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TGFβ links EBV to multisystem inflammatory syndrome in children.
Nature
March 2025
German Rheumatology Research Center, a Leibniz-Institute (DRFZ), Berlin, Germany.
In a subset of children and adolescents, SARS-CoV-2 infection induces a severe acute hyperinflammatory shock termed multisystem inflammatory syndrome in children (MIS-C) at four to eight weeks after infection. MIS-C is characterized by a specific T cell expansion and systemic hyperinflammation. The pathogenesis of MIS-C remains largely unknown.
View Article and Find Full Text PDFAnalysis of HPV-16 viral load, integration status, and p16 expression in relation to EBV co-infection and cervical lesion severity.
Sci Rep
March 2025
Department of Bacteriology and Virology, School of Medicine, Shiraz University of Medical Science, Shiraz, Iran.
Cervical cancer, one of the most common cancers in women, is primarily driven by high-risk human papillomaviruses (HPV) infections, particularly HPV-16. Co-infection with Epstein-Barr virus (EBV) has been reported to exacerbate disease progression by influencing HPV genome integration. This study examines HPV-16 integration status, p16INK4a expression, and their relationship with EBV co-infection and viral load in cervical cancer cases.
View Article and Find Full Text PDFReal-world evidence regarding cancer, mortality, and graft failure risk with de novo belatacept use among kidney transplant recipients in the United States.
Am J Transplant
March 2025
Division of Cancer Epidemiology and Genetics, National Cancer Institute, MD.
Belatacept is a selective T-cell co-stimulation blocker used in maintenance immunosuppression for kidney transplant recipients (KTRs), but evidence on cancer risk and other outcomes is limited. This retrospective cohort study used linked US transplant and cancer registry data on KTRs treated with belatacept (N=1514) or tacrolimus (N=7570) as initial maintenance therapy. We used multivariable Cox regression models to compare incidence of invasive cancer, cutaneous squamous cell carcinoma (cSCC), posttransplant lymphoproliferative disorder (PTLD), death, and graft failure/retransplantation (GF/RT) between belatacept and tacrolimus users.
View Article and Find Full Text PDFAntibody reactivity against EBNA1 and GlialCAM differentiates multiple sclerosis patients from healthy controls.
Proc Natl Acad Sci U S A
March 2025
Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Multiple sclerosis (MS) is an autoimmune demyelinating disorder of the central nervous system (CNS), which is linked to Epstein-Barr virus (EBV) infection, preceding the disease. The molecular mechanisms underlying this connection are only partially understood. We previously described molecular mimicry between the EBV transcription factor EBV nuclear antigen 1 (EBNA1) and three human CNS proteins: anoctamin-2 (ANO2), alpha-B crystallin (CRYAB), and glial cellular adhesion molecule (GlialCAM).
View Article and Find Full Text PDFIntroduction: The immune system protects against pathogens, and its dysfunction leads to primary and secondary immunodeficiencies, increasing infection susceptibility. Epstein-Barr virus (EBV) reactivation is linked to immune homeostasis disorders, particularly in common variable immunodeficiency (CVID) and chronic lymphocytic leukemia (CLL). Toll-like receptor (TLR) pathways play a crucial role in innate immunity, and their deregulation may contribute to immune dysfunction.
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