoonotic human infections. Testing 100 immune-response genes in 121 dromedaries from United Arab Emirates (UAE) for potential association with present MERS-CoV infection, we identified candidate genes with important functions in the adaptive, MHC-class I (HLA-A-24-like) and II (HLA-DPB1-like), and innate immune response (PTPN4, MAGOHB), and in cilia coating the respiratory tract (DNAH7). Some of these genes previously have been associated with viral replication in SARS-CoV-1/-2 in humans, others have an important role in the movement of bronchial cilia. These results suggest similar host genetic pathways associated with these betacoronaviruses, although further work is required to better understand the MERS-CoV disease dynamics in both dromedaries and humans. Full article
(This article belongs to the Special Issue SARS-CoV-2, Viral Interference and the Type I/III IFN Antiviral Innate Immune Response)
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9 pages, 1774 KiB  
Commentary
Shedding Light on the Possible Link between ADAMTS13 and Vaccine—Induced Thrombotic Thrombocytopenia
by Anna Szóstek-Mioduchowska and Paweł Kordowitzki
Cells 2021, 10(10), 2785; https://doi.org/10.3390/cells10102785 - 18 Oct 2021
Cited by 9 | Viewed by 2747
Abstract
Several recent reports have highlighted the onset of vaccine-induced thrombotic thrombocytopaenia (VITT) in some recipients (approximately 1 case out of 100k exposures) of the ChAdOx1 nCoV-19 vaccine (AstraZeneca). Although the underlying events leading to this blood-clotting phenomenon has yet to be elucidated, several [...] Read more.
Several recent reports have highlighted the onset of vaccine-induced thrombotic thrombocytopaenia (VITT) in some recipients (approximately 1 case out of 100k exposures) of the ChAdOx1 nCoV-19 vaccine (AstraZeneca). Although the underlying events leading to this blood-clotting phenomenon has yet to be elucidated, several critical observations present a compelling potential mechanism. Thrombus formation requires the von Willebrand (VWF) protein to be in ultra-large multimeric state. The conservation of this state is controlled by the ADAMTS13 enzyme, whose proteolytic activity reduces the size of VWF multimers, keeping blood clotting at bay. However, ADAMTS13 cannot act on VWF that is bound to platelet factor 4 (PF4). As such, it is of particular interest to note that a common feature between subjects presenting with VITT is high titres of antibodies against PF4. This raises the possibility that these antibodies preserve the stability of ultra-large VWF complexes, leading to the formation of endothelium-anchored VWF strings, which are capable of recruiting circulating platelets and causing uncontrolled thrombosis in terminal capillaries. Here, we share our viewpoint about the current understanding of the VITT pathogenesis involving the prevention of ADAMTS13’s activity on VWF by PF4 antibody-mediated stabilisation/ protection of the PF4-VWF complex. Full article
(This article belongs to the Special Issue SARS-CoV-2, Viral Interference and the Type I/III IFN Antiviral Innate Immune Response)
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