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Article ; Online: COVID-19 associated myopathy.

Aschman, Tom / Stenzel, Werner

2022 Volume 35, Issue 5, Page(s) 622–628

Abstract: Purpose of review: The global spread of severe acute respiratory syndrome coronavirus 2 resulted in many cases of acute and postacute muscular symptoms. In this review, we try to decipher the potential underlying pathomechanisms and summarize the ... ...

Abstract	Purpose of review: The global spread of severe acute respiratory syndrome coronavirus 2 resulted in many cases of acute and postacute muscular symptoms. In this review, we try to decipher the potential underlying pathomechanisms and summarize the potential links between viral infection and muscle affection. Recent findings: Disregarding single case studies that do not allow safe conclusions due to the high number of infections, histopathological evidence of myositis has only been reported in deceased individuals with severe COVID-19. Postacute myalgia and weakness seem to occur in a subset of patients up to one year after initial infection, reminiscent of postinfectious syndromes (PIS) described in prior epidemics and pandemics of the past. Summary: COVID-19 associated myopathy likely comprises different entities with heterogeneous pathomechanisms. Individual factors such as disease severity and duration, age, sex, constitutional susceptibilities, and preexisting conditions are important to consider when formulating a diagnosis. Persisting symptoms show overlapping features with PIS or postintensive care syndrome. In lack of strong evidence for a direct infection of myocytes, inflammatory myopathies associated with COVID-19 are presumably immune-mediated. Differential diagnosis of rheumatological and nonmuscular neurological origin coinciding with the infection need to be considered, due to the extremely high numbers of newly occurring infections the last 2 years.
MeSH term(s)	COVID-19/complications ; Humans ; Muscular Diseases/epidemiology ; Muscular Diseases/etiology ; Pandemics ; SARS-CoV-2 ; Virus Diseases
Language	English
Publishing date	2022-08-11
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1182686-1
ISSN	1473-6551 ; 1350-7540
ISSN (online)	1473-6551
ISSN	1350-7540
DOI	10.1097/WCO.0000000000001101
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Article ; Online: Unconvincing Evidence of SARS-CoV-2-Associated Myositis in Autopsied Muscles-Reply.

Aschman, Tom / Goebel, Hans-Hilmar / Stenzel, Werner Peter

JAMA neurology

2022 Volume 79, Issue 1, Page(s) 92–93

MeSH term(s)	Autopsy ; COVID-19 ; Humans ; Muscles ; Myositis ; SARS-CoV-2
Language	English
Publishing date	2022-01-13
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2702023-X
ISSN	2168-6157 ; 2168-6149
ISSN (online)	2168-6157
ISSN	2168-6149
DOI	10.1001/jamaneurol.2021.4339
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Article ; Online: What SARS-CoV-2 does to our brains.

Aschman, Tom / Mothes, Ronja / Heppner, Frank L / Radbruch, Helena

Immunity

2022 Volume 55, Issue 7, Page(s) 1159–1172

Abstract: Neurological symptoms in SARS-CoV-2-infected patients have been reported, but their cause remains unclear. In theory, the neurological symptoms observed after SARS-CoV-2 infection could be (1) directly caused by the virus infecting brain cells, (2) ... ...

Abstract	Neurological symptoms in SARS-CoV-2-infected patients have been reported, but their cause remains unclear. In theory, the neurological symptoms observed after SARS-CoV-2 infection could be (1) directly caused by the virus infecting brain cells, (2) indirectly by our body's local or systemic immune response toward the virus, (3) by coincidental phenomena, or (4) a combination of these factors. As indisputable evidence of intact and replicating SARS-CoV-2 particles in the central nervous system (CNS) is currently lacking, we suggest focusing on the host's immune reaction when trying to understand the neurocognitive symptoms associated with SARS-CoV-2 infection. In this perspective, we discuss the possible immune-mediated mechanisms causing functional or structural CNS alterations during acute infection as well as in the post-infectious context. We also review the available literature on CNS affection in the context of COVID-19 infection, as well as observations from animal studies on the molecular pathways involved in sickness behavior.
MeSH term(s)	Animals ; Brain ; COVID-19 ; Central Nervous System ; SARS-CoV-2
Language	English
Publishing date	2022-06-20
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2022.06.013
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Article ; Online: Interferon Lambda Regulates Cellular and Humoral Immunity in Pristane-Induced Lupus.

Aschman, Tom / Schaffer, Sandra / Biniaris Georgallis, Stylianos Iason / Triantafyllopoulou, Antigoni / Staeheli, Peter / Voll, Reinhard E

International journal of molecular sciences

2021 Volume 22, Issue 21

Abstract: A pivotal role of type I interferons in systemic lupus erythematosus (SLE) is widely accepted. Type III interferons (IFN-λ) however, the most recently discovered cytokines grouped within the interferon family, have not been extensively studied in lupus ... ...

Abstract	A pivotal role of type I interferons in systemic lupus erythematosus (SLE) is widely accepted. Type III interferons (IFN-λ) however, the most recently discovered cytokines grouped within the interferon family, have not been extensively studied in lupus disease models yet. Growing evidence suggests a role for IFN-λ in regulating both innate and adaptive immune responses, and increased serum concentrations have been described in multiple autoimmune diseases including SLE. Using the pristane-induced lupus model, we found that mice with defective IFN-λ receptors (
MeSH term(s)	Animals ; Immunity, Cellular ; Immunity, Humoral ; Interferons/genetics ; Interferons/immunology ; Leukocytes/immunology ; Lupus Erythematosus, Systemic/chemically induced ; Lupus Erythematosus, Systemic/genetics ; Lupus Erythematosus, Systemic/immunology ; Mice ; Mice, Knockout ; Receptors, Interferon/deficiency ; Receptors, Interferon/immunology ; Terpenes/adverse effects ; Terpenes/pharmacology
Chemical Substances	IFNLR1 protein, mouse ; Receptors, Interferon ; Terpenes ; interferon type III ; pristane (26HZV48DT1) ; Interferons (9008-11-1)
Language	English
Publishing date	2021-10-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms222111747
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Article ; Online: Daratumumab for treatment-refractory antibody-mediated diseases in neurology.

Scheibe, Franziska / Ostendorf, Lennard / Prüss, Harald / Radbruch, Helena / Aschman, Tom / Hoffmann, Sarah / Blau, Igor-Wolfgang / Meisel, Christian / Alexander, Tobias / Meisel, Andreas

European journal of neurology

2022 Volume 29, Issue 6, Page(s) 1847–1854

Abstract: Background and purpose: A fraction of patients with antibody-mediated autoimmune diseases remain unresponsive to first-/second-line and sometimes even to escalation immunotherapies. Because these patients are still affected by poor outcome and increased ...

Abstract	Background and purpose: A fraction of patients with antibody-mediated autoimmune diseases remain unresponsive to first-/second-line and sometimes even to escalation immunotherapies. Because these patients are still affected by poor outcome and increased mortality, we investigated the safety and efficacy of the plasma cell-depleting anti-CD38 antibody daratumumab in life-threatening, antibody-mediated autoimmune diseases. Methods: In this retrospective, single-center case series, seven patients with autoantibody-driven neurological autoimmune diseases (autoimmune encephalitis, n = 5; neurofascin antibody-associated chronic inflammatory demyelinating polyneuropathy associated with sporadic late onset nemaline myopathy, n = 1; seronegative myasthenia gravis, n = 1) unresponsive to a median of four (range = 4-9) immunotherapies were treated with four to 20 cycles of 16 mg/kg daratumumab. Results: Daratumumab allowed a substantial clinical improvement in all patients, as measured by modified Rankin Scale (mRS; before treatment: mRS =5, n = 7; after treatment: median mRS =4, range = 0-5), Clinical Assessment Scale in Autoimmune Encephalitis (from median 21 to 3 points, n = 5), Inflammatory Neuropathy Cause and Treatment disability score (from 7 to 0 points, n = 1), and Quantitative Myasthenia Gravis score (from 16 to 8 points, n = 1). Daratumumab induced a substantial reduction of disease-specific autoreactive antibodies, total IgG (serum, 66%, n = 7; cerebrospinal fluid, 58%, n = 5), and vaccine-induced titers for rubella (50%) and tetanus toxoid (74%). Treatment-related toxicities Grade 3 or higher occurred in five patients, including one death. Conclusions: Our findings suggest that daratumumab provided a clinically relevant depletion of autoreactive long-lived plasma cells, identifying plasma cell-targeted therapies as promising escalation therapy for highly active, otherwise treatment-refractory autoantibody-mediated neurological diseases.
MeSH term(s)	Antibodies, Monoclonal ; Autoantibodies ; Encephalitis ; Hashimoto Disease ; Humans ; Myasthenia Gravis ; Nervous System Diseases/drug therapy ; Neurology ; Retrospective Studies
Chemical Substances	Antibodies, Monoclonal ; Autoantibodies ; daratumumab (4Z63YK6E0E)
Language	English
Publishing date	2022-02-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1280785-0
ISSN	1468-1331 ; 1351-5101 ; 1471-0552
ISSN (online)	1468-1331
ISSN	1351-5101 ; 1471-0552
DOI	10.1111/ene.15266
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Zs.MO 592: Show issues

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Article ; Online: Interferon Lambda Regulates Cellular and Humoral Immunity in Pristane-Induced Lupus

Tom Aschman / Sandra Schaffer / Stylianos Iason Biniaris Georgallis / Antigoni Triantafyllopoulou / Peter Staeheli / Reinhard E. Voll

International Journal of Molecular Sciences, Vol 22, Iss 11747, p

2021 Volume 11747

Abstract	A pivotal role of type I interferons in systemic lupus erythematosus (SLE) is widely accepted. Type III interferons (IFN-λ) however, the most recently discovered cytokines grouped within the interferon family, have not been extensively studied in lupus disease models yet. Growing evidence suggests a role for IFN-λ in regulating both innate and adaptive immune responses, and increased serum concentrations have been described in multiple autoimmune diseases including SLE. Using the pristane-induced lupus model, we found that mice with defective IFN-λ receptors ( Ifnlr1 −/− ) showed increased survival rates, decreased lipogranuloma formation and reduced anti-dsDNA autoantibody titers in the early phase of autoimmunity development compared to pristane-treated wild-type mice. Moreover, Ifnlr1 −/− mice treated with pristane had reduced numbers of inflammatory mononuclear phagocytes and cNK cells in their kidneys, resembling untreated control mice. Systemically, circulating B cells and monocytes (CD115 + Ly6C + ) were reduced in pristane-treated Ifnlr1 −/− mice. The present study supports a significant role for type III interferons in the pathogenesis of pristane-induced murine autoimmunity as well as in systemic and renal inflammation. Although the absence of type III interferon receptors does not completely prevent the development of autoantibodies, type III interferon signaling accelerates the development of autoimmunity and promotes a pro-inflammatory environment in autoimmune-prone hosts.
Keywords	SLE ; lupus ; type III interferons ; Ifnlr1 ; interferon lambda ; pristane ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	333
Language	English
Publishing date	2021-10-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Post-COVID exercise intolerance is associated with capillary alterations and immune dysregulations in skeletal muscles.

Aschman, Tom / Wyler, Emanuel / Baum, Oliver / Hentschel, Andreas / Rust, Rebekka / Legler, Franziska / Preusse, Corinna / Meyer-Arndt, Lil / Büttnerova, Ivana / Förster, Alexandra / Cengiz, Derya / Alves, Luiz Gustavo Teixeira / Schneider, Julia / Kedor, Claudia / Bellmann-Strobl, Judith / Sanchin, Aminaa / Goebel, Hans-Hilmar / Landthaler, Markus / Corman, Victor /

Roos, Andreas / Heppner, Frank L / Radbruch, Helena / Paul, Friedemann / Scheibenbogen, Carmen / Dengler, Nora F / Stenzel, Werner

Acta neuropathologica communications

2023 Volume 11, Issue 1, Page(s) 193

Abstract: The SARS-CoV-2 pandemic not only resulted in millions of acute infections worldwide, but also in many cases of post-infectious syndromes, colloquially referred to as "long COVID". Due to the heterogeneous nature of symptoms and scarcity of available ... ...

Abstract	The SARS-CoV-2 pandemic not only resulted in millions of acute infections worldwide, but also in many cases of post-infectious syndromes, colloquially referred to as "long COVID". Due to the heterogeneous nature of symptoms and scarcity of available tissue samples, little is known about the underlying mechanisms. We present an in-depth analysis of skeletal muscle biopsies obtained from eleven patients suffering from enduring fatigue and post-exertional malaise after an infection with SARS-CoV-2. Compared to two independent historical control cohorts, patients with post-COVID exertion intolerance had fewer capillaries, thicker capillary basement membranes and increased numbers of CD169
MeSH term(s)	Humans ; Capillaries ; COVID-19 ; SARS-CoV-2 ; Muscle, Skeletal ; Fatigue
Language	English
Publishing date	2023-12-08
Publishing country	England
Document type	Journal Article
ZDB-ID	2715589-4
ISSN	2051-5960 ; 2051-5960
ISSN (online)	2051-5960
ISSN	2051-5960
DOI	10.1186/s40478-023-01662-2
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Article ; Online: Distinct tissue niches direct lung immunopathology via CCL18 and CCL21 in severe COVID-19.

Mothes, Ronja / Pascual-Reguant, Anna / Koehler, Ralf / Liebeskind, Juliane / Liebheit, Alina / Bauherr, Sandy / Philipsen, Lars / Dittmayer, Carsten / Laue, Michael / von Manitius, Regina / Elezkurtaj, Sefer / Durek, Pawel / Heinrich, Frederik / Heinz, Gitta A / Guerra, Gabriela M / Obermayer, Benedikt / Meinhardt, Jenny / Ihlow, Jana / Radke, Josefine /

Heppner, Frank L / Enghard, Philipp / Stockmann, Helena / Aschman, Tom / Schneider, Julia / Corman, Victor M / Sander, Leif E / Mashreghi, Mir-Farzin / Conrad, Thomas / Hocke, Andreas C / Niesner, Raluca A / Radbruch, Helena / Hauser, Anja E

Nature communications

2023 Volume 14, Issue 1, Page(s) 791

Abstract: Prolonged lung pathology has been associated with COVID-19, yet the cellular and molecular mechanisms behind this chronic inflammatory disease are poorly understood. In this study, we combine advanced imaging and spatial transcriptomics to shed light on ... ...

Abstract	Prolonged lung pathology has been associated with COVID-19, yet the cellular and molecular mechanisms behind this chronic inflammatory disease are poorly understood. In this study, we combine advanced imaging and spatial transcriptomics to shed light on the local immune response in severe COVID-19. We show that activated adventitial niches are crucial microenvironments contributing to the orchestration of prolonged lung immunopathology. Up-regulation of the chemokines CCL21 and CCL18 associates to endothelial-to-mesenchymal transition and tissue fibrosis within these niches. CCL21 over-expression additionally links to the local accumulation of T cells expressing the cognate receptor CCR7. These T cells are imprinted with an exhausted phenotype and form lymphoid aggregates that can organize in ectopic lymphoid structures. Our work proposes immune-stromal interaction mechanisms promoting a self-sustained and non-resolving local immune response that extends beyond active viral infection and perpetuates tissue remodeling.
MeSH term(s)	Humans ; Chemokine CCL21 ; Chemokines, CC ; COVID-19/immunology ; Fibrosis ; Lung ; T-Lymphocytes/immunology
Chemical Substances	CCL18 protein, human ; CCL21 protein, human ; Chemokine CCL21 ; Chemokines, CC
Language	English
Publishing date	2023-02-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-36333-2
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Article ; Online: COVID-19: Autopsy findings in six patients between 26 and 46 years of age.

Greuel, Selina / Ihlow, Jana / Dragomir, Mihnea-Paul / Streit, Simon / Corman, Victor Max / Haberbosch, Linus / Winkler, David / Meinhardt, Jenny / Aschman, Tom / Schneider, Julia / Trotsyuk, Iryna / Kunze, Catarina Alisa / Maurer, Lukas / Radbruch, Helena / Heppner, Frank L / Horst, David / Elezkurtaj, Sefer

International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases

2021 Volume 108, Page(s) 274–281

Abstract: Objectives: Studies on coronavirus disease 2019 (COVID-19) usually focus on middle-aged and older adults. However, younger patients may present with severe COVID-19 with potentially fatal outcomes. For optimized, more specialized therapeutic regimens in ...

Abstract	Objectives: Studies on coronavirus disease 2019 (COVID-19) usually focus on middle-aged and older adults. However, younger patients may present with severe COVID-19 with potentially fatal outcomes. For optimized, more specialized therapeutic regimens in this particular patient group, a better understanding of the underlying pathomechanisms is of utmost importance. Methods: Our study investigated relevant, pre-existing medical conditions, clinical histories, and autopsy findings, together with SARS-CoV-2-RNA, determined by qPCR, and laboratory data in six COVID-19 decedents aged 50 years or younger, who were autopsied at the Charité University Hospital. Results: From a total of 76 COVID-19 patients who underwent an autopsy at our institution, six (7.9%) were 50 years old or younger. Most of these younger COVID-19 decedents presented with pre-existing medical conditions prior to SARS-CoV-2 infection. These included overweight and obesity, arterial hypertension, asthma, and obstructive sleep apnea, as well as graft-versus-host disease following cancer and bone marrow transplantation. Furthermore, clinical histories and autopsy results revealed a disproportionally high prevalence of thromboembolism and ischemic organ damage in this patient cohort. Histopathology and laboratory results indicated coagulopathies, signs of immune dysregulation, and liver damage. Conclusions: In conclusion, pre-existing health conditions may increase the risk of severe and fatal COVID-19 in younger patients, who may be especially prone to developing thromboembolic complications, immune dysregulation, and liver damage.
MeSH term(s)	Aged ; Autopsy ; COVID-19 ; Humans ; Hypertension ; Middle Aged ; Overweight ; SARS-CoV-2
Language	English
Publishing date	2021-06-03
Publishing country	Canada
Document type	Journal Article
ZDB-ID	1331197-9
ISSN	1878-3511 ; 1201-9712
ISSN (online)	1878-3511
ISSN	1201-9712
DOI	10.1016/j.ijid.2021.05.069
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Article ; Online: Association Between SARS-CoV-2 Infection and Immune-Mediated Myopathy in Patients Who Have Died.

Aschman, Tom / Schneider, Julia / Greuel, Selina / Meinhardt, Jenny / Streit, Simon / Goebel, Hans-Hilmar / Büttnerova, Ivana / Elezkurtaj, Sefer / Scheibe, Franziska / Radke, Josefine / Meisel, Christian / Drosten, Christian / Radbruch, Helena / Heppner, Frank L / Corman, Victor Max / Stenzel, Werner

JAMA neurology

2021 Volume 78, Issue 8, Page(s) 948–960

Abstract: Importance: Myalgia, increased levels of creatine kinase, and persistent muscle weakness have been reported in patients with COVID-19.: Objective: To study skeletal muscle and myocardial inflammation in patients with COVID-19 who had died.: Design, ...

Abstract	Importance: Myalgia, increased levels of creatine kinase, and persistent muscle weakness have been reported in patients with COVID-19. Objective: To study skeletal muscle and myocardial inflammation in patients with COVID-19 who had died. Design, setting, and participants: This case-control autopsy series was conducted in a university hospital as a multidisciplinary postmortem investigation. Patients with COVID-19 or other critical illnesses who had died between March 2020 and February 2021 and on whom an autopsy was performed were included. Individuals for whom informed consent to autopsy was available and the postmortem interval was less than 6 days were randomly selected. Individuals who were infected with SARS-CoV-2 per polymerase chain reaction test results and had clinical features suggestive of COVID-19 were compared with individuals with negative SARS-CoV-2 polymerase chain reaction test results and an absence of clinical features suggestive of COVID-19. Main outcomes and measures: Inflammation of skeletal muscle tissue was assessed by quantification of immune cell infiltrates, expression of major histocompatibility complex (MHC) class I and class II antigens on the sarcolemma, and a blinded evaluation on a visual analog scale ranging from absence of pathology to the most pronounced pathology. Inflammation of cardiac muscles was assessed by quantification of immune cell infiltrates. Results: Forty-three patients with COVID-19 (median [interquartile range] age, 72 [16] years; 31 men [72%]) and 11 patients with diseases other than COVID-19 (median [interquartile range] age, 71 [5] years; 7 men [64%]) were included. Skeletal muscle samples from the patients who died with COVID-19 showed a higher overall pathology score (mean [SD], 3.4 [1.8] vs 1.5 [1.0]; 95% CI, 0-3; P < .001) and a higher inflammation score (mean [SD], 3.5 [2.1] vs 1.0 [0.6]; 95% CI, 0-4; P < .001). Relevant expression of MHC class I antigens on the sarcolemma was present in 23 of 42 specimens from patients with COVID-19 (55%) and upregulation of MHC class II antigens in 7 of 42 specimens from patients with COVID-19 (17%), but neither were found in any of the controls. Increased numbers of natural killer cells (median [interquartile range], 8 [8] vs 3 [4] cells per 10 high-power fields; 95% CI, 1-10 cells per 10 high-power fields; P < .001) were found. Skeletal muscles showed more inflammatory features than cardiac muscles, and inflammation was most pronounced in patients with COVID-19 with chronic courses. In some muscle specimens, SARS-CoV-2 RNA was detected by reverse transcription-polymerase chain reaction, but no evidence for a direct viral infection of myofibers was found by immunohistochemistry and electron microscopy. Conclusions and relevance: In this case-control study of patients who had died with and without COVID-19, most individuals with severe COVID-19 showed signs of myositis ranging from mild to severe. Inflammation of skeletal muscles was associated with the duration of illness and was more pronounced than cardiac inflammation. Detection of viral load was low or negative in most skeletal and cardiac muscles and probably attributable to circulating viral RNA rather than genuine infection of myocytes. This suggests that SARS-CoV-2 may be associated with a postinfectious, immune-mediated myopathy.
MeSH term(s)	Aged ; Aged, 80 and over ; Autopsy ; CD8-Positive T-Lymphocytes/pathology ; COVID-19/metabolism ; COVID-19/pathology ; COVID-19 Nucleic Acid Testing ; COVID-19 Serological Testing ; Case-Control Studies ; Female ; Histocompatibility Antigens Class I/metabolism ; Histocompatibility Antigens Class II/metabolism ; Humans ; Killer Cells, Natural/pathology ; Leukocytes/pathology ; Macrophages/pathology ; Male ; Middle Aged ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Myocarditis/metabolism ; Myocarditis/pathology ; Myocardium/metabolism ; Myocardium/pathology ; Myositis/metabolism ; Myositis/pathology ; RNA, Viral/metabolism ; SARS-CoV-2 ; Sarcolemma/metabolism ; Time Factors
Chemical Substances	Histocompatibility Antigens Class I ; Histocompatibility Antigens Class II ; RNA, Viral
Language	English
Publishing date	2021-06-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2702023-X
ISSN	2168-6157 ; 2168-6149
ISSN (online)	2168-6157
ISSN	2168-6149
DOI	10.1001/jamaneurol.2021.2004
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