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Objectives: The immune response in children elicited by SARS-CoV-2 Omicron infection alone or in combination with COVID-19 vaccination (hybrid immunity) is poorly understood. We examined the humoral and cellular immune response following SARS-CoV-2 Omicron infection in unvaccinated children and children who were previously vaccinated with COVID-19 mRNA vaccine.
Methods: Participants were recruited as part of a household cohort study conducted during the Omicron predominant wave (Jan to July 2022) in Victoria, Australia. Blood samples were collected at 1, 3, 6 and 12 months following COVID-19 diagnosis. Humoral immune responses to SARS-CoV-2 Spike proteins from Wuhan, Omicron BA.1, BA.4/5 and JN.1, as well as cellular immune responses to Wuhan and BA.1 were assessed.
Results: A total of 43 children and 113 samples were included in the analysis. Following Omicron infection, unvaccinated children generated low antibody responses but elicited Spike-specific CD4 and CD8 T-cell responses. In contrast, vaccinated children infected with the Omicron variant mounted robust humoral and cellular immune responses to both ancestral strain and Omicron subvariants. Hybrid immunity persisted for at least 6 months post infection, with cellular immune memory characterised by the generation of Spike-specific polyfunctional CD8 T-cell responses.
Conclusion: SARS-CoV-2 hybrid immunity in children is characterised by persisting SARS-CoV-2 antibodies and robust CD4 and CD8 T-cell activation and polyfunctional responses. Our findings contribute to understanding hybrid immunity in children and may have implications regarding COVID-19 vaccination and SARS-CoV-2 re-infections.
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http://dx.doi.org/10.1002/cti2.70008 | DOI Listing |
Lung
September 2025
The Wellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, 97 Lisburn Road, Belfast, Belfast BT9 7BL, UK.
Introduction: Rhinovirus (RV) is the leading cause of exacerbations of lung disease. A sensory neuronal model, derived from human dental pulp stem cells and differentiated into peripheral neuronal equivalents (PNEs), was used to examine RV's effects on airway sensory nerves. We investigated whether RV can directly infect and alter PNEs or whether it exerts effects indirectly via the release of mediators from infected epithelial cells.
View Article and Find Full Text PDFAnn Surg Oncol
September 2025
Department of Thoracic Surgery, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou, Fujian Province, China.
Background: RUNX3 acts as a tumor suppressor gene in non-small-cell lung cancer (NSCLC), yet its specific biological mechanism is still unclear. This study aimed to uncover tumor microenvironment (TME) changes in NSCLC with varying RUNX3 expression statuses through single-cell RNA sequencing.
Patients And Methods: In total, seven patients with NSCLC with detailed pathological data were involved, with three both paracancerous and cancerous tissue samples.
Curr Microbiol
September 2025
Department of Spine Surgery, Honghui Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
This review article describes recent research advances in the relationship between spinal cord injury (SCI) and the gut microbiota and each other's inflammatory response. SCI is a serious neurological disease that directly damages physiological function. Recent studies have shown that SCI significantly affected the composition and function of the gut microbiota, and even caused intestinal inflammation.
View Article and Find Full Text PDFImmunol Invest
September 2025
Respiratory and Critical Care Medicine, The 940th Hospital of Joint Logistics Support Force of chinese PLA, Lanzhou, China.
Background: Pulmonary neuroendocrine cells (PNECs) are specialized airway epithelial cells with dual sensory and secretory functions. They release bioactive mediators --including neuropeptides such as calcitonin gene-related peptide (CGRP) and gastrin-releasing peptide (GRP), and neurotransmitters such as 5-hydroxytryptamine (5-HT) and γ-aminobutyric acid (GABA) --that regulate airway smooth-muscle tone, mucus production, and immune responses. In chronic obstructive pulmonary disease (COPD), these PNEC-derived mediators contribute to airway inflammation, remodeling, and smooth-muscle dysfunction.
View Article and Find Full Text PDFTrends Pharmacol Sci
September 2025
Department of Biosciences and Bioinformatics & Suzhou Municipal Key Lab of Biomedical Sciences and Translational Immunology, School of Science, Xi'an Jiaotong-Liverpool University, Suzhou, China; Biomedical Research Center, School of Science, Engineering and Environment, University of Salford, Manch
Regulatory T cells (Tregs) play a pivotal role in maintaining immune tolerance and sustaining immunological homeostasis. Emerging evidence indicates that Treg characteristics and functional alterations can significantly contribute to the pathogenesis of autoimmune diseases including type 1 diabetes mellitus (T1DM). Notably, recent studies have established a positive correlation between diminished numbers of Tregs and the onset of T1DM.
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