Background: Hepatitis C viral (HCV) infection has been shown to lead to auto-immune phenomena.
Aims: We review the prevalence of serological auto-immune disorders associated to HCV infection and to clarify their clinical significance.
Methods: Literature review.
Results: The serological immune response to HCV infection may include the development of cryoglobulinemia, rheumatoid factor, anticardiolipin, antinuclear, anti-liver-kidney-microsome 1 and anti-smooth muscle antibodies. Serological auto-immune manifestations were explained by the lymphotropism of HCV and the polyclonal activation of B cells. Interferon-based treatment of HCV infection may precipitate or exacerbate the associated auto-immune disease.
Conclusion: In patients with serological auto-immune disorders associated with HCV infection, a very careful analysis of clinical and biological features is needed. Application of classification criteria of systemic auto-immune diseases and testing more specific antibodies can resolve this point.
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Med Care
February 2025
Department of Medicine, Section of Infectious Diseases & Global Health, University of Chicago, Chicago, IL.
Background: Restrictive Medicaid policies regarding hepatitis C virus (HCV) treatment may exacerbate rural health care disparities for people who use drugs (PWUD). We assessed associations between Medicaid restrictions and HCV treatment among rural PWUD.
Methods: We compiled state-specific Medicaid treatment policies across 8 US rural sites in 10 states and merged these with participant survey data.
Cells
December 2024
Infectious Diseases Department, Clinica Universitaria Colombia, Clínica Colsanitas S.A., Bogotá 111321, Colombia.
Inflammation can positively and negatively affect tumorigenesis based on the duration, scope, and sequence of related events through the regulation of signaling pathways. A transcriptomic analysis of five pulmonary arterial hypertension, twelve Crohn's disease, and twelve ulcerative colitis high throughput sequencing datasets using R language specialized libraries and gene enrichment analyses identified a regulatory network in each inflammatory disease. IRF9 and LINC01089 in pulmonary arterial hypertension are related to the regulation of signaling pathways like MAPK, NOTCH, human papillomavirus, and hepatitis c infection.
View Article and Find Full Text PDFHealthcare (Basel)
December 2024
Center for Global Emergency Care, Johns Hopkins University, Baltimore, MD 21209, USA.
: Direct-acting antiviral agents (DAAs) have significantly reduced Hepatitis C Virus (HCV) transmission and improved health outcomes since their FDA approval in 2011. Despite these advances, over 70 million people remain untreated globally, with a disproportionately high burden in low- and middle-income countries (LMICs). : Through a structured search of open access informational sources and an informal peer-reviewed literature review, HCV treatment barriers were identified, compiled, and analyzed.
View Article and Find Full Text PDFCureus
December 2024
Pulmonology, Israeli-Georgian Multiprofile Medical Center "Healthycore", Tbilisi, GEO.
This study describes a 64-year-old female with a history of hepatitis C and cryoglobulinemia, who presented with respiratory symptoms, including dry cough, shortness of breath, and fever, alongside joint pain and fatigue. Initial workup revealed interstitial pneumonia, supported by chest imaging, and the patient was treated for pneumonia with standard antibiotic therapy. Despite no renal involvement, a hallmark of cryoglobulinemia, further testing confirmed elevated serum cryoglobulin levels.
View Article and Find Full Text PDFMetabol Open
March 2025
Hepatogastroenterology and Infectious Diseases Department, Faculty of Medicine, Al-Azhar University, Cairo, Egypt.
Background: Tissue damage by viral hepatitis is a major cause of morbidity and mortality worldwide. Oxidation reactions and reactive oxygen species (ROS) transform proteins and lipids in plasma low-density lipoproteins (LDL) into the abnormal oxidized LDL (ox-LDL). Hepatitis C virus (HCV) infection induces oxidative/nitrosative stress from multiple sources, including the inducible nitric oxide synthase (iNOS), the mitochondrial electron transport chain, hepatocyte NAD(P)H oxidases (NOX enzymes), and inflammation.
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