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Autoimmunity and COVID-19
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Autoimmunity and COVID-19

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 12484

Special Issue Editor

Prof. Dr. Yehuda Shoenfeld

E-Mail Website
Guest Editor
Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Reichman University, Herzelya 4610101, Israel
Interests: autoimmune diseases; clinical immunology; systemic lupus erythematosus; rheumatology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

COVID-19 was found to be an autoimmune virus inducing a panoply of autoantibodies as well as diversity of autoimmune diseases. Moreover, it was also noted to induce exacerbations of autoimmune conditions. The mechanisms by which the virus achieves this are complex and entail hyperstimulation of the immune system and molecular mimicry.

This Special Issue is dedicated to the many facets of the relationships between the virus, the immune system, and the induction of autoimmunity. Series of cases are invited as well as mechanisms by which diseases are induced by the virus. The subject of post-COVID syndrome will also be discussed with all its clinical manifestations and autoimmune aspects, especially of the autonomic nervous system; papers dedicated to ways of therapy of this prolonged condition are welcome as well.

Prof. Dr. Yehuda Shoenfeld
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.

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Keywords

  • COVID-19
  • post-COVID
  • autoimmunity
  • autoimmune diseases
  • autonomic nervous system

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Published Papers (5 papers)

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Research

16 pages, 3987 KiB  
Article
The Immunological Profile of SARS-CoV-2 Infection in Children Is Linked to Clinical Severity and Age
by Claudia Vanetti, Vito Lampasona, Marta Stracuzzi, Claudio Fenizia, Mara Biasin, Irma Saulle, Fiona Limanaqi, Ahmed Abdelsalam, Cristian Loretelli, Laura Paradiso, Emma Longoni, Lucia Barcellini, Lorenzo Piemonti, Ilaria Marzinotto, Stefania Dispinseri, Antonella Amendola, Clara Fappani, Elisabetta Tanzi, Mario Salvatore Clerici, Gabriella Scarlatti, Gian Vincenzo Zuccotti, Vania Giacomet and Daria Trabattoniadd Show full author list remove Hide full author list
Int. J. Mol. Sci. 2023, 24(7), 6779; https://doi.org/10.3390/ijms24076779 - 5 Apr 2023
Cited by 2 | Viewed by 1956
Abstract
Coronavirus disease 19 (COVID-19) is clinically less severe in children, even if the wide variety and degree of severity of symptoms reported in children pose a still-unresolved challenge for clinicians. We performed an in-depth analysis of the immunological profiles of 18 hospitalized SARS-CoV-2-infected [...] Read more.
Coronavirus disease 19 (COVID-19) is clinically less severe in children, even if the wide variety and degree of severity of symptoms reported in children pose a still-unresolved challenge for clinicians. We performed an in-depth analysis of the immunological profiles of 18 hospitalized SARS-CoV-2-infected children, whose results were compared to those obtained from 13 age- and sex-matched healthy controls (HC). The patients were categorized as paucisymptomatic/moderate (55.6%) or severe/critical (44.5%) according to established diagnostic criteria and further stratified into the categories of infants (1–12 months), children (1–12 years), and adolescents (>12 years). We assessed SARS-CoV-2-specific RBD antibodies (Ab), neutralizing antibodies (nAb), and circulating cytokines/chemokines in the plasma, and the SARS-CoV-2-specific immune response was measured in PBMCs by gene expression and secretome analyses. Our results showed peculiar circulating cytokine/chemokine profiles among patients sharing a similar clinical phenotype. A cluster of patients consisting of infants with severe symptoms presented hyperinflammatory profiles, together with extremely polarized antibody profiles. In a second cluster consisting of paucisymptomatic patients, a less pronounced increase in the level of inflammatory cytokines, together with an association between the selected cytokines and humoral responses, was observed. A third cluster, again consisting of paucisymptomatic patients, showed a circulating cytokine/chemokine profile which overlapped with that of the HC. The SARS-CoV-2-stimulated production of pro-inflammatory proteins, T lymphocyte activation, and migration-specific proteins, were significantly increased in SARS-CoV-2-infected children compared to the HC. Our findings suggest that immune response activation in the course of SARS-CoV-2 infection in children is directly correlated with clinical severity and, to a lesser extent, age. Full article
(This article belongs to the Special Issue Autoimmunity and COVID-19)
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14 pages, 1565 KiB  
Article
SARS-CoV-2 Lysate Stimulation Impairs the Release of Platelet-like Particles and Megakaryopoiesis in the MEG-01 Cell Line
by Valentina Lopardo, Francesco Montella, Roberta Maria Esposito, Carla Zannella, Silvana Mirella Aliberti, Mario Capunzo, Gianluigi Franci, Annibale Alessandro Puca and Elena Ciaglia
Int. J. Mol. Sci. 2023, 24(5), 4723; https://doi.org/10.3390/ijms24054723 - 1 Mar 2023
Cited by 2 | Viewed by 2558
Abstract
SARS-CoV-2 infection causes a considerable inflammatory response coupled with impaired platelet reactivity, which can lead to platelet disorders recognized as negative prognostic factors in COVID-19 patients. The virus may cause thrombocytopenia or thrombocytosis during the different disease stages by destroying or activating platelets [...] Read more.
SARS-CoV-2 infection causes a considerable inflammatory response coupled with impaired platelet reactivity, which can lead to platelet disorders recognized as negative prognostic factors in COVID-19 patients. The virus may cause thrombocytopenia or thrombocytosis during the different disease stages by destroying or activating platelets and influencing platelet production. While it is known that several viruses can impair megakaryopoiesis by generating an improper production and activation of platelets, the potential involvement of SARS-CoV-2 in affecting megakaryopoiesis is poorly understood. To this purpose, we explored, in vitro, the impact of SARS-CoV-2 stimulation in the MEG-01 cell line, a human megakaryoblastic leukemia cell line, considering its spontaneous capacity of releasing platelet-like particles (PLPs). We interrogated the effect of heat-inactivated SARS-CoV-2 lysate in the release of PLPs and activation from MEG-01, the signaling pathway influenced by SARS-CoV-2, and the functional effect on macrophagic skewing. The results highlight the potential influence of SARS-CoV-2 in the early stages of megakaryopoiesis by enhancing the production and activation of platelets, very likely due to the impairment of STATs signaling and AMPK activity. Overall, these findings provide new insight into the role of SARS-CoV-2 in affecting megakaryocyte–platelet compartment, possibly unlocking another avenue by which SARS-CoV-2 moves. Full article
(This article belongs to the Special Issue Autoimmunity and COVID-19)
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18 pages, 2961 KiB  
Article
Plasma Proteomic Variables Related to COVID-19 Severity: An Untargeted nLC-MS/MS Investigation
by Lisa Pagani, Clizia Chinello, Giulia Risca, Giulia Capitoli, Lucrezia Criscuolo, Andrea Lombardi, Riccardo Ungaro, Davide Mangioni, Isabella Piga, Antonio Muscatello, Francesco Blasi, Andrea Favalli, Martina Martinovic, Andrea Gori, Alessandra Bandera, Renata Grifantini and Fulvio Magni
Int. J. Mol. Sci. 2023, 24(4), 3570; https://doi.org/10.3390/ijms24043570 - 10 Feb 2023
Cited by 10 | Viewed by 2601
Abstract
Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) infection leads to a wide range of clinical manifestations and determines the need for personalized and precision medicine. To better understand the biological determinants of this heterogeneity, we explored the plasma proteome of 43 COVID-19 patients with [...] Read more.
Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) infection leads to a wide range of clinical manifestations and determines the need for personalized and precision medicine. To better understand the biological determinants of this heterogeneity, we explored the plasma proteome of 43 COVID-19 patients with different outcomes by an untargeted liquid chromatography-mass spectrometry approach. The comparison between asymptomatic or pauci-symptomatic subjects (MILDs), and hospitalised patients in need of oxygen support therapy (SEVEREs) highlighted 29 proteins emerged as differentially expressed: 12 overexpressed in MILDs and 17 in SEVEREs. Moreover, a supervised analysis based on a decision-tree recognised three proteins (Fetuin-A, Ig lambda-2chain-C-region, Vitronectin) that are able to robustly discriminate between the two classes independently from the infection stage. In silico functional annotation of the 29 deregulated proteins pinpointed several functions possibly related to the severity; no pathway was associated exclusively to MILDs, while several only to SEVEREs, and some associated to both MILDs and SEVEREs; SARS-CoV-2 signalling pathway was significantly enriched by proteins up-expressed in SEVEREs (SAA1/2, CRP, HP, LRG1) and in MILDs (GSN, HRG). In conclusion, our analysis could provide key information for ‘proteomically’ defining possible upstream mechanisms and mediators triggering or limiting the domino effect of the immune-related response and characterizing severe exacerbations. Full article
(This article belongs to the Special Issue Autoimmunity and COVID-19)
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14 pages, 1189 KiB  
Article
Longitudinal Analysis of Antiphospholipid Antibody Dynamics after Infection with SARS-CoV-2 or Vaccination with BNT162b2
by Manca Ogrič, Polona Žigon, Snezna Sodin-Semrl, Mirjana Zlatković-Švenda, Marija Zdravković, Milica Ovuka, Tinka Švec, Katja Lakota, Peter Radšel, Žiga Rotar and Saša Čučnik
Int. J. Mol. Sci. 2023, 24(1), 211; https://doi.org/10.3390/ijms24010211 - 22 Dec 2022
Cited by 5 | Viewed by 2401
Abstract
Antiphospholipid antibodies (aPL) comprise a group of autoantibodies that reflect prothrombotic risk in antiphospholipid syndrome (APS) but may also be present in a small proportion of healthy individuals. They are often transiently elevated in infections, including SARS-CoV-2, and may also be associated with [...] Read more.
Antiphospholipid antibodies (aPL) comprise a group of autoantibodies that reflect prothrombotic risk in antiphospholipid syndrome (APS) but may also be present in a small proportion of healthy individuals. They are often transiently elevated in infections, including SARS-CoV-2, and may also be associated with vaccine-induced autoimmunity. Therefore, we aimed to investigate the dynamics of aPL in COVID-19 patients and in individuals (healthcare professionals—HCPs) after receiving BNT162b2 vaccine and to compare aPL levels and positivity with those found in APS patients. We measured solid-phase identifiable aPL, including anticardiolipin (aCL), anti-β2 glycoprotein I (anti-β2GPI), and anti-prothrombin/phosphatidylserine (aPS/PT) antibodies in 58 HCPs before and after vaccination (at 3 weeks, 3, 6, and 9 months after the second dose, and 3 weeks after the third booster dose), in 45 COVID-19 patients hospitalized in the ICU, in 89 COVID-19 patients hospitalized in the non-ICU (at admission, at hospital discharge, and at follow-up), and in 52 patients with APS. The most frequently induced aPL in COVID-19 patients (hospitalized in non-ICU) were aCL (50.6% of patients had positive levels at at least one time point), followed by anti-β2GPI (21.3% of patients had positive levels at at least one time point). In 9/89 COVID-19 patients, positive aPL levels persisted for three months. One HCP developed aCL IgG after vaccination but the persistence could not be confirmed, and two HCPs developed persistent anti-β2GPI IgG after vaccination with no increase during a 1-year follow-up period. Solid-phase aPL were detected in 84.6% of APS patients, in 49.4% of COVID-19 patients hospitalized in the non-ICU, in 33.3% of COVID-19 patients hospitalized in the ICU, and in only 17.2% of vaccinated HCPs. aPL levels and multiple positivity were significantly lower in both infected groups and in vaccinated individuals compared with APS patients. In conclusion, BNT162b2 mRNA vaccine may have induced aPL in a few individuals, whereas SARS-CoV-2 infection itself results in a higher percentage of aPL induction, but the levels, persistence, and multiple positivity of aPL do not follow the pattern observed in APS. Full article
(This article belongs to the Special Issue Autoimmunity and COVID-19)
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19 pages, 3238 KiB  
Article
Natural IgG against S-Protein and RBD of SARS-CoV-2 Do Not Bind and Hydrolyze DNA and Are Not Autoimmune
by Anna M. Timofeeva, Sergey E. Sedykh, Evgeny A. Ermakov, Andrey L. Matveev, Eva I. Odegova, Tatiana A. Sedykh, Dmitry N. Shcherbakov, Iuliia A. Merkuleva, Ekaterina A. Volosnikova, Valentina S. Nesmeyanova, Nina V. Tikunova and Georgy A. Nevinsky
Int. J. Mol. Sci. 2022, 23(22), 13681; https://doi.org/10.3390/ijms232213681 - 8 Nov 2022
Cited by 9 | Viewed by 2123
Abstract
Since the onset of the COVID-19 pandemic, numerous publications have appeared describing autoimmune pathologies developing after a coronavirus infection, with several papers reporting autoantibody production during the acute period of the disease. Several viral diseases are known to trigger autoimmune processes, and the [...] Read more.
Since the onset of the COVID-19 pandemic, numerous publications have appeared describing autoimmune pathologies developing after a coronavirus infection, with several papers reporting autoantibody production during the acute period of the disease. Several viral diseases are known to trigger autoimmune processes, and the appearance of catalytic antibodies with DNase activity is one of the earliest markers of several autoimmune pathologies. Therefore, we analyzed whether IgG antibodies from blood plasma of SARS-CoV-2 patients after recovery could bind and hydrolyze DNA. We analyzed how vaccination of patients with adenovirus Sputnik V vaccine influences the production of abzymes with DNase activity. Four groups were selected for the analysis, each containing 25 patients according to their relative titers of antibodies to S-protein: with high and median titers, vaccinated with Sputnik V with high titers, and a control group of donors with negative titers. The relative titers of antibodies against DNA and the relative DNase activity of IgGs depended very much on the individual patient and the donor, and no significant correlation was found between the relative values of antibodies titers and their DNase activity. Our results indicate that COVID-19 disease and vaccination with adenoviral Sputnik V vaccine do not result in the development or enhancement of strong autoimmune reactions as in the typical autoimmune diseases associated with the production of anti-DNA and DNA hydrolyzing antibodies. Full article
(This article belongs to the Special Issue Autoimmunity and COVID-19)
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