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      COVID‐19 coagulopathies: Human blood proteins mimic SARS‐CoV‐2 virus, vaccine proteins and bacterial co‐infections inducing autoimmunity : Combinations of bacteria and SARS‐CoV‐2 synergize to induce autoantibodies targeting cardiolipin, cardiolipin‐binding proteins, platelet factor 4, prothrombin, and coagulation factors.

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          Abstract

          Severe COVID‐19 is often accompanied by coagulopathies such as thrombocytopenia and abnormal clotting. Rarely, such complications follow SARS‐CoV‐2 vaccination. The cause of these coagulopathies is unknown. It is hypothesized that coagulopathies accompanying SARS‐CoV‐2 infections and vaccinations result from bacterial co‐infections that synergize with virus‐induced autoimmunity due to antigenic mimicry of blood proteins by both bacterial and viral antigens. Coagulopathies occur mainly in severe COVID‐19 characterized by bacterial co‐infections with Streptococci, Staphylococci, Klebsiella, Escherichia coli, and Acinetobacter baumannii. These bacteria express unusually large numbers of antigens mimicking human blood antigens, as do both SARS‐CoV‐2 and adenoviruses. Bacteria mimic cardiolipin, prothrombin, albumin, and platelet factor 4 (PF4). SARS‐CoV‐2 mimics complement factors, Rh antigens, platelet phosphodiesterases, Factors IX and X, von Willebrand Factor (VWF), and VWF protease ADAMTS13. Adenoviruses mimic prothrombin and platelet factor 4. Bacterial prophylaxis, avoidance of vaccinating bacterially infected individuals, and antigen deletion for vaccines may reduce coagulopathy risk. Also see the video abstract here: https://youtu.be/zWDOsghrPg8

          Abstract

          SARS‐CoV‐2 and bacteria synergize to induce COVID‐19 autoimmune coagulopathies. VIral proteins mimic blood proteins including Rh antigens, phosphodiesterases (PDE), and cardiolipin‐binding proteins (β2GPI) while bacteria express cardiolipin, complement‐, and coagulation‐factor‐like proteins. These antigens induce complementary antibodies (Ab), circulating immune complexes, cytokine over‐production via Toll‐like receptor (TLR) hyperactivation and autoimmune disease.

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          Most cited references141

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          Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study

          Summary Background Since December, 2019, Wuhan, China, has experienced an outbreak of coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Epidemiological and clinical characteristics of patients with COVID-19 have been reported but risk factors for mortality and a detailed clinical course of illness, including viral shedding, have not been well described. Methods In this retrospective, multicentre cohort study, we included all adult inpatients (≥18 years old) with laboratory-confirmed COVID-19 from Jinyintan Hospital and Wuhan Pulmonary Hospital (Wuhan, China) who had been discharged or had died by Jan 31, 2020. Demographic, clinical, treatment, and laboratory data, including serial samples for viral RNA detection, were extracted from electronic medical records and compared between survivors and non-survivors. We used univariable and multivariable logistic regression methods to explore the risk factors associated with in-hospital death. Findings 191 patients (135 from Jinyintan Hospital and 56 from Wuhan Pulmonary Hospital) were included in this study, of whom 137 were discharged and 54 died in hospital. 91 (48%) patients had a comorbidity, with hypertension being the most common (58 [30%] patients), followed by diabetes (36 [19%] patients) and coronary heart disease (15 [8%] patients). Multivariable regression showed increasing odds of in-hospital death associated with older age (odds ratio 1·10, 95% CI 1·03–1·17, per year increase; p=0·0043), higher Sequential Organ Failure Assessment (SOFA) score (5·65, 2·61–12·23; p<0·0001), and d-dimer greater than 1 μg/mL (18·42, 2·64–128·55; p=0·0033) on admission. Median duration of viral shedding was 20·0 days (IQR 17·0–24·0) in survivors, but SARS-CoV-2 was detectable until death in non-survivors. The longest observed duration of viral shedding in survivors was 37 days. Interpretation The potential risk factors of older age, high SOFA score, and d-dimer greater than 1 μg/mL could help clinicians to identify patients with poor prognosis at an early stage. Prolonged viral shedding provides the rationale for a strategy of isolation of infected patients and optimal antiviral interventions in the future. Funding Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences; National Science Grant for Distinguished Young Scholars; National Key Research and Development Program of China; The Beijing Science and Technology Project; and Major Projects of National Science and Technology on New Drug Creation and Development.
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            Neutrophil extracellular traps kill bacteria.

            Neutrophils engulf and kill bacteria when their antimicrobial granules fuse with the phagosome. Here, we describe that, upon activation, neutrophils release granule proteins and chromatin that together form extracellular fibers that bind Gram-positive and -negative bacteria. These neutrophil extracellular traps (NETs) degrade virulence factors and kill bacteria. NETs are abundant in vivo in experimental dysentery and spontaneous human appendicitis, two examples of acute inflammation. NETs appear to be a form of innate response that binds microorganisms, prevents them from spreading, and ensures a high local concentration of antimicrobial agents to degrade virulence factors and kill bacteria.
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              Clinical characteristics of 140 patients infected by SARS‐CoV‐2 in Wuhan, China

              Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been widely spread. We aim to investigate the clinical characteristic and allergy status of patients infected with SARS-CoV-2.
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                Author and article information

                Contributors
                rootbern@msu.edu
                Journal
                Bioessays
                Bioessays
                10.1002/(ISSN)1521-1878
                BIES
                Bioessays
                John Wiley and Sons Inc. (Hoboken )
                0265-9247
                1521-1878
                22 October 2021
                December 2021
                22 October 2021
                : 43
                : 12 ( doiID: 10.1002/bies.v43.12 )
                : 2100158
                Affiliations
                [ 1 ] Michigan State University East Lansing Michigan USA
                Author notes
                [*] [* ] Correspondence

                Robert Root‐Bernstein, Michigan State University, East Lansing, MI 48824, USA

                Email: rootbern@ 123456msu.edu

                Author information
                https://orcid.org/0000-0002-3298-9306
                Article
                BIES202100158
                10.1002/bies.202100158
                8646673
                34677872
                74b56153-1c4f-4be1-a22f-9d6e4351b6ea
                © 2021 Wiley Periodicals LLC

                This article is being made freely available through PubMed Central as part of the COVID-19 public health emergency response. It can be used for unrestricted research re-use and analysis in any form or by any means with acknowledgement of the original source, for the duration of the public health emergency.

                History
                : 28 September 2021
                : 23 June 2021
                : 30 September 2021
                Page count
                Figures: 4, Tables: 3, Pages: 17, Words: 11655
                Categories
                Hypothesis
                Hypothesis
                Custom metadata
                2.0
                December 2021
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.0.9 mode:remove_FC converted:06.12.2021

                Cell biology
                cardiolipin,coagulation factors,phosphodiesterase,platelet,streptococci,thrombocytopenia,thrombosis

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