ArticleDisease models & mechanisms2022
Molecular signature of postmortem lung tissue from COVID-19 patients suggests distinct trajectories driving mortality.
Article in Disease models & mechanisms, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Meta-analysis of Transcriptomic Data from Lung Autopsy and Cellular Models of SARS-CoV-2 Infection.Biochemical genetics · 2024Pooled it
- Effect of aberrant fructose metabolism following SARS-CoV-2 infection on colorectal cancer patients' poor prognosis.PLoS computational biology · 2024Article
- A Machine Learning Model for the Prediction of COVID-19 Severity Using RNA-Seq, Clinical, and Co-Morbidity Data.Diagnostics (Basel, Switzerland) · 2024Article
- SARS-CoV-2 Viral Replication Persists in the Human Lung for Several Weeks after Symptom Onset.American journal of respiratory and critical care medicine · 2024Article
- Microplastics dysregulate innate immunity in the SARS-CoV-2 infected lung.Frontiers in immunology · 2024Article
- Human-derived air-liquid interface cultures decipher Alzheimer's disease-SARS-CoV-2 crosstalk in the olfactory mucosa.Journal of neuroinflammation · 2023Article
- Bacterial Biomarkers of the Oropharyngeal and Oral Cavity during SARS-CoV-2 Infection.Microorganisms · 2023Article
- Crossroads in virology: current challenges and future perspectives in the age of emerging viruses.Disease models & mechanisms · 2023Article
- Understanding the neurological implications of acute and long COVID using brain organoids.Disease models & mechanisms · 2023Review
- Review
- Uncovering common pathobiological processes between COVID-19 and pulmonary arterial hypertension by integrating Omics data.Pulmonary circulation · 2023Article
- A study on the morbid histopathological changes in COVID-19 patients with or without comorbidities using minimally invasive tissue sampling.Journal of medical virology · 2023Article
- Review
- ACE2 protein expression in lung tissues of severe COVID-19 infection.Scientific reports · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To elucidate the molecular mechanisms that manifest lung abnormalities during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections, we performed whole-transcriptome sequencing of lung autopsies from 31 patients with severe COVID-19 and ten uninfected controls. Using metatranscriptomics, we identified the existence of two distinct molecular signatures of lethal COVID-19. The dominant 'classical' signature (n=23) showed upregulation of the unfolded protein response, steroid biosynthesis and complement activation, supported by massive metabolic reprogramming leading to characteristic lung damage. The rarer signature (n=8) that potentially represents 'cytokine release syndrome' (CRS) showed upregulation of cytokines such as IL1 and CCL19, but absence of complement activation. We found that a majority of patients cleared SARS-CoV-2 infection, but they suffered from acute dysbiosis with characteristic enrichment of opportunistic pathogens such as Staphylococcus cohnii in 'classical' patients and Pasteurella multocida in CRS patients. Our results suggest two distinct models of lung pathology in severe COVID-19 patients, which can be identified through complement activation, presence of specific cytokines and characteristic microbiome. These findings can be used to design personalized therapy using in silico identified drug molecules or in mitigating specific secondary infections.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.