Key result
Transcriptionally active erythroparvovirus infection in heart failure patients was associated with significant upregulation of miR-98, miR-222, miR-106b, and miR-197 (P < 0.005).
Why the study?
miRNAs influence viral infection outcomes and may selectively suppress transcriptionally active erythroparvovirus, representing potential targets for antiviral therapies in heart failure.
Observational (n=75)
Specific miRNAs (miR-98, miR-222, miR-106b, miR-197) are upregulated in heart failure patients with active erythroparvovirus infection, offering a potential novel diagnostic tool.
May inform miRNA-based antiviral strategies in unexplained cardiomyopathy; hypothesis-generating and requires prospective validation.
AIMS: miRNAs, small non-coding RNAs, play key roles in gene regulation, cell differentiation and tissue development. They influence viral infection outcomes by directly interacting with viral genomes or modifying the host microenvironment. This study demonstrates miRNAs' ability to selectively suppress transcriptionally active erythroparvovirus, highlighting their potential in antiviral therapies. METHODS AND RESULTS: Seventy-five endomyocardial biopsy (EMB) specimens from patients with unexplained heart failure were analysed. The samples included 19 with dilated cardiomyopathy and inflammation (DCMi), 12 with dilated cardiomyopathy (DCM), 25 with inflammation and active erythroparvovirus infection, 13 with active erythroparvovirus infection only and 6 from undiagnosed patients as controls. miRNA expression was measured using TaqMan assays. miR-98, miR-222, miR-106b and miR-197 were significantly upregulated in patients with transcriptionally active erythroparvovirus infection, independent of inflammation (P < 0.005). These miRNAs differentiated these patients from all other groups with over 90% specificity. CONCLUSIONS: These specific miRNAs offer a novel diagnostic tool for active erythroparvovirus infections and hold promise as therapeutic targets, providing safer alternatives to traditional antiviral treatments.
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Aleshcheva et al. (2025) conducted an observational in Unexplained heart failure (n=75). Transcriptionally active erythroparvovirus infection vs. Patients without active erythroparvovirus infection was evaluated on Upregulation of miR-98, miR-222, miR-106b and miR-197 (p=< 0.005). Transcriptionally active erythroparvovirus infection in heart failure patients was associated with significant upregulation of miR-98, miR-222, miR-106b, and miR-197 (P < 0.005).
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