Neuropathology of patients with COVID-19 in Germany: a post-mortem case series
Open accessAbstract
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).
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No other anti-SARS-CoV-2 antibody yielded specific signal over controls.
“However, no other antibody–including those also used in recent publications9,30–yielded specific signal over controls.”
From Dysregulation of brain and choroid plexus cell types in severe COVID-19 (2021) · cites this paper as [9]
A recent article found SARS-CoV-2 virus in 53% of brain tissues of people who died by COVID-19.
“A recent article found SARS-CoV-2 virus in 53% of brain tissues of people who died by COVID-19, even though brain lesions were non-specific and could not be attributed to SARS-CoV-2 lesions directly [157].”
From Cognitive decline following acute viral infections: literature review and projections for post-COVID-19 (2022) · cites this paper as [157]
Brain lesions in people who died by COVID-19 were non-specific and could not be directly attributed to SARS-CoV-2 lesions.
“A recent article found SARS-CoV-2 virus in 53% of brain tissues of people who died by COVID-19, even though brain lesions were non-specific and could not be attributed to SARS-CoV-2 lesions directly [157].”
From Cognitive decline following acute viral infections: literature review and projections for post-COVID-19 (2022) · cites this paper as [157]
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- Authors
- Matschke, J., Lütgehetmann, M., Hagel, C., Sperhake, J. P., Schröder, A. S., Edler, C., Mushumba, H., Fitzek, A., Allweiss, L., Dandri, M., Dottermusch, M., Heinemann, A., Pfefferle, S., Schwabenland, M., Sumner Magruder, D., Bonn, S., Prinz, M., Gerloff, C., Püschel, K., Krasemann, S., Aepfelbacher, M., & Glatzel, M.
- Affiliations
- University Medical Center Hamburg-Eppendorf (DE)
- University of Freiburg (DE)
- German Center for Neurodegenerative Diseases (DE)
- Corresponding author
- Glatzel, Markus
- ORCID
- Venue
- The Lancet Neurology
- Publisher
- Elsevier BV
- Published
- 2020-11
- Volume
- 19
- Issue
- 11
- Pages
- 919-929
- ISSN
- 1474-4422 (ISSN-L)
- PMC
- PMC7535629
- OpenAlex
- W3090344202
- Cited by
- 1,300
- References
- 35
- Citations by year
- 2026: 51 · 2025: 105 · 2024: 170 · 2023: 251 · 2022: 332 · 2021: 361 · 2020: 25
- FWCI
- 104.90
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Lancet Neurology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DZNE Pub (submittedVersion)
- Funders
- Deutsche Forschungsgemeinschaft (SFB1286, SFB877)
- Deutsches Zentrum für Infektionsforschung
- Topics
- Health Sciences › Medicine › Neurology › Long-Term Effects of COVID-19
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- COVID-19 pandemic, SARS-CoV-2, neuropathology, neuroinflammation, astrocyte activation, microglial activation, cytotoxic T lymphocytes, brainstem, cerebellum, olfactory bulb, basal ganglia, postmortem brain
- MeSH terms
- Neuropathology, Betacoronavirus, COVID-19, SARS-CoV-2, Aged, Aged, 80 and over, Autopsy, Brain, Female, Germany, Humans, Male, Middle Aged, Pneumonia, Viral, Coronavirus Infections, Pandemics, Transcriptome
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