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SARS-CoV-2 proteins

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    Secondary analysis of transcriptomes of SARS-CoV-2 infection MESHD models to characterize COVID-19 MESHD

    Authors: Anil G Jegga

    doi:10.1101/2020.08.27.270835 Date: 2020-08-28 Source: bioRxiv

    Knowledge about the molecular mechanisms driving COVID-19 MESHD pathophysiology and outcomes is still limited. To learn more about COVID-19 MESHD pathophysiology we performed secondary analyses of transcriptomic data from two in vitro (Calu-3 and Vero E6 cells) and one in vivo (Ad5- hACE2 HGNC-sensitized mice) models of SARS-CoV-2 infection MESHD. We found 1467 conserved differentially expressed host genes (differentially expressed in at least two of the three model system transcriptomes compared) in SARS-CoV-2 infection MESHD. To find potential genetic factors associated with COVID-19 MESHD, we analyzed these conserved differentially expressed genes using known human genotype-phenotype associations. Genome-wide association study enrichment analysis showed evidence of enrichment for GWA loci associated with platelet functions, blood pressure, body mass index, respiratory functions, and neurodegenerative and neuropsychiatric diseases MESHD, among others. Since human protein complexes are known to be directly related to viral infection, we combined and analyzed the conserved transcriptomic signature with SARS-CoV-2-host protein-protein interaction data and found more than 150 gene clusters. Of these, 29 clusters (with 5 or more genes in each cluster) had at least one gene encoding protein that interacts with SARS-CoV-2 proteome. These clusters were enriched for different cell types in lung including epithelial, endothelial, and immune cell types suggesting their pathophysiological relevancy to COVID-19 MESHD. Finally, pathway analysis on the conserved differentially expressed genes and gene clusters showed alterations in several pathways and biological processes that could enable in understanding or hypothesizing molecular signatures inducing pathophysiological changes, risks, or sequelae of COVID-19 MESHD.

    18F-FDG brain PET metabolism in post- SARS-CoV-2 infection MESHD: substrate for persistent/delayed disorders?

    Authors: Eric Guedj; Matthieu Million; Pierre Dudouet; Hervé Tissot-Dupont; Fabienne Bregeon; Serge Cammilleri; Didier Raoult

    doi:10.21203/rs.3.rs-40021/v1 Date: 2020-07-03 Source: ResearchSquare

    Purpose: Several brain complications of SARS-CoV-2 infection MESHD have been reported. It has been moreover speculated that this neurotropism could potentially cause a delayed outbreak of neuropsychiatric and neurodegenerative diseases MESHD of neuroinflammatory origin. A propagation mechanism has been proposed across the cribriform plate of the ethmoid bone, from the nose to the olfactory epithelium, and possibly afterwards to other limbic structures, and deeper parts of the brain including the brainstem. Methods: Review of clinical examination, and whole-brain voxel-based analysis of 18F-FDG PET metabolism in comparison to healthy subjects (p-voxel<0.001, p-cluster<0.05), of two patients with confirmed diagnosis of SARS-CoV-2 pneumonia MESHD explored at the post-viral stage of the disease.Results: Hypometabolism of the olfactory/rectus gyrus was found on the two patients, especially one with 4 weeks prolonged anosmia MESHD. Additional hypometabolisms were found within bilateral amygdala, hippocampus, cingulate cortex, thalamus, pons and medulla brainstem in the other patient who complained of delayed onset of an atypical painful syndrome MESHD.Conclusion: These preliminary findings reinforce the hypotheses of SARS-CoV-2 neurotropism MESHD through the olfactory bulb, and the possible extension of this impairment to other limbic structures and to the brainstem. 18F-FDG PET hypometabolism could constitute a cerebral quantitative biomarker of this involvement. Post-viral cohort studies are required to specify the exact relationship between limbic/brainstem hypometabolisms and the possible persistent disorders, especially involving cognitive or emotion disturbances MESHD, residual respiratory symptoms or painful complaints.

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MeSH Disease
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SARS-CoV-2 Proteins


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