ArticleJournal of translational medicine2018
CCR5del32 genotype in human enteroviral cardiomyopathy leads to spontaneous virus clearance and improved outcome compared to wildtype CCR5.
Article in Journal of translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Review
- Major Group-B Enterovirus populations deleted in the noncoding 5' region of genomic RNA modulate activation of the type I interferon pathway in cardiomyocytes and induce myocarditis.PLoS pathogens · 2024Article
- Advancing Precision Medicine in Myocarditis: Current Status and Future Perspectives in Endomyocardial Biopsy-Based Diagnostics and Therapeutic Approaches.Journal of clinical medicine · 2023Review
- Fulminant Coxsackievirus Myocarditis in an Immunocompetent Adult: A Case Report and Literature Analysis.Cureus · 2022Article
- Cpxm2 as a novel candidate for cardiac hypertrophy and failure in hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2022Article
- Cardiovascular consequences of viral infections: from COVID to other viral diseases.Cardiovascular research · 2021Review
- Review
- Myocarditis and inflammatory cardiomyopathy: current evidence and future directions.Nature reviews. Cardiology · 2021Review
- CCR5Δ32 in Brazil: Impacts of a European Genetic Variant on a Highly Admixed Population.Frontiers in immunology · 2021Review
- Modulation of the acute defence reaction by eplerenone prevents cardiac disease progression in viral myocarditis.ESC heart failure · 2020Article
- Beyond HIV infection: Neglected and varied impacts of CCR5 and CCR5Δ32 on viral diseases.Virus research · 2020Review
- Serum alarmin S100A8/S100A9 levels and its potential role as biomarker in myocarditis.ESC heart failure · 2020Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundEnteroviral cardiomyopathy is a life-threatening disease, and detection of enterovirus (EV) RNA in the initial endomyocardial biopsy is associated with adverse prognosis and increased mortality. Some patients with EV infection may spontaneously eliminate the virus and recover, whereas those with virus persistence deteriorate and progress to heart failure. Interferon-beta (IFN-β) therapy eliminates the virus, resulting in increased survival of treated patients. CCR5 is expressed on antigen-presenting cells (both macrophages and dendritic cells) and immune effector cells (T-lymphocytes with memory/effector phenotype and natural killer cells). Its 32-bp deletion (CCR5del32) is the most frequent human coding sequence mutation. This study addresses the correlation of CCR5 polymorphism to the clinical course of EV infection and the necessity for IFN-β treatment.
methodsWe examined 97 consecutive patients with chronic/inflammatory cardiomyopathy and biopsy-proven EV infection and reliable information on clinical outcomes by CCr5 genotyping. These data were evaluated in relation to virus persistence in follow-up biopsies and survival rates over a 15-year period.
resultsGenotyping revealed a strong correlation between the CCR5del32 genotype and spontaneous virus clearance with improved outcomes. All patients with CCR5del32 eliminated EV spontaneously and none of them died within the observed period. In the group of untreated CCR5 wildtype patients, 33% died (Kaplan-Meier log-rank p = 0.010). However, CCR5 wildtype individuals treated with IFN-β are more likely to survive than without therapy (Kaplan-Meier log-rank p = 0.004) in identical proportions to individuals with the CCR5del32 genotype.
conclusionsThese data suggest that CCR5 genotyping is a novel predictive genetic marker for the clinical course of human EV cardiomyopathies. Hereby clinicians can identify those EV positive individuals who will eliminate the virus spontaneously based on CCR5 phenotype and those patients with CCR5 wildtype genotype who would be eligible for immediate antiviral IFN-β treatment to minimize irreversible cardiac damage.
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