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Diagnostics
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COVID-19, Post-COVID and Autoimmunity
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COVID-19, Post-COVID and Autoimmunity

A special issue of Diagnostics (ISSN 2075-4418). This special issue belongs to the section "Diagnostic Microbiology and Infectious Disease".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 14246

Special Issue Editors

Dr. Leonid Churilov

E-Mail Website
Guest Editor
Laboratory of the Mosaic of Autoimmunity, Saint Petersburg State University, 199034 Saint Petersburg, Russia
Interests: pathophysiology; experimental medicine; immunology; history of medicine; endocrine and metabolic disorders
Special Issues, Collections and Topics in MDPI journals
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,

Since various autoimmune diseases have much in common, a new interdisciplinary branch of medicine—autoimmunology—is shaping in front of our eyes. About 90 autoimmune entities have been described, which implicate virtually all organs and systems and belong to the sphere of all medical specializations. There is strong evidence for the existence of autoimmune/autoinflammatory links in pathogenesis of severe COVID-19 cases, and especially of its complications, including post-COVID syndrome, which is one of the lessons of current pandemic. Virtually, SARS-CoV-2 is showing the properties of the “autoimmunity virus”. At the same time, practical healthcare needs worldwide target prophylaxis and effective modalities for autoimmune disorder diagnostics and treatment. New diseases as well as new means for their specific prevention, diagnosis and treatment may raise new questions within the field of autoimmune pathology. Despite the great positive results of anti-COVID-19 vaccination worldwide, there is concern regarding episodes of autoimmune adverse events in some individuals; this phenomenon needs to be carefully monitored and explored for greater safety. In the presence of primary individual hereditary predisposition, pathological autoimmunity can manifest differently under the influence of various exogenous factors—interplaying at different life periods of an individual person, while autoimmune disorders in the human body seem to flow from one nosological entity to another, keeping a similar background like a “kaleidoscope of autoimmunity”. The novel etiological factor of autoimmune disorders in SARS-CoV-2 requires special attention from medical scholars and clinicians. This Special Issue of Diagnostics (IF 3.706) is devoted to autoimmunity in relation to the COVID-19 pandemic.

You are welcome to contribute your original papers, reviews and case reports devoted to autoimmunity in light of COVID-19 and its consequences or prevention.

Dr. Leonid P. Churilov
Prof. Dr. Yehuda Shoenfeld
Guest Editors

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. Diagnostics 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 2600 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.

 

Keywords

  • autoimmunity
  • COVID-19
  • post-COVID syndrome
  • pathogenesis
  • diagnosis

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Published Papers (4 papers)

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17 pages, 1655 KiB  
Article
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Post-COVID Syndrome: A Common Neuroimmune Ground?
by Varvara A. Ryabkova, Natalia Y. Gavrilova, Tamara V. Fedotkina, Leonid P. Churilov and Yehuda Shoenfeld
Diagnostics 2023, 13(1), 66; https://doi.org/10.3390/diagnostics13010066 - 26 Dec 2022
Cited by 15 | Viewed by 5525
Abstract
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating chronic disease of unknown etiology, sharing a similar clinical presentation with the increasingly recognized post-COVID syndrome. We performed the first cross-sectional study of ME/CFS in a community population in Russia. Then we described and compared [...] Read more.
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating chronic disease of unknown etiology, sharing a similar clinical presentation with the increasingly recognized post-COVID syndrome. We performed the first cross-sectional study of ME/CFS in a community population in Russia. Then we described and compared some clinical and pathophysiological characteristics of ME/CFS and post-COVID syndrome as neuroimmune disorders. Of the cohort of 76 individuals who suggested themselves as suffering from ME/CFS, 56 were diagnosed with ME/CFS by clinicians according to ≥1 of the four most commonly used case definitions. Of the cohort of 14 individuals with post-COVID-19 syndrome, 14 met the diagnostic criteria for ME/CFS. The severity of anxiety/depressive symptoms did not correlate with the severity of fatigue either in ME/CFS or in post-COVID ME/CFS. Still, a positive correlation was found between the severity of fatigue and 20 other symptoms of ME/CFS related to the domains of “post-exertional exhaustion”, “immune dysfunction”, “sleep disturbances”, “dysfunction of the autonomic nervous system”, “neurological sensory/motor disorders” and “pain syndromes”. Immunological abnormalities were identified in 12/12 patients with ME/CFS according to the results of laboratory testing. The prevalence of postural orthostatic tachycardia assessed in the active orthostatic test amounted to 37.5% in ME/CFS and 75.0% in post-COVID ME/CFS (the latter was higher than in healthy controls, p = 0.02). There was a more pronounced increase in heart rate starting from the 6th minute of the test in post-COVID ME/CFS compared with the control group. Assessment of the functional characteristics of microcirculation by laser doppler flowmetry revealed obvious and very similar changes in ME/CFS and post-COVID ME/CFS compared to the healthy controls. The identified laser doppler flowmetry pattern corresponded to the hyperemic form of microcirculation disorders usually observed in acute inflammatory response or in case of systemic vasoconstriction failure. Full article
(This article belongs to the Special Issue COVID-19, Post-COVID and Autoimmunity)
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12 pages, 1726 KiB  
Article
High Plasma Levels of Activated Factor VII-Antithrombin Complex Point to Increased Tissue Factor Expression in Patients with SARS-CoV-2 Pneumonia: A Potential Link with COVID-19 Prothrombotic Diathesis
by Nicola Martinelli, Anna Maria Rigoni, Sergio De Marchi, Nicola Osti, Martino Donini, Martina Montagnana, Annalisa Castagna, Patrizia Pattini, Silvia Udali, Lucia De Franceschi, Elisa Tinazzi, Filippo Mazzi, Sara Moruzzi, Giuseppe Argentino, Lorenzo Delfino, Giulia Sartori, Anna Maria Azzini, Evelina Tacconelli, Patrick Van Dreden, Giuseppe Lippi, Domenico Girelli, Oliviero Olivieri, Simonetta Friso and Francesca Pizzoloadd Show full author list remove Hide full author list
Diagnostics 2022, 12(11), 2792; https://doi.org/10.3390/diagnostics12112792 - 14 Nov 2022
Cited by 5 | Viewed by 2437
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causal agent of coronavirus disease 2019 (COVID-19), in which coagulation abnormalities and endothelial dysfunction play a key pathogenic role. Tissue factor (TF) expression is triggered by endothelial dysfunction. Activated factor VII-antithrombin (FVIIa-AT) complex reflects [...] Read more.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causal agent of coronavirus disease 2019 (COVID-19), in which coagulation abnormalities and endothelial dysfunction play a key pathogenic role. Tissue factor (TF) expression is triggered by endothelial dysfunction. Activated factor VII-antithrombin (FVIIa-AT) complex reflects indirectly FVIIa-TF interaction and has been proposed as a potential biomarker of prothrombotic diathesis. FVIIa-AT plasma concentration was measured in 40 patients (30 males and 10 females; 64.8 ± 12.3 years) admitted with SARS-CoV-2 pneumonia during the first pandemic wave in Italy. Two sex- and age-matched cohorts without COVID-19, with or without signs of systemic inflammation, were used to compare FVIIa-AT data. The FVIIa-AT plasma levels in COVID-19 patients were higher than those in non-COVID-19 subjects, either with or without inflammation, while no difference was observed among non-COVID-19 subjects. The association between COVID-19 and FVIIa-AT levels remained significant after adjustment for sex, age, C-reactive protein, renal function, fibrinogen, prothrombin time and activated partial thromboplastin time. Our results indicate that SARS-CoV-2 infection, at least during the first pandemic wave, was characterized by high FVIIa-AT levels, which may suggest an enhanced FVIIa-TF interaction in COVID-19, potentially consistent with SARS-CoV-2-induced endotheliopathy. Full article
(This article belongs to the Special Issue COVID-19, Post-COVID and Autoimmunity)
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10 pages, 2373 KiB  
Case Report
Multisystem Inflammatory Syndrome in Adults Associated with Recent Infection with COVID-19
by Ondrej Zahornacky, Štefan Porubčin, Alena Rovnakova and Pavol Jarcuska
Diagnostics 2023, 13(5), 983; https://doi.org/10.3390/diagnostics13050983 - 4 Mar 2023
Cited by 7 | Viewed by 1888
Abstract
Multisystem inflammatory syndrome in adults (MIS-A) is an uncommon but severe and still understudied post-infectious complication of COVID-19. Clinically, the disease manifests itself most often 2–6 weeks after overcoming the infection. Young and middle-aged patients are especially affected. The clinical picture of the [...] Read more.
Multisystem inflammatory syndrome in adults (MIS-A) is an uncommon but severe and still understudied post-infectious complication of COVID-19. Clinically, the disease manifests itself most often 2–6 weeks after overcoming the infection. Young and middle-aged patients are especially affected. The clinical picture of the disease is very diverse. The dominant symptoms are mainly fever and myalgia, usually accompanied by various, especially extrapulmonary, manifestations. Cardiac damage (often in the form of cardiogenic shock) and significantly increased inflammatory parameters are often associated with MIS-A, while respiratory symptoms, including hypoxia, are less frequent. Due to the seriousness of the disease and the possibility of rapid progression, the basis of a successful treatment of the patient is early diagnosis, based mainly on anamnesis (overcoming the disease of COVID-19 in the recent past) and clinical symptoms, which often imitate other severe conditions such as, e.g., sepsis, septic shock, or toxic shock syndrome. Because of the danger of missing the treatment, it is necessary to initiate it immediately after the suspicion of MIS-A is expressed, without waiting for the results of microbiological and serological examinations. The cornerstone of pharmacological therapy is the administration of corticosteroids and intravenous immunoglobulins, to which the majority of patients clinically react. In this article, the authors describe the case report of a 21-year-old patient admitted to the Clinic of Infectology and Travel Medicine for febrility up to 40.5 °C, myalgia, arthralgia, headache, vomiting, and diarrhea three weeks after overcoming COVID-19. However, as part of the routine differential diagnosis of fevers (imaging and laboratory examinations), their cause was not clarified. Due to the overall worsening of the condition, the patient was transferred to the ICU with suspicion of developing MIS-A (he met all clinical and laboratory criteria). Given the above, reserve antibiotics, intravenous corticosteroids, and immunoglobulins were added to the treatment due to the risk of missing them, with a good clinical and laboratory effect. After stabilizing the condition and adjusting the laboratory parameters, the patient was transferred to a standard bed and sent home. Full article
(This article belongs to the Special Issue COVID-19, Post-COVID and Autoimmunity)
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10 pages, 1719 KiB  
Case Report
Large-Vessel Giant Cell Arteritis following COVID-19—What Can HLA Typing Reveal?
by Maja Stojanovic, Aleksandra Barac, Ana Petkovic, Nikola Vojvodic, Strahinja Odalovic, Zorana Andric, Rada Miskovic, Dragana Jovanovic, Sanja Dimic-Janjic, Sanja Dragasevic, Sanvila Raskovic and Mihailo I. Stjepanovic
Diagnostics 2023, 13(3), 484; https://doi.org/10.3390/diagnostics13030484 - 28 Jan 2023
Cited by 3 | Viewed by 2510
Abstract
Giant cell arteritis (GCA) is an immune-mediated vasculitis that affects large arteries. It has been hypothesized that viruses may trigger inflammation within the vessel walls. Genetic studies on human leukocyte antigens (HLAs) have previously reported HLA-DRB1*04 as a susceptible allele for GCA and [...] Read more.
Giant cell arteritis (GCA) is an immune-mediated vasculitis that affects large arteries. It has been hypothesized that viruses may trigger inflammation within the vessel walls. Genetic studies on human leukocyte antigens (HLAs) have previously reported HLA-DRB1*04 as a susceptible allele for GCA and HLA-DRB1*15 as a protective allele for GCA. Here, we discuss the clinical presentation, laboratory findings, HLA class I and class II analysis results, and management of patients with extracranial large-vessel (LV) GCA, detected at least six weeks after recovery from COVID-19. This case series encompassed three patients with LV-GCA (two males and a female with an age range of 63–69 years) whose leading clinical presentation included the presence of constitutional symptoms and significantly elevated inflammatory markers. The diagnosis of LV-GCA was confirmed by CT angiography and FDG-PET/CT, revealing inflammation in the large vessels. All were treated with corticosteroids, while two received adjunctive therapy. By analyzing HLA profiles, we found no presence of the susceptible HLA-DRB1*04 allele, while the HLA-DRB1*15 allele was detected in two patients. In conclusion, LV-GCA may be triggered by COVID-19. We highlight the importance of the early identification of LV-GCA following SARS-CoV-2 infection, which may be delayed due to the overlapping clinical features of GCA and COVID-19. The prompt initiation of therapy is necessary in order to avoid severe vascular complications. Future studies will better define the role of specific HLA alleles in patients who developed GCA following COVID-19. Full article
(This article belongs to the Special Issue COVID-19, Post-COVID and Autoimmunity)
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