Detection of parvovirus B19 and human herpesvirus 6 in pediatric dilated cardiomyopathy: Impact after heart transplantation

Das, Bibhuti B.; Prusty, Bhupesh K.; Niu, Jianli; Huang, Meei‐Li; Zhu, Haiying; Eliassen, Eva; Kuypers, Jane; Jerome, Keith R.

doi:10.4103/apc.apc_124_19

Cited by 5 publications

(3 citation statements)

References 30 publications

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“…Furthermore, CVB3 is known to be the most extensively studied virus in both patients and animal models with myocarditis [ 21 ]. Over the past two decades, human herpesvirus 6 (HHV-6) has been associated with paediatric cardiomyopathy and DCM [ 22 ]. Parvovirus B19 (PVB19), a member of Erythroviruses, has also been reported in the paediatric population, which may lead to heart failure with high mortality [ 23 ].…”

Section: Triggers Of Myocarditismentioning

confidence: 99%

Immune mechanisms of group B coxsackievirus induced viral myocarditis

et al. 2023

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Viral myocarditis is known to be a primary cause of dilated cardiomyopathy (DCM) that can lead to heart failure and sudden cardiac death and is invariably caused by myocardial viral infection following active inflammatory destruction of the myocardium. Although acute viral myocarditis frequently recovers on its own, current chronic myocarditis therapies are unsatisfactory, where the persistence of viral or immunological insults to the heart may play a role. Cellular and mouse experimental models that utilized the most prevalent Coxsackievirus group B type 3 (CVB3) virus infection causing myocarditis have illustrated the pathophysiology of viral myocarditis. In this review, immunological insights into the different stages of development of viral myocarditis were discussed, concentrating on the mechanisms of innate and adaptive immunity in the development of CVB3-induced myocarditis.

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Section: Triggers Of Myocarditismentioning

confidence: 99%

Immune mechanisms of group B coxsackievirus induced viral myocarditis

et al. 2023

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“…Clinical relevance of HHV6 infection of the myocardium has been shown in particular for paediatric patients after heart transplantation. 86 There is strong evidence that co-infection with other viruses, in particular with B19V, contributes to cardiac dysfunction since exclusive cardiac infection with HHV6 occurs only rarely. 87 The HHV6 genome may integrate into the telomere region of somatic cells or germ line cells [chromosomally integrated HHV6 (ciHHV6)].…”

Section: Human Herpesvirusesmentioning

confidence: 99%

Cardiovascular consequences of viral infections: from COVID to other viral diseases

Schultheiss

Baumeier

Pietsch

et al. 2021

Cardiovascular Research

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Infection of the heart muscle with cardiotropic viruses is one of the major etiologies of myocarditis and acute and chronic inflammatory cardiomyopathy (DCMi). However, viral myocarditis and subsequent dilated cardiomyopathy (DCM) is still a challenging disease to diagnose and to treat and is therefore a significant public health issue globally. Advances in clinical examination and thorough molecular genetic analysis of intramyocardial viruses and their activation status have incrementally improved our understanding of molecular pathogenesis and pathophysiology of viral infections of the heart muscle. To date, several cardiotropic viruses have been implicated as causes of myocarditis and DCMi. These include, among others, classical cardiotropic enteroviruses (coxsackieviruses B), the most commonly detected parvovirus B19, and human herpes virus 6. A newcomer is the respiratory virus that has triggered the worst pandemic in a century, SARS-CoV-2, whose involvement and impact in viral cardiovascular disease is under scrutiny. Despite extensive research into the pathomechanisms of viral infections of the cardiovascular system, our knowledge regarding their treatment and management is still incomplete. Accordingly, in this review we aim to explore and summarize the current knowledge and available evidence on viral infections of the heart. We focus on diagnostics, clinical relevance and cardiovascular consequences, pathophysiology, and current and novel treatment strategies.

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“…Anyhow, it is proposed that a high viral load of over 500 ge (genome equivalents) and active replication of PVB19 could result in myocarditis in about 64.7% of myocarditis patients [6]. Additional co-infection with another cardiotropic virus in parallel to a PVB19 infection might even elevate the chance of myocarditis development [7,8]. Kuhl et al were able to support this hypothesis: They observed a clear difference between latent and transcriptionally active PVB19 in human endomyocardial biopsies.…”

Section: Relevance Of Cvb3 and Pvb19 In Viral Myocarditismentioning

confidence: 99%

Virus-Host Interactions of Enteroviruses and Parvovirus B19 in Myocarditis

Peischard

Strutz‐Seebohm

et al. 2021

Cell Physiol Biochem

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Viral diseases are a major threat to modern society and the global health system. It is therefore of utter relevance to understand the way viruses affect the host as a basis to find new treatment solutions. The understanding of viral myocarditis (VMC) is incomplete and effective treatment options are lacking. This review will discuss the mechanism, effects, and treatment options of the most frequent myocarditis-causing viruses namely enteroviruses such as Coxsackievirus B3 (CVB3) and Parvovirus B19 (PVB19) on the human heart. Thereby, we focus on: 1. Viral entry: CVB3 use Coxsackievirus-Adenovirus-Receptor (CAR) and Decay Accelerating Factor (DAF) to enter cardiac myocytes while PVB19 use the receptor globoside (Gb4) to enter cardiac endothelial cells. 2. Immune system responses: The innate immune system mediated by activated cardiac toll-like receptors (TLRs) worsen inflammation in CVB3-infected mouse hearts. Different types of cells of the adaptive immune system are recruited to the site of inflammation that have either protective or adverse effects during VMC. 3. Autophagy: CVB3 evades autophagosomal degradation and misuses the autophasomal pathway for viral replication and release. 4. Viral replication sites: CVB3 promotes the formation of double membrane vesicles (DMVs), which it uses as replication sites. PVB19 uses the host cell nucleus as the replication site and uses the host cell DNA replication system. 5. Cell cycle manipulation: CVB3 attenuates the cell cycle at the G1/S phase, which promotes viral transcription and replication. PVB19 exerts cell cycle arrest in the S phase using its viral endonuclease activity. 6. Regulation of apoptosis: Enteroviruses prevent apoptosis during early stages of infection and promote cell death during later stages by using the viral proteases 2A and 3C, and viroporin 2B. PVB19 promotes apoptosis using the non-structural proteins NS1 and the 11 kDa protein. 7. Energy metabolism: Dysregulation of respiratory chain complex expression, activity and ROS production may be altered in CVB3- and PVB19-mediated myocarditis. 8. Ion channel modulation: CVB3-expression was indicated to alter calcium and potassium currents in Xenopus laevis oocytes and rodent cardiomyocytes. The phospholipase 2-like activity of PVB19 may alter several calcium, potassium and sodium channels. By understanding the general pathophysiological mechanisms of well-studied myocarditis-linked viruses, we might be provided with a guideline to handle other less-studied human viruses.

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Detection of parvovirus B19 and human herpesvirus 6 in pediatric dilated cardiomyopathy: Impact after heart transplantation

Cited by 5 publications

References 30 publications

Immune mechanisms of group B coxsackievirus induced viral myocarditis

Immune mechanisms of group B coxsackievirus induced viral myocarditis

Cardiovascular consequences of viral infections: from COVID to other viral diseases

Virus-Host Interactions of Enteroviruses and Parvovirus B19 in Myocarditis

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