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CSF single cell transcriptomic changes associated with post-acute sequelae of SARS CoV 2 infection

ABSTRACT: Natural history and mechanisms for persistent cognitive symptoms (also known as “brain fog”) following acute and often mild COVID-19 are unknown. In a large prospective cohort of people who recovered from acute COVID-19 in the New York City/New Jersey area, we found the presence of cognitive dysfunction to closely associate with fatigue symptoms and, in some people, brain imaging abnormalities. In a smaller subset of people who underwent cerebrospinal fluid analysis at a median of 9 months after their initial infection, there was no evidence to suggest changes related to Alzheimer’s disease or neurodegeneration. However, single cell gene expression analysis of immune cells (T cells, border associated macrophages, microglia-like myeloid cells, myeloid dendritic cells) from the cerebrospinal fluid showed many changes seen in models of acute SARS-CoV-2 infection. Longitudinal follow-up additionally showed recovery from cognitive dysfunction to be very slow, and associate with greater – not less – activation of interferon-related inflammatory processes in both single cell transcriptomic and targeted fluid proteomic studies. These findings suggest persistent brain fog following COVID-19 to resemble more viral infection than autoimmune disorders.

ORGANISM(S): Homo sapiens

PROVIDER: GSE241385 | GEO | 2024/05/20

REPOSITORIES: GEO

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Project description:Neurologic manifestations are among the most frequently reported complications of COVID-19. However, given the paucity of tissue samples and highly infectious nature of the etiologic agent of COVID-19, we have limited information to understand the neuropathogenesis of COVID-19. Therefore to better understand the impact of COVID-19 in brain, we employed mass-spectrometry-based proteomics using data-independent acquisition mode (DIA) to investigate cerebrospinal fluid (CSF) proteins collected from two different non-human primates, Rhesus Macaque and African Green Monkeys for the neurologic effects of the infection. These monkeys exhibited minimal to mild pulmonary pathology but moderate to severe CNS pathology. Our results indicate that CSF proteome changes after infection resolution correspond with bronchial virus abundance during early infection and revealed substantial differences between the infected NHPs and their age-matched uninfected controls, suggesting these differences could reflect altered secretion of CNS factors in response to SARS-CoV-2-induced neuropathology. We also observed the infected animals to exhibit much scattered data distributions as compared to the tightly clustered corresponding controls which suggest the heterogeneity of the CSF proteome change and the host response to the viral infection. In addition, dysregulated CSF proteins were preferentially enriched in functional pathways associated with progressive neurodegenerative disorders, hemostasis and innate immune responses that could influence neuroinflammatory responses following COVID-19. Mapping dysregulated proteins to the Human Brain Protein Atlas found that these proteins tended to be enriched in brain regions that exhibit more frequent injury following COVID-19. It therefore appears reasonable to speculate that such CSF protein changes could serve as signatures for neurologic injury, identify important regulatory pathways in this process, and potentially reveal therapeutic targets to prevent or attenuate the development of neurologic injuries following COVID-19.

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CSF single cell transcriptomic changes associated with post-acute sequelae of SARS CoV 2 infection

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