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Neurological Sciences ; 43(Supplement 1):S323-S324, 2022.
Article in English | EMBASE | ID: covidwho-2174297


Objectives: Neurological manifestations are common in COVID-19, the disease caused by SARS-CoV-2. Despite reports of detection of SARS-CoV-2 in the brain and cerebrospinal fluid of COVID-19 patients, it's still unclear whether the virus can infect the central nervous system, and which neuropathological alterations can be ascribed to viral tropism, rather than immunemediated mechanisms. In the present study, we assess the neuropathological alterations occurring in COVID-19 subjects deceased during the acute stages of the disease and compare these findings with the neuropathological alterations occurring in pneumonia / respiratory failure patients. Materials: 24 COVID-19 patients and 18 sex- and age-matched controls who died due to pneumonia / respiratory failure were included in the study. Clinical and demographical data was retrospectively obtained. The brain was sampled and underwent extensive neuropathological sampling, with particular focus on the brainstem. Method(s): Immunoperoxidase and immunofluorescent staining for 20 different antibodies (CD3, CD20, CD61, CD68, TMEM119, HLA-DR, pTAU, Beta-Amyloid, Beta-III Tubulin, GFAP, ACE2R, TMPRSS2, etc) was performed to assess the neuropathological alterations and two SARS-CoV-2 specific antibodies were employed to assess viral tropism. RT-PCR analyses for SARS-CoV-2 genomic sequences was performed to complement these findings. Morphometrical evaluation of brainstem regions of interest was performed to asses microglial activation and density. Result(s): Aside from a wide spectrum of neuropathological alterations, including hypoxic/ischemic damage, perivascular lympho-monocytic cuffing and other aspecific findings, SARS-CoV-2-immunoreactive neurons were detected in the vagal nuclei of the medulla and in the substantia nigra of 5 COVID- 19 subjects. Viral RNA was also detected by real-time RT-PCR. Quantification of reactive microglia revealed an anatomically segregated pattern of inflammation within affected brainstem regions, and was higher when compared to controls. Discussion(s): These findings suggest that while acute fatal COVID-19 is characterized by neuropathological alterations, such as hypoxic / ischaemic damage, microthromboses and microgliosis, mediated mainly by systemic infection and the ongoing cytokine storm, SARS-CoV-2 neurotropism is a possible, yet not frequent, consequence of infection without immediately appreciable neuropathological alterations, at least in the acute phases of the disease. Conclusion(s): These findings indicate the need to further investigation of the role of SARS-CoV-2 neurotropism in the general population, not only in severe / fatal COVID-19 cases, including whether SARS-CoV-2 neurotropism may determine specific neuropathological sequelae in cases of prolonged infection or in patients suffering from the long-term effects of COVID-19.

Clinical Neuropathology ; 40(4):S110, 2021.
Article in English | EMBASE | ID: covidwho-1325931


Introduction: SARS-CoV-2 is a novel strain of Coronavirus that mainly targets the respiratory tract, but with important implications also for the CNS. Data deriving from autopsy studies supports the neuroinvasive potential of SARS-CoV-2, even though infection appears to be limited to sparse cells within the brainstem and was not associated with the severity of neuropathological changes. Objectives: In the following study, we assess the neuropathological changes of 14 patients who died following a diagnosis of Sars-CoV-2 infection in Padova, Italy from March 2020 to January 2021. Methods: The cerebrum, cerebellum, brainstem, cranial nerves and meninges were sampled and histopathological evaluation was performed by histochemistry and immunohistochemistry for GFAP, CD8, CD61, CD68 and HLA-DR antibodies. SARS-CoV-2 proteins and RNA were investigated through immunohistochemistry, RTPCR and in-situ hybridization. Results: Small vessel thromboses were identified in two patients, while fresh territory ischaemic lesions were identified in three patients. Astrogliosis and microglial activation were more pronounced at the level of the brainstem in all subjects. SARS-CoV-2 proteins were found within the brainstem and meninges of 4 patients. In one patient, SARS-CoV-2 proteins and RNA were identified throughout the whole rostrocaudal extent of the brainstem and basal ganglia, with prominent involvement of neurons and oligodendrocytes in the mesencephalon, rostral pons and medulla. Conclusion: Although limited by the number of our cohort, the study contributes to define the neuroinvasive potential of SARS-CoV-2 within the CNS. In line with available literature, SARS-CoV-2 invasion does not appear to correlate with the severity of neuropathological changes.