Arthritogenic alphaviruses pose a significant public health concern due to their ability to cause joint inflammation, with emerging evidence of potential neurological consequences. In this review, we examine the immunopathology and immune evasion strategies employed by these viruses, highlighting their complex mechanisms of pathogenesis and neurological implications. We delve into how these viruses manipulate host immune responses, modulate inflammatory pathways, and potentially establish persistent infections. Further, we explore their ability to breach the blood-brain barrier, triggering neurological complications, and how co-infections exacerbate neurological outcomes. This review synthesizes current research to provide a comprehensive overview of the immunopathological mechanisms driving arthritogenic alphavirus infections and their impact on neurological health. By highlighting knowledge gaps, it underscores the need for research to unravel the complexities of virus-host interactions. This deeper understanding is crucial for developing targeted therapies to address both joint and neurological manifestations of these infections.
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http://dx.doi.org/10.3389/fcimb.2024.1421571 | DOI Listing |
Nutrients
December 2024
Department of Immunopathology, Faculty of Medicine, Medical University of Lodz, Zeligowskiego 7/9, 90-752 Lodz, Poland.
Asthma (a chronic inflammatory disease of the airways) is characterized by a variable course, response to treatment, and prognosis. Its incidence has increased significantly in recent decades. Unfortunately, modern lifestyle and environmental factors contribute to the further increase in the incidence of this disease.
View Article and Find Full Text PDFSci Immunol
January 2025
Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Human recombination-activating gene (RAG) deficiency can manifest with distinct clinical and immunological phenotypes. By applying a multiomics approach to a large group of -mutated patients, we aimed at characterizing the immunopathology associated with each phenotype. Although defective T and B cell development is common to all phenotypes, patients with hypomorphic variants can generate T and B cells with signatures of immune dysregulation and produce autoantibodies to a broad range of self-antigens, including type I interferons.
View Article and Find Full Text PDFMicrobiol Spectr
January 2025
Department of Molecular and Comparative Pathobiology, Johns Hopkins University, School of Medicine, Baltimore, Maryland, USA.
Unlabelled: is a protozoan parasite that causes human and animal African trypanosomiases (HAT and AAT). Cardiac symptoms are commonly reported in HAT patients, and intracardiac parasites with accompanying myocarditis have been observed in both natural hosts and animal models of infection. Despite the importance of as a cause of cardiac dysfunction and the dramatic socioeconomic impact of African trypanosomiases in sub-Saharan Africa, there are currently no reproducible murine models of associated cardiomyopathy.
View Article and Find Full Text PDFVaccines (Basel)
November 2024
Laboratory of Biology of Cellular Interactions, Department of Morphology, Federal University of Minas Gerais, Belo Horizonte 31270-901, MG, Brazil.
Background/objectives: Considering the large number of candidates in vaccine-testing studies against different pathogens and the amount of time spent in the preclinical and clinical trials, there is a pressing need to develop an improved in vivo system to quickly screen vaccine candidates. The model of a polyester-polyurethane sponge implant provides a rapid analysis of the specific stimulus-response, allowing the study of a compartmentalized microenvironment. The sponge implant's defined measurements were standardized as a compartment to assess the immune response triggered by the vaccinal antigen.
View Article and Find Full Text PDFJ Clin Med
December 2024
Department of Rheumatology, Hospital Universitario Marqués de Valdecilla, IDIVAL, Immunopathology Group, Avda. Valdecilla s/n., 39008 Santander, Spain.
Patients with rheumatic immune-mediated diseases (rheumatic-IMID) and latent tuberculosis (LTBI) are at an increased risk of developing active tuberculosis (TB); therefore, screening is recommended before starting biological treatment. The aims of this study were as follows: (i) to assess the prevalence of LTBI, (ii) to determine the importance of using a booster test in TST-negative patients, (iii) to compare the tuberculin skin test (TST) with the interferon-gamma release assay (IGRA), (iv) to perform a review of the prevalence of LTBI. A cross-sectional hospital study was performed, including patients diagnosed with rheumatic-IMID who underwent a TST and/or IGRA during the period 2016-2020.
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