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Objective: Untreated perinatal HIV-1 infection is often associated with rapid disease progression in children with HIV (CWH), characterized by high viral loads and early mortality. TRIM22 is a host restriction factor, which directly inhibits HIV-1 transcription, and its genotype variation is associated with disease progression in adults. We tested the hypothesis that TRIM22 genotype is associated with disease progression in CWH.
Design: ART-naive CWH, aged 6-16 years, were recruited from primary care clinics in Harare, Zimbabwe. We performed a candidate gene association study of TRIM22 genotype and haplotypes with markers of disease progression and indicators of advanced disease.
Methods: TRIM22 exons three and four were sequenced by Sanger sequencing and single nucleotide polymorphisms were associated with markers of disease progression (CD4+ T-cell count and HIV viral load) and clinical indicators of advanced HIV disease (presence of stunting and chronic diarrhoea). Associations were tested using multivariate linear and logistic regression models.
Results: A total of 241 children, median age 11.4 years, 50% female, were included. Stunting was present in 16% of participants. Five SNPs were analyzed including rs7935564, rs2291842, rs78484876, rs1063303 and rs61735273. The median CD4+ count was 342 (IQR: 195-533) cells/μl and median HIV-1 viral load 34 199 (IQR: 8211-90 662) IU/ml. TRIM22 genotype and haplotypes were not associated with CD4+ T-cell count, HIV-1 viral load, stunting or chronic diarrhoea.
Conclusion: TRIM22 genotype was not associated with markers of HIV disease progression markers or advanced disease in CWH.
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http://dx.doi.org/10.1097/QAD.0000000000003053 | DOI Listing |
J Pathol Transl Med
September 2025
Department of Biochemistry, Faculty of Pharmacy, Cairo University, Cairo, Egypt.
Background: Prostate cancer is one of the most common malignancies in males worldwide. Serum prostate-specific antigen is a frequently employed biomarker in the diagnosis and risk stratification of prostate cancer; however, it is known for its low predictive accuracy for disease progression. New prognostic biomarkers are needed to distinguish aggressive prostate cancer from low-risk disease.
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September 2025
Department of Histology and Embryology and Vascular Biology Student Research Club, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, 85-092 Bydgoszcz, Poland, E-Mail:
Migrasomes are newly discovered, migration-dependent organelles that mediate the release of cellular contents into the extracellular environment through a process known as migracytosis. Since their identification in 2014, growing evidence has highlighted their critical roles in intercellular communication, organ development, mitochondrial quality control, and disease pathogenesis. Migrasome biogenesis is a complex, multi-step process tightly regulated by lipid composition, tetraspanin-enriched microdomains, and molecular pathways involving sphingomyelin synthase 2, Rab35, and integrins.
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September 2025
Department of Neurology, Danish Dementia Research Centre, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark.
Background: Early identification of pathological α-synuclein deposition (αSynD) may improve understanding of Lewy body disorder (LBD) progression and enable timely disease-modifying treatments.
Objectives: We investigated αSynD using a seed amplification assay and assessed prodromal LBD symptoms in individuals with idiopathic olfactory dysfunction (iOD).
Methods: In this cross-sectional, case-control study, we included iOD participants and normosmic healthy controls (HC) aged 55 to 75 years without diagnoses of dementia with Lewy bodies, Parkinson's disease (PD), or other major neurological disorders.
Macrophage Migration Inhibitory Factor (MIF) is a pleiotropic cytokine that acts as a central regulator of inflammation and immune responses across diverse organ systems. Functioning upstream in immune activation cascades, MIF influences macrophage polarization, T and B cell differentiation, and cytokine expression through CD74, CXCR2/4/7, and downstream signaling via NF-κB, ERK1/2, and PI3K/AKT pathways. This review provides a comprehensive analysis of MIF's mechanistic functions under both physiological and pathological conditions, highlighting its dual role as a protective mediator during acute stress and as a pro-inflammatory amplifier in chronic disease.
View Article and Find Full Text PDFZhong Nan Da Xue Xue Bao Yi Xue Ban
May 2025
School of Sports Medicine and Rehabilitation, Beijing Sport University, Beijing 100084, China.
Multimorbidity of chronic diseases is one of the most common health issues among older adults, and the resulting demand for long-term medical care and management imposes a considerable burden on healthcare systems. Muscle strength, a core indicator of overall health status, is closely associated with the risk of developing multimorbidity of chronic diseases in older adults. Decline in muscle strength not only increases the risk of multimorbidity of chronic diseases but also interacts with it to exacerbate disease burden.
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