Home > Publications Database > Neuropathology of patients with COVID-19 in Germany: a post-mortem case series > print |
001 | 154197 | ||
005 | 20240618100829.0 | ||
024 | 7 | _ | |a pmc:PMC7535629 |2 pmc |
024 | 7 | _ | |a 10.1016/S1474-4422(20)30308-2 |2 doi |
024 | 7 | _ | |a 1474-4422 |2 ISSN |
024 | 7 | _ | |a 1474-4465 |2 ISSN |
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037 | _ | _ | |a DZNE-2021-00059 |
082 | _ | _ | |a 610 |
100 | 1 | _ | |a Matschke, Jakob |b 0 |
245 | _ | _ | |a Neuropathology of patients with COVID-19 in Germany: a post-mortem case series |
260 | _ | _ | |a London |c 2020 |b Lancet Publ. Group |
336 | 7 | _ | |a article |2 DRIVER |
336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1718698038_13421 |2 PUB:(DE-HGF) |
336 | 7 | _ | |a ARTICLE |2 BibTeX |
336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
520 | _ | _ | |a Background: Prominent clinical symptoms of COVID-19 include CNS manifestations. However, it is unclear whether severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of COVID-19, gains access to the CNS and whether it causes neuropathological changes. We investigated the brain tissue of patients who died from COVID-19 for glial responses, inflammatory changes, and the presence of SARS-CoV-2 in the CNS.Methods: In this post-mortem case series, we investigated the neuropathological features in the brains of patients who died between March 13 and April 24, 2020, in Hamburg, Germany. Inclusion criteria comprised a positive test for SARS-CoV-2 by quantitative RT-PCR (qRT-PCR) and availability of adequate samples. We did a neuropathological workup including histological staining and immunohistochemical staining for activated astrocytes, activated microglia, and cytotoxic T lymphocytes in the olfactory bulb, basal ganglia, brainstem, and cerebellum. Additionally, we investigated the presence and localisation of SARS-CoV-2 by qRT-PCR and by immunohistochemistry in selected patients and brain regions.Findings: 43 patients were included in our study. Patients died in hospitals, nursing homes, or at home, and were aged between 51 years and 94 years (median 76 years [IQR 70-86]). We detected fresh territorial ischaemic lesions in six (14%) patients. 37 (86%) patients had astrogliosis in all assessed regions. Activation of microglia and infiltration by cytotoxic T lymphocytes was most pronounced in the brainstem and cerebellum, and meningeal cytotoxic T lymphocyte infiltration was seen in 34 (79%) patients. SARS-CoV-2 could be detected in the brains of 21 (53%) of 40 examined patients, with SARS-CoV-2 viral proteins found in cranial nerves originating from the lower brainstem and in isolated cells of the brainstem. The presence of SARS-CoV-2 in the CNS was not associated with the severity of neuropathological changes.Interpretation: In general, neuropathological changes in patients with COVID-19 seem to be mild, with pronounced neuroinflammatory changes in the brainstem being the most common finding. There was no evidence for CNS damage directly caused by SARS-CoV-2. The generalisability of these findings needs to be validated in future studies as the number of cases and availability of clinical data were low and no age-matched and sex-matched controls were included.Funding: German Research Foundation, Federal State of Hamburg, EU (eRARE), German Center for Infection Research (DZIF). |
536 | _ | _ | |a 342 - Disease Mechanisms and Model Systems (POF3-342) |0 G:(DE-HGF)POF3-342 |c POF3-342 |f POF III |x 0 |
588 | _ | _ | |a Dataset connected to CrossRef |
650 | _ | 2 | |a Aged |2 MeSH |
650 | _ | 2 | |a Aged, 80 and over |2 MeSH |
650 | _ | 2 | |a Autopsy: methods |2 MeSH |
650 | _ | 2 | |a Betacoronavirus: isolation & purification |2 MeSH |
650 | _ | 2 | |a Brain: pathology |2 MeSH |
650 | _ | 2 | |a Brain: virology |2 MeSH |
650 | _ | 2 | |a COVID-19 |2 MeSH |
650 | _ | 2 | |a Coronavirus Infections: epidemiology |2 MeSH |
650 | _ | 2 | |a Coronavirus Infections: genetics |2 MeSH |
650 | _ | 2 | |a Coronavirus Infections: pathology |2 MeSH |
650 | _ | 2 | |a Female |2 MeSH |
650 | _ | 2 | |a Germany: epidemiology |2 MeSH |
650 | _ | 2 | |a Humans |2 MeSH |
650 | _ | 2 | |a Male |2 MeSH |
650 | _ | 2 | |a Middle Aged |2 MeSH |
650 | _ | 2 | |a Neuropathology |2 MeSH |
650 | _ | 2 | |a Pandemics |2 MeSH |
650 | _ | 2 | |a Pneumonia, Viral: epidemiology |2 MeSH |
650 | _ | 2 | |a Pneumonia, Viral: genetics |2 MeSH |
650 | _ | 2 | |a Pneumonia, Viral: pathology |2 MeSH |
650 | _ | 2 | |a SARS-CoV-2 |2 MeSH |
650 | _ | 2 | |a Transcriptome: genetics |2 MeSH |
700 | 1 | _ | |a Lütgehetmann, Marc |b 1 |
700 | 1 | _ | |a Hagel, Christian |b 2 |
700 | 1 | _ | |a Sperhake, Jan P |b 3 |
700 | 1 | _ | |a Schröder, Ann Sophie |0 P:(DE-HGF)0 |b 4 |
700 | 1 | _ | |a Edler, Carolin |b 5 |
700 | 1 | _ | |a Mushumba, Herbert |b 6 |
700 | 1 | _ | |a Fitzek, Antonia |b 7 |
700 | 1 | _ | |a Allweiss, Lena |b 8 |
700 | 1 | _ | |a Dandri, Maura |b 9 |
700 | 1 | _ | |a Dottermusch, Matthias |b 10 |
700 | 1 | _ | |a Heinemann, Axel |b 11 |
700 | 1 | _ | |a Pfefferle, Susanne |b 12 |
700 | 1 | _ | |a Schwabenland, Marius |b 13 |
700 | 1 | _ | |a Sumner Magruder, Daniel |b 14 |
700 | 1 | _ | |a Bonn, Stefan |0 P:(DE-2719)2810547 |b 15 |u dzne |
700 | 1 | _ | |a Prinz, Marco |b 16 |
700 | 1 | _ | |a Gerloff, Christian |b 17 |
700 | 1 | _ | |a Püschel, Klaus |b 18 |
700 | 1 | _ | |a Krasemann, Susanne |b 19 |
700 | 1 | _ | |a Aepfelbacher, Martin |b 20 |
700 | 1 | _ | |a Glatzel, Markus |b 21 |
773 | _ | _ | |a 10.1016/S1474-4422(20)30308-2 |g Vol. 19, no. 11, p. 919 - 929 |0 PERI:(DE-600)2079704-7 |n 11 |p 919 - 929 |t The lancet |v 19 |y 2020 |x 1474-4422 |
856 | 4 | _ | |u https://pub.dzne.de/record/154197/files/DZNE-2021-00059_Restricted.pdf |
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