COVID-19 mortality is associated with pre-existing impaired innate immunity in health conditions
PeerJ, ISSN: 2167-8359, Vol: 10, Page: e13227
2022
- 3Citations
- 34Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations3
- Citation Indexes3
- Captures34
- Readers34
- 34
Article Description
COVID-19 can be life-threatening to individuals with chronic diseases. To prevent severe outcomes, it is critical that we comprehend pre-existing molecular abnormalities found in common health conditions that predispose patients to poor prognoses. In this study, we focused on 14 pre-existing health conditions for which increased hazard ratios of COVID-19 mortality have been documented. We hypothesized that dysregulated gene expression in these pre-existing health conditions were risk factors of COVID-19 related death, and the magnitude of dysregulation (measured by fold change) were correlated with the severity of COVID-19 outcome (measured by hazard ratio). To test this hypothesis, we analyzed transcriptomics data sets archived before the pandemic in which no sample had COVID-19. For a given pre-existing health condition, we identified differentially expressed genes by comparing individuals affected by this health condition with those unaffected. Among genes differentially expressed in multiple health conditions, the fold changes of 70 upregulated genes and 181 downregulated genes were correlated with hazard ratios of COVID-19 mortality. These pre-existing dysregulations were molecular risk factors of severe COVID-19 outcomes. These genes were enriched with endoplasmic reticulum and mitochondria function, proinflammatory reaction, interferon production, and programmed cell death that participate in viral replication and innate immune responses to viral infections. Our results suggest that impaired innate immunity in pre-existing health conditions is associated with increased hazard of COVID-19 mortality. The discovered molecular risk factors are potential prognostic biomarkers and targets for therapeutic intervention.
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