Corpus overview


MeSH Disease

Human Phenotype


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    Persistence of viral RNA, widespread thrombosis MESHD thrombosis and abnormal HP and abnormal cellular syncytia are hallmarks of COVID-19 lung pathology

    Authors: Mauro Giacca; Rossana Bussani; Edoardo Schneider; Lorena Zentilin; Chiara Collesi; Hashim Ali; Luca Braga; Ilaria Secco; Maria Concetta Volpe; Andrea Colliva; Fabrizio Zanconati; Giorgio Berlot; Furio Silvestri; Serena Zacchigna

    doi:10.1101/2020.06.22.20136358 Date: 2020-06-26 Source: medRxiv

    COVID-19 is a deadly pulmonary disease MESHD with unique clinical features. A thorough understanding of the molecular and histological correlates of the disease MESHD is still missing, especially because post-mortem analysis of COVID-19-affected organs has been so far scant and often anecdotical. Here we report the results of the systematic analysis of 41 consecutive post-mortem samples from individuals who died of COVID-19. We found that the disease MESHD is characterized by extensive alveolar damage and thrombosis MESHD of the lung micro- and macro-vasculature. Thrombi were in different stages of organization, consistent with an ongoing, endogenous thrombotic process. In all the analyzed samples, in situ RNA hybridization showed that pneumocytes and vascular endothelial cells had massive presence of viral RNA even at the later stages of the disease MESHD. An additional feature of the disease MESHD was the presence, in the vast majority of patients, of a large number of dysmorphic pneumocytes, often forming large syncytial elements, a consequence of the fusogenic activity of the viral Spike protein, detected with specific antibodies SERO. Despite occasional presence of virus-positive cells in the heart, no overt signs of viral infection MESHD were detected in other organs, which showed common alterations compatible with prolonged hypoxia MESHD, multifocal organ disease MESHD or previous comorbidities. In summary, COVID-19 is a unique interstitial pneumonia MESHD pneumonia HP with extensive lung thrombosis MESHD, long-term persistence of viral replication in pneumocytes and endothelial cells, along with the presence of infected cellular syncytia in the lung. We propose that several of the COVID-19 disease MESHD features are due to the persistence of virus-infected cells in the lungs of the infected individuals for the duration of the disease MESHD.

    Lung biopsy cells transcriptional landscape from COVID-19 patient stratified lung injury MESHD in SARS-CoV-2 infection MESHD through impaired pulmonary surfactant metabolism

    Authors: Abul B.M.M.K. Islam; Md. Abdullah-Al-Kamran Khan

    doi:10.1101/2020.05.07.082297 Date: 2020-05-08 Source: bioRxiv

    Clinical management of COVID-19 is still complicated due to the lack of therapeutic interventions to reduce the breathing problems, respiratory complications and acute lung injury MESHD - which are the major complications of most of the mild to critically affected patients and the molecular mechanisms behind these clinical features are still largely unknown. In this study, we have used the RNA-seq gene expression pattern in the COVID-19 affected lung biopsy cells and compared it with the effects observed in typical cell lines infected with SARS-CoV-2 and SARS-CoV. We performed functional overrepresentation analyses using these differentially expressed genes to signify the processes/pathways which could be deregulated during SARS-CoV-2 infection MESHD resulting in the symptomatic impairments observed in COVID-19. Our results showed that the significantly altered processes include inflammatory responses, antiviral cytokine signaling, interferon responses, and interleukin signaling etc. along with downmodulated processes related to lungs functionality like-responses to hypoxia MESHD, lung development, respiratory processes, cholesterol biosynthesis and surfactant metabolism. We also found that the viral protein interacting hosts proteins involved in similar pathways like: respiratory failure HP, lung diseases MESHD, asthma MESHD asthma HP, and hypoxia MESHD responses etc., suggesting viral proteins might be deregulating the processes related to acute lung injury MESHD/breathing complications in COVID-19 patients. Protein-protein interaction networks of these processes and map of gene expression of deregulated genes revealed that several viral proteins can directly or indirectly modulate the host genes/proteins of those lung related processes along with several host transcription factors and miRNAs. Surfactant proteins and their regulators SPD, SPC, TTF1 etc. which maintains the stability of the pulmonary tissue are found to be downregulated through viral NSP5, NSP12 that could lead to deficient gaseous exchange by the surface films. Mitochondrial dysfunction owing to the aberration of NDUFA10, NDUFAF5, SAMM50 etc. by NSP12; abnormal thrombosis HP thrombosis MESHD in lungs through atypical PLAT, EGR1 functions by viral ORF8, NSP12; dulled hypoxia MESHD responses due to unusual shift in HIF-1 downstream signaling might be the causative elements behind the acute lung injury MESHD in COVID-19 patients. Our study put forward a distinct mechanism of probable virus induced lung damage apart from cytokine storm and advocate the need of further research for alternate therapy in this direction.

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MeSH Disease
Human Phenotype

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