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      SARS-CoV-2 antibodies in inflammatory neurological conditions: a multicentre retrospective comparative study


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          It is well established that neurological and non-neurological autoimmune disorders can be triggered by viral infections. It remains unclear whether SARS-CoV-2 infection induces similar conditions and whether they show a distinctive phenotype. We retrospectively identified patients with acute inflammatory CNS conditions referred to our laboratory for antibody testing during the pandemic (March 1 to August 31, 2020). We screened SARS-COV-2 IgA/IgG in all sera by ELISA and confirmed the positivity with additional assays. Clinical and paraclinical data of SARS-COV-2-IgG seropositive patients were compared to those of seronegative cases matched for clinical phenotype, geographical zone, and timeframe. SARS-CoV-2-IgG positivity was detected in 16/339 (4%) sera, with paired CSF positivity in 3/16. 5 of these patients had atypical demyelinating disorders and 11 autoimmune encephalitis syndromes. 9/16 patients had a previous history of SARS-CoV-2 infection and 6 of them were symptomatic. In comparison with 32 consecutive seronegative controls, SARS-CoV-2-IgG-positive patients were older, frequently presented with encephalopathy, had lower rates of CSF pleocytosis and other neurological autoantibodies, and were less likely to receive immunotherapy. When SARS-CoV-2 seropositive versus seronegative cases with demyelinating disorders were compared no differences were seen. Whereas seropositive encephalitis patients less commonly showed increased CSF cells and protein, our data suggest that an antecedent symptomatic or asymptomatic SARS-CoV-2 infection can be detected in patients with autoimmune neurological conditions. These cases are rare, usually do not have specific neuroglial antibodies.

          Supplementary Information

          The online version contains supplementary material available at 10.1007/s12026-023-09384-2.

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          A new coronavirus associated with human respiratory disease in China

          Emerging infectious diseases, such as severe acute respiratory syndrome (SARS) and Zika virus disease, present a major threat to public health 1–3 . Despite intense research efforts, how, when and where new diseases appear are still a source of considerable uncertainty. A severe respiratory disease was recently reported in Wuhan, Hubei province, China. As of 25 January 2020, at least 1,975 cases had been reported since the first patient was hospitalized on 12 December 2019. Epidemiological investigations have suggested that the outbreak was associated with a seafood market in Wuhan. Here we study a single patient who was a worker at the market and who was admitted to the Central Hospital of Wuhan on 26 December 2019 while experiencing a severe respiratory syndrome that included fever, dizziness and a cough. Metagenomic RNA sequencing 4 of a sample of bronchoalveolar lavage fluid from the patient identified a new RNA virus strain from the family Coronaviridae, which is designated here ‘WH-Human 1’ coronavirus (and has also been referred to as ‘2019-nCoV’). Phylogenetic analysis of the complete viral genome (29,903 nucleotides) revealed that the virus was most closely related (89.1% nucleotide similarity) to a group of SARS-like coronaviruses (genus Betacoronavirus, subgenus Sarbecovirus) that had previously been found in bats in China 5 . This outbreak highlights the ongoing ability of viral spill-over from animals to cause severe disease in humans.
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            Neurological associations of COVID-19

            Summary Background The COVID-19 pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is of a scale not seen since the 1918 influenza pandemic. Although the predominant clinical presentation is with respiratory disease, neurological manifestations are being recognised increasingly. On the basis of knowledge of other coronaviruses, especially those that caused the severe acute respiratory syndrome and Middle East respiratory syndrome epidemics, cases of CNS and peripheral nervous system disease caused by SARS-CoV-2 might be expected to be rare. Recent developments A growing number of case reports and series describe a wide array of neurological manifestations in 901 patients, but many have insufficient detail, reflecting the challenge of studying such patients. Encephalopathy has been reported for 93 patients in total, including 16 (7%) of 214 hospitalised patients with COVID-19 in Wuhan, China, and 40 (69%) of 58 patients in intensive care with COVID-19 in France. Encephalitis has been described in eight patients to date, and Guillain-Barré syndrome in 19 patients. SARS-CoV-2 has been detected in the CSF of some patients. Anosmia and ageusia are common, and can occur in the absence of other clinical features. Unexpectedly, acute cerebrovascular disease is also emerging as an important complication, with cohort studies reporting stroke in 2–6% of patients hospitalised with COVID-19. So far, 96 patients with stroke have been described, who frequently had vascular events in the context of a pro-inflammatory hypercoagulable state with elevated C-reactive protein, D-dimer, and ferritin. Where next? Careful clinical, diagnostic, and epidemiological studies are needed to help define the manifestations and burden of neurological disease caused by SARS-CoV-2. Precise case definitions must be used to distinguish non-specific complications of severe disease (eg, hypoxic encephalopathy and critical care neuropathy) from those caused directly or indirectly by the virus, including infectious, para-infectious, and post-infectious encephalitis, hypercoagulable states leading to stroke, and acute neuropathies such as Guillain-Barré syndrome. Recognition of neurological disease associated with SARS-CoV-2 in patients whose respiratory infection is mild or asymptomatic might prove challenging, especially if the primary COVID-19 illness occurred weeks earlier. The proportion of infections leading to neurological disease will probably remain small. However, these patients might be left with severe neurological sequelae. With so many people infected, the overall number of neurological patients, and their associated health burden and social and economic costs might be large. Health-care planners and policy makers must prepare for this eventuality, while the many ongoing studies investigating neurological associations increase our knowledge base.
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              A clinical approach to diagnosis of autoimmune encephalitis.

              Encephalitis is a severe inflammatory disorder of the brain with many possible causes and a complex differential diagnosis. Advances in autoimmune encephalitis research in the past 10 years have led to the identification of new syndromes and biomarkers that have transformed the diagnostic approach to these disorders. However, existing criteria for autoimmune encephalitis are too reliant on antibody testing and response to immunotherapy, which might delay the diagnosis. We reviewed the literature and gathered the experience of a team of experts with the aims of developing a practical, syndrome-based diagnostic approach to autoimmune encephalitis and providing guidelines to navigate through the differential diagnosis. Because autoantibody test results and response to therapy are not available at disease onset, we based the initial diagnostic approach on neurological assessment and conventional tests that are accessible to most clinicians. Through logical differential diagnosis, levels of evidence for autoimmune encephalitis (possible, probable, or definite) are achieved, which can lead to prompt immunotherapy.

                Author and article information

                Immunol Res
                Immunol Res
                Immunologic Research
                Springer US (New York )
                12 May 2023
                12 May 2023
                : 1-8
                [1 ]GRID grid.5611.3, ISNI 0000 0004 1763 1124, Department of Neurosciences, Biomedicine and Movement Sciences, , Neurology Unit, University of Verona, ; Verona, Italy
                [2 ]GRID grid.4991.5, ISNI 0000 0004 1936 8948, Oxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, , University of Oxford, ; Oxford, UK
                [3 ]GRID grid.8348.7, ISNI 0000 0001 2306 7492, Department of Neurology, , John Radcliffe Hospital, Oxford University Hospitals, ; Oxford, UK
                [4 ]GRID grid.4991.5, ISNI 0000 0004 1936 8948, Oxford Epilepsy Research Group, , University of Oxford, ; Oxford, UK
                [5 ]Department of Laboratory Medicine and Pathology, Rochester, MN USA
                [6 ]GRID grid.66875.3a, ISNI 0000 0004 0459 167X, Department of Neurology Mayo Clinic, ; Rochester, MN USA
                [7 ]GRID grid.7637.5, ISNI 0000000417571846, Department of Clinical and Experimental Sciences, , Neurology Unit, University of Brescia, ; Brescia, Italy
                [8 ]GRID grid.415090.9, ISNI 0000 0004 1763 5424, Neurology Unit, Poliambulanza Hospital, Brescia, ; Brescia, Italy
                [9 ]GRID grid.412725.7, Multiple Sclerosis Center, ASST - Spedali Civili of Brescia, ; Brescia, Montichiari Italy
                [10 ]GRID grid.413172.2, Multiple Sclerosis Center “A. Cardarelli” Hospital, ; Naples, Italy
                [11 ]GRID grid.413172.2, Neurological Clinic and Stroke Unit “A. Cardarelli” Hospital, ; Naples, Italy
                [12 ]GRID grid.478938.9, ISNI 0000 0004 0619 6710, Encephalitis Society, ; 32 Castlegate, Malton, UK
                [13 ]GRID grid.10025.36, ISNI 0000 0004 1936 8470, Department of Clinical Infection, Microbiology and Immunology, , University of Liverpool , ; Liverpool, England
                [14 ]GRID grid.5611.3, ISNI 0000 0004 1763 1124, Section of Clinical Biochemistry, , University of Verona, ; Verona, Italy
                [15 ]GRID grid.513352.3, Service of Laboratory Medicine, , Pederzoli Hospital, Peschiera del Garda, ; Verona, Italy
                Author information
                © The Author(s) 2023

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                : 16 February 2023
                : 18 April 2023
                Funded by: Università degli Studi di Verona
                Original Article

                sars-cov-2,encephalitis,demyelinating disorders,viral trigger


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