ArticlePloS one2026
Elevated mortality and upregulated SARS-CoV-2-associated pathways in innate and adaptive immune cells from individuals with Down syndrome.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Immune Dysregulation in Down Syndrome: Implications for Infectious Susceptibility and Vaccine Response.Journal of clinical immunology · 2026Review
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Authors and funding
18 authors.
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Abstract
Trisomy 21 increases the risk of severe outcomes and mortality in hospitalized individuals with Down syndrome (DS) following SARS-CoV-2 infection. Using data from the Brazilian Epidemiological Surveillance Information System Influenza (SIVEP-Gripe), we analyzed 102,767 hospitalized COVID-19 patients (1,115 DS and 101,652 non-DS, NDS). DS patients had a higher prevalence of comorbidities and required ventilatory support, ICU admission, and intubation more frequently than NDS patients (p < 0.001). Mortality was 4.5 times higher in DS patients aged 0-30 years (26.3% vs. 5.9%, p < 0.001) and remained 2.22 times higher after adjusting for comorbidities. DS patients over 30 years also exhibited a 22% increase in mortality (PR 1.22, p < 0.001). Gene expression analysis of pre-pandemic monocytes and T cells from DS individuals revealed upregulated pathways linked to SARS-CoV-2 infection, including interferon signaling and cytokine interactions. This baseline immune dysregulation may contribute to severe COVID-19 outcomes in DS patients. Identifying these altered pathways could inform targeted therapeutic strategies to improve immune homeostasis and clinical outcomes. To the best of our knowledge, this is the first study integrating nationwide clinical outcomes with pre-pandemic immune transcriptomic data to mechanistically explain the heightened COVID-19 severity in individuals with DS.
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