Molecular Mechanisms behind Persistent Presence of Parvovirus B19 in Human Dilated Myocardium

Daiva Bironaitė1, Ieva Kažukauskienė2, Julius Bogomolovas3

  • 1Department of Regenerative Medicine, State Research Institute Center for Innovative Medicine, Vilnius, Lithuania. daibironai@gmail.com.

Insights

Parvovirus B19 (PVB19) persistence in dilated cardiomyopathy (DCM) patients impairs mitochondria and remodels the extracellular matrix (ECM) via matrix metalloproteinases (MMPs). Antiviral therapy may benefit PVB19-positive DCM patients.

Area of Science:

  • Cardiology
  • Virology
  • Pathology

Background:

  • The role of parvovirus B19 (PVB19) in idiopathic dilated cardiomyopathy (DCM) pathogenesis is unclear.
  • PVB19 infection is a potential trigger for cardiac conditions.

Purpose of the Study:

  • To investigate the impact of chronic PVB19 persistence on myocardial inflammation, fibrosis, apoptosis, and mitochondrial function in nonischemic DCM patients.
  • To explore potential therapeutic strategies for PVB19-positive DCM.

Main Methods:

  • Analysis of endomyocardial biopsies (EMBs) and sera from PVB19-positive and negative DCM patients.
  • Measurement of inflammatory cell infiltration (CD3, CD45Ro, CD68), cytokine secretion (TNFα, IL-6), fibrosis, apoptosis markers, and mitochondrial proteins (Bcl-2, Hsp60).
  • Assessed matrix metalloproteinases (MMPs) involved in extracellular matrix (ECM) degradation.

Main Results:

  • Chronic PVB19 in myocardium did not increase inflammatory cell infiltration or pro-inflammatory cytokines.
  • Fibrosis was lower in PVB19-positive EMBs, but ECM-degrading MMP1 and MMP2 were upregulated twofold.
  • Mitochondrial impairment was indicated by a threefold decrease in antiapoptotic Bcl-2 and Hsp60 in PVB19-positive biopsies, with no significant apoptosis or necrosis activation.

Conclusions:

  • PVB19 persistence in DCM can lead to myocardial ECM remodeling via MMPs and mitochondrial dysfunction.
  • Biomarker analysis suggests potential for future apoptotic pathway activation rather than fibrosis.
  • Antiviral therapy may be beneficial for PVB19-positive DCM patients by mitigating pathological myocardial remodeling.

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