12
views
0
recommends
+1 Recommend
1 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Human molecular chaperones share with SARS-CoV-2 antigenic epitopes potentially capable of eliciting autoimmunity against endothelial cells: possible role of molecular mimicry in COVID-19

      brief-report

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), the cause of COVID-19 disease, has the potential to elicit autoimmunity because mimicry of human molecular chaperones by viral proteins. We compared viral proteins with human molecular chaperones, many of which are heat shock proteins, to determine if they share amino acid-sequence segments with immunogenic-antigenic potential, which can elicit cross-reactive antibodies and effector immune cells with the capacity to damage-destroy human cells by a mechanism of autoimmunity. We identified the chaperones that can putatively participate in molecular mimicry phenomena after SARS-CoV-2 infection, focusing on those for which endothelial cell plasma-cell membrane localization has already been demonstrated. We also postulate that post-translational modifications, induced by physical (shear) and chemical (metabolic) stress caused respectively by the risk factors hypertension and diabetes, might have a role in determining plasma-cell membrane localization and, in turn, autoimmune-induced endothelial damage.

          Electronic supplementary material

          The online version of this article (10.1007/s12192-020-01148-3) contains supplementary material, which is available to authorized users.

          Related collections

          Most cited references27

          • Record: found
          • Abstract: found
          • Article: not found

          Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19

          Progressive respiratory failure is the primary cause of death in the coronavirus disease 2019 (Covid-19) pandemic. Despite widespread interest in the pathophysiology of the disease, relatively little is known about the associated morphologic and molecular changes in the peripheral lung of patients who die from Covid-19.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: found
            Is Open Access

            Prediction models for diagnosis and prognosis of covid-19 infection: systematic review and critical appraisal

            Abstract Objective To review and critically appraise published and preprint reports of prediction models for diagnosing coronavirus disease 2019 (covid-19) in patients with suspected infection, for prognosis of patients with covid-19, and for detecting people in the general population at risk of being admitted to hospital for covid-19 pneumonia. Design Rapid systematic review and critical appraisal. Data sources PubMed and Embase through Ovid, Arxiv, medRxiv, and bioRxiv up to 24 March 2020. Study selection Studies that developed or validated a multivariable covid-19 related prediction model. Data extraction At least two authors independently extracted data using the CHARMS (critical appraisal and data extraction for systematic reviews of prediction modelling studies) checklist; risk of bias was assessed using PROBAST (prediction model risk of bias assessment tool). Results 2696 titles were screened, and 27 studies describing 31 prediction models were included. Three models were identified for predicting hospital admission from pneumonia and other events (as proxy outcomes for covid-19 pneumonia) in the general population; 18 diagnostic models for detecting covid-19 infection (13 were machine learning based on computed tomography scans); and 10 prognostic models for predicting mortality risk, progression to severe disease, or length of hospital stay. Only one study used patient data from outside of China. The most reported predictors of presence of covid-19 in patients with suspected disease included age, body temperature, and signs and symptoms. The most reported predictors of severe prognosis in patients with covid-19 included age, sex, features derived from computed tomography scans, C reactive protein, lactic dehydrogenase, and lymphocyte count. C index estimates ranged from 0.73 to 0.81 in prediction models for the general population (reported for all three models), from 0.81 to more than 0.99 in diagnostic models (reported for 13 of the 18 models), and from 0.85 to 0.98 in prognostic models (reported for six of the 10 models). All studies were rated at high risk of bias, mostly because of non-representative selection of control patients, exclusion of patients who had not experienced the event of interest by the end of the study, and high risk of model overfitting. Reporting quality varied substantially between studies. Most reports did not include a description of the study population or intended use of the models, and calibration of predictions was rarely assessed. Conclusion Prediction models for covid-19 are quickly entering the academic literature to support medical decision making at a time when they are urgently needed. This review indicates that proposed models are poorly reported, at high risk of bias, and their reported performance is probably optimistic. Immediate sharing of well documented individual participant data from covid-19 studies is needed for collaborative efforts to develop more rigorous prediction models and validate existing ones. The predictors identified in included studies could be considered as candidate predictors for new models. Methodological guidance should be followed because unreliable predictions could cause more harm than benefit in guiding clinical decisions. Finally, studies should adhere to the TRIPOD (transparent reporting of a multivariable prediction model for individual prognosis or diagnosis) reporting guideline. Systematic review registration Protocol https://osf.io/ehc47/, registration https://osf.io/wy245.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Heat-shock proteins, molecular chaperones, and the stress response: evolutionary and ecological physiology.

              Molecular chaperones, including the heat-shock proteins (Hsps), are a ubiquitous feature of cells in which these proteins cope with stress-induced denaturation of other proteins. Hsps have received the most attention in model organisms undergoing experimental stress in the laboratory, and the function of Hsps at the molecular and cellular level is becoming well understood in this context. A complementary focus is now emerging on the Hsps of both model and nonmodel organisms undergoing stress in nature, on the roles of Hsps in the stress physiology of whole multicellular eukaryotes and the tissues and organs they comprise, and on the ecological and evolutionary correlates of variation in Hsps and the genes that encode them. This focus discloses that (a) expression of Hsps can occur in nature, (b) all species have hsp genes but they vary in the patterns of their expression, (c) Hsp expression can be correlated with resistance to stress, and (d) species' thresholds for Hsp expression are correlated with levels of stress that they naturally undergo. These conclusions are now well established and may require little additional confirmation; many significant questions remain unanswered concerning both the mechanisms of Hsp-mediated stress tolerance at the organismal level and the evolutionary mechanisms that have diversified the hsp genes.
                Bookmark

                Author and article information

                Contributors
                francesco.cappello@unipa.it
                Journal
                Cell Stress Chaperones
                Cell Stress Chaperones
                Cell Stress & Chaperones
                Springer Netherlands (Dordrecht )
                1355-8145
                1466-1268
                4 August 2020
                : 1-5
                Affiliations
                [1 ]GRID grid.10776.37, ISNI 0000 0004 1762 5517, Department of Biomedicine, Neuroscience and Advanced Diagnostics (BIND), , University of Palermo, ; Palermo, Italy
                [2 ]GRID grid.440907.e, ISNI 0000 0004 1784 3645, Département d’Informatique de l’ÉNS, ÉNS, CNRS, , Université PSL, ; Paris, France
                [3 ]Centre de Recherche Inria de Paris, Paris, France
                [4 ]GRID grid.10776.37, ISNI 0000 0004 1762 5517, Department of Mathematics and Computer Science, , University of Palermo, ; Palermo, Italy
                [5 ]GRID grid.25697.3f, ISNI 0000 0001 2172 4233, Centre Léon Bérard, Cancer Research Center of Lyon, , Université de Lyon, Université Claude Bernard Lyon 1, INSERM 1052, CNRS 5286, ; Lyon, France
                [6 ]GRID grid.411024.2, ISNI 0000 0001 2175 4264, Department of Microbiology and Immunology, School of Medicine, , University of Maryland at Baltimore-Institute of Marine and Environmental Technology (IMET), ; Baltimore, MD 21202 USA
                [7 ]GRID grid.428936.2, Euro-Mediterranean Institute of Science and Technology (IEMEST), ; Palermo, Italy
                Author information
                http://orcid.org/0000-0001-9288-1148
                Article
                1148
                10.1007/s12192-020-01148-3
                7402394
                32754823
                83e93d08-af67-4838-90f1-74c029dbcd1c
                © Cell Stress Society International 2020

                This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

                History
                : 10 July 2020
                : 27 July 2020
                : 30 July 2020
                Categories
                Short Communication

                Molecular biology
                severe acute respiratory syndrome coronavirus 2,covid-19,molecular chaperones,molecular mimicry,autoimmunity,endothelialitis

                Comments

                Comment on this article