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Background: Immunocompromised individuals are expected to be more prone to severe diseases and, subsequently, death. Genetic disorders and polymorphisms in genes involved in the immune system, such as human leukocyte antigen (HLA), inflammatory cytokines, and killer-cell immunoglobulin-like receptors, can be involved in the immune system's response to various pathogens. In the current survey, the data were received from the world health organization, collected around the world.
Results: Spearman's coefficient correlation test for evaluating the relationship between the Daily Death Rates (DDR) and immunological variables showed a statistically significant correlation between the DDR and all immunological variables except TNFa857T, TNFa863A IL2330G, and IL2166T ( < 0.001). Also, there was a statistically significant correlation between the DDR and some HLA markers.
Conclusion: This meta-analysis study shows that predictive biomarkers and mortality of COVID-19 are associated with HLA markers. However, these results should be confirmed in a more structured agreement. It is worth noting that the design of new studies should consider potential diseases with poor prognoses because they are related to these immune genetic markers.
Supplementary Information: The online version contains supplementary material available at 10.1186/s42269-022-00844-7.
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http://dx.doi.org/10.1186/s42269-022-00844-7 | DOI Listing |
Cardiovasc Res
September 2025
Center for Cardiovascular Research, Division of Cardiology, Department of Medicine, Washington University in Saint Louis, St. Louis, MO, USA.
Aims: Although the ability of the heart to adapt to environmental stress has been studied extensively, the molecular and cellular mechanisms responsible for cardioprotection are not yet fully understood. In this study, we sought to elucidate these mechanisms for cytoprotection using a model of stress-induced cardiomyopathy.
Methods And Results: We administered Toll-like receptor (TLR) agonists or diluent to wild-type mice and assessed for cardioprotection against injury from a high intraperitoneal dose of isoproterenol (ISO) administered 7 days later.
Elife
September 2025
Department of Biology, University of Copenhagen, Copenhagen, Denmark.
Sickness-induced sleep is a behavior conserved across species that promotes recovery from illness, yet the underlying mechanisms are poorly understood. Here, we show that interleukin-6-like cytokine signaling from the gut to brain glial cells regulates sleep. Under healthy conditions, this pathway promotes wakefulness.
View Article and Find Full Text PDFPLoS One
September 2025
Centre for Experimental Pathogen Host Research, School of Medicine, University College Dublin, Dublin, Ireland.
Background: Acute viral respiratory infections (AVRIs) rank among the most common causes of hospitalisation worldwide, imposing significant healthcare burdens and driving the development of pharmacological treatments. However, inconsistent outcome reporting across clinical trials limits evidence synthesis and its translation into clinical practice. A core outcome set (COS) for pharmacological treatments in hospitalised adults with AVRIs is essential to standardise trial outcomes and improve research comparability.
View Article and Find Full Text PDFPLoS One
September 2025
Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Background: Disulfidptosis, a novel cellular death manner, has yet to be fully explored within the context of pulmonary arterial hypertension (PAH). This study aims to identify genes implicated in PAH that are involved in disulfidptosis.
Method: Based on data from the GEO database, this study employed co-expression analysis, Weighted Gene Co-Expression Network Analysis (WGCNA), hub gene identification, and Gene Set Enrichment Analysis (GSEA) to uncover genes associated with PAH and disulfidptosis.
ACS Chem Neurosci
September 2025
Department of Medical Biology, Faculty of Medicine, Bahçeşehir University, Istanbul 34353, Turkey.
IL-17A is a pro-inflammatory cytokine that significantly contributes to the pathogenesis of autoimmune diseases, including multiple sclerosis (MS). Previous studies have suggested that PARP-1 inhibitors can modulate IL-17A-mediated inflammation, prompting the investigation of Niraparib, an FDA-approved PARP-1 inhibitor, as a potential therapeutic agent for MS. In this study, we hypothesized that Niraparib could disrupt the interaction between IL-17A and its receptor, IL-17RA.
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