Virus-Host Coevolution in a Persistently Coxsackievirus B3-Infected Cardiomyocyte Cell Line

Pinkert, Sandra; Klingel, Karin; Lindig, Vanessa; Dörner, Andrea; Zeichhardt, Heinz; Spiller, O. Brad; Fechner, Henry

doi:10.1128/jvi.00621-11

Cited by 49 publications

(72 citation statements)

References 62 publications

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“…Indeed, resistance to lysis associated with a decrease of CAR expression was found during CVB3 persistence in a murine cardiac myocyte cell line. 18 The persistently infected cells were completely cured by using fluoxetine, and then subcultured for one year. The expression of PDX-1 was still reduced in cured cells at similar levels than in untreated cells.…”

Section: Discussionmentioning

confidence: 99%

“…In steady-state infections, almost all the cells are infected with no lytic replication cycle, whereas in carrierstate culture systems, only a small proportion of cells are involved with a significant virus replication. 18,24 Data available on CVB persistence in vitro are compatible with a carrier-state persistent infection. 18,25,26 Virus persistence is thought to result from a coevolution between the host cell and the virus, and this supposes changes in some of their characteristics 18 Viral factors during CVB persistence have been studied in several reports.…”

mentioning

confidence: 98%

“…18,24 Data available on CVB persistence in vitro are compatible with a carrier-state persistent infection. 18,25,26 Virus persistence is thought to result from a coevolution between the host cell and the virus, and this supposes changes in some of their characteristics 18 Viral factors during CVB persistence have been studied in several reports. These factors include genomic changes such as mutations with amino acid substitutions, 27 a deletion in the 5 0 non coding region, [28][29][30][31] or the persistence as a stable and atypical double-stranded RNA genomic form.…”

mentioning

confidence: 98%

“…Indeed, CVB are able to establish persistent infection in vitro as well as in vivo. 18 Viral persistence has been suggested as a major mechanism in the enteroviral pathogenesis of CVB-related chronic diseases such as T1D. 19,20 Previous in vitro studies confirmed that CVB can persist in pancreatic islets.…”

mentioning

confidence: 99%

“…These factors include genomic changes such as mutations with amino acid substitutions, 27 a deletion in the 5 0 non coding region, [28][29][30][31] or the persistence as a stable and atypical double-stranded RNA genomic form. 32 Among host factors, the role of a reduced expression of receptors 18,33,34 and the cellular activation status have been reported. [35][36][37] Other cellular factors such as miRNAs could also play a role in viral persistence.…”

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confidence: 99%

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Persistence of Coxsackievirus B4 in pancreatic ductal-like cells results in cellular and viral changes

et al. 2017

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Introduction: Although known as cytolytic viruses, group B coxackieviruses (CVB) are able to establish a persistent infection in vitro and in vivo. Viral persistence has been reported as a key mechanism in the pathogenesis of CVB-associated chronic diseases such as type 1 diabetes (T1D). The impact of CVB4 persistence on human pancreas ductal-like cells was investigated. Methods: A persistent CVB4 infection was established in ductal-like cells. PDX-1 expression, resistance to CVB4-induced lysis and CAR expression were evaluated. The profile of cellular microRNAs (miRNAs) was investigated through miRNA-sequencing. Viral phenotypic changes were examined, and genomic modifications were assessed by sequencing of the viral genome. Results: The CVB4 persistence in ductal-like cells was productive, with continuous release of infectious particles. Persistently infected cells displayed a resistance to CVB4-induced lysis upon superinfection and expression of PDX-1 and CAR was decreased. These changes were maintained even after virus clearance. The patterns of cellular miRNA expression in mock-infected and in CVB4-persistently infected ductal-like cells were clearly different. The persistent infection-derived virus (PIDV) was still able to induce cytopathic effect but its plaques were smaller than the parental virus. Several mutations appeared in various PIDV genome regions, but amino acid substitutions did not affect the predicted site of interaction with CAR. Conclusion: Cellular and viral changes occur during persistent infection of human pancreas ductal-like cells with CVB4. The persistence of cellular changes even after virus clearance supports the hypothesis of a long-lasting impact of persistent CVB infection on the cells.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 98%

mentioning

confidence: 98%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Persistence of Coxsackievirus B4 in pancreatic ductal-like cells results in cellular and viral changes

et al. 2017

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Type dependent patterns of human adenovirus persistence in human T‐lymphocyte cell lines

Markel

Lam

Harste

et al. 2013

Journal of Medical Virology

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Disseminated adenovirus infections cause significant mortality in stem cell transplanted patients and are suspected to originate from asymptomatic adenovirus persistence ("latency") in lymphocytes. The infection of three human T-lymphocyte lines (Jurkat, PM1, and CEM) with human adenovirus types of species A (HAdV-A31), B (HAdV-B3, -B11), and C (HAdV-C2, -C5) was investigated for 150 days in order to establish in vitro models for adenovirus persistence. HAdV-C5 persisted with continuous production of infectious virus progeny (about 10(7) TCID50 /ml) in PM1 cells. More than 100 copies of HAdV-C5-DNA per cell were detected by real-time PCR but hexon immunostaining showed that only 7.5% of the cells were infected ("carrier state infection"). Coxsackie and adenovirus receptor (CAR) expression was decreased in comparison to mock infected cultures suggesting selection of a semi-permissive subpopulation of PM-1 cells. By contrast, latency of HAdV-DNA (10(-3) -10(-4) copies/cell) without production of infectious virus progeny was observed in HAdV-C2 infection of PM1 and Jurkat, HAdV-A31 infection of PM1, and HAdV-B3 infection of Jurkat cells. In addition, transcription of E1A, DNA polymerase and hexon mRNA was not detected by RT-PCR suggesting an equivalent of clinical "HAdV latency." Persistence of HAdV-DNA was not observed in abortive infections of PM1 cells with HAdV-B3 and -B11 and in productive, lytical infections of Jurkat cells with HAdV-C5, HAdV-B11, and HAdV-A31. In conclusion, lytic and persistent infections with and without production of infectious virus were observed depending on the type of adenovirus. Genetic determinants for viral persistence may be investigated using these newly established infection models.

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Combating coxsackievirus B infections

Nekoua

Mercier

Vergez

et al. 2022

Reviews in Medical Virology

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Coxsackieviruses B (CVB) are small, non‐enveloped, single‐stranded RNA viruses belonging to the Enterovirus genus of the Picornaviridae family. They are common worldwide and cause a wide variety of human diseases ranging from those having relatively mild symptoms to severe acute and chronic pathologies such as cardiomyopathy and type 1 diabetes. The development of safe and effective strategies to combat these viruses remains a challenge. The present review outlines current approaches to control CVB infections and associated diseases. Various drugs targeting viral or host proteins involved in viral replication as well as vaccines have been developed and shown potential to prevent or combat CVB infections in vitro and in vivo in animal models. Repurposed drugs and alternative strategies targeting miRNAs or based on plant extracts and probiotics and their derivatives have also shown antiviral effects against CVB. In addition, clinical trials with vaccines and drugs are underway and offer hope for the prevention or treatment of CVB‐induced diseases.

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Virus-Host Coevolution in a Persistently Coxsackievirus B3-Infected Cardiomyocyte Cell Line

Abstract: Coevolution of virus and host is a process that emerges in persistent virus

Cited by 49 publications

References 62 publications

Persistence of Coxsackievirus B4 in pancreatic ductal-like cells results in cellular and viral changes

Persistence of Coxsackievirus B4 in pancreatic ductal-like cells results in cellular and viral changes

Type dependent patterns of human adenovirus persistence in human T‐lymphocyte cell lines

Combating coxsackievirus B infections

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