miR‐466 is putative negative regulator of Coxsackie virus and Adenovirus Receptor

Lam, Wai Yip; Cheung, Ariel C.Y.; Tung, Christine K.C.; Yeung, Albert T.; Ngai, Karry L. K.; Lui, Vivian Wai Yan; Chan, Paul K.S.; Tsui, Stephen Kwok‐Wing

doi:10.1016/j.febslet.2014.12.006

Cited by 13 publications

(9 citation statements)

References 60 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CAR mRNA was quantified by real-time RT-qPCR by using the SuperScript III Platinum One-Step Quantitative RT-PCR System (Thermofisher Scientific) and oligonucleotides described by Lam and colleagues. 60 The quantification was performed on the Mx3000p Ò instrument (Agilent technologies) with the following program: 50 C for 15 minutes, 95 C for 2 minutes, and 40 cycles of amplification consisting of 15 seconds at 95 C and 30 seconds at 60 C. The expression of the b-actin mRNA was used for normalization.…”

Section: Pdx-1 and Car Gene Expressionmentioning

confidence: 99%

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

et al. 2017

View full text Add to dashboard Cite

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.

show abstract

Section: Pdx-1 and Car Gene Expressionmentioning

confidence: 99%

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

et al. 2017

View full text Add to dashboard Cite

show abstract

“…CAR mRNA was quantified by real-time RT-qPCR using the SuperScript III Platinum One-Step Quantitative RT-PCR System (Life Technologies/Thermofischer Scientific). The oligonucleotides were already published [ 40 ]. The quantification was carried out on the Mx3000p® (Stratagene) with the following program: 50 °C for 15 min, 95 °C for 2 min and 40 cycles of amplification consisting of 15 s at 95 °C and 30 s at 60 °C.…”

Section: Methodsmentioning

confidence: 99%

Coxsackievirus B4 Can Infect Human Peripheral Blood-Derived Macrophages

Alidjinou

Sané

Trauet

et al. 2015

Viruses

View full text Add to dashboard Cite

Beyond acute infections, group B coxsackieviruses (CVB) are also reported to play a role in the development of chronic diseases, like type 1 diabetes. The viral pathogenesis mainly relies on the interplay between the viruses and innate immune response in genetically-susceptible individuals. We investigated the interaction between CVB4 and macrophages considered as major players in immune response. Monocyte-derived macrophages (MDM) generated with either M-CSF or GM-CSF were inoculated with CVB4, and infection, inflammation, viral replication and persistence were assessed. M-CSF-induced MDM, but not GM-CSF-induced MDM, can be infected by CVB4. In addition, enhancing serum was not needed to infect MDM in contrast with parental monocytes. The expression of viral receptor (CAR) mRNA was similar in both M-CSF and GM-CSF MDM. CVB4 induced high levels of pro-inflammatory cytokines (IL-6 and TNFα) in both MDM populations. CVB4 effectively replicated and persisted in M-CSF MDM, but IFNα was produced in the early phase of infection only. Our results demonstrate that CVB4 can replicate and persist in MDM. Further investigations are required to determine whether the interaction between the virus and MDM plays a role in the pathogenesis of CVB-induced chronic diseases.

show abstract

“…For example, EV68 3C protease cleaved host cell TIR-domain-containing adapter-inducing interferon-β (TRIF), a key molecule downstream of TLR3, to abolish NF-κB signaling and IFN-β production and enabled viruses to escape the host innate immune response [ 83 ]. In addition to viral proteases, miRNAs have also been characterized as a critical players in host signaling transduction [ 54 , 55 , 58 , 78 , 79 , 91 , 92 , 93 , 94 , 95 , 96 , 97 ]. In the investigation of Coxsackie virus-induced cardiovascular pathogenesis, the destruction of cell-cell interactions is one of its key mechanisms.…”

Section: Host Cellular Mirnas In Enterovirus Pathogenesismentioning

confidence: 99%

“…Enterovirus 2A and 3C proteases digested the host eukaryotic initiation factor 4G (eIF4G) and Poly(A)-binding protein (PABP), and these cleavages led to the shutdown of host cell protein synthesis and further promoted apoptosis, along with nuclear condensation and DNA fragmentation [ 85 , 86 , 90 ]. In addition to viral proteases, miRNAs have also been characterized as critical players in host protein synthesis shutdown and signaling regulation [ 54 , 55 , 59 , 78 , 79 , 91 , 92 , 93 , 94 , 95 , 96 , 97 , 108 ]. The role of miRNAs in the virus-induced translational switch has recently begun to be investigated.…”

Section: Host Cellular Mirnas In Enterovirus Pathogenesismentioning

confidence: 99%

MicroRNA and Pathogenesis of Enterovirus Infection

Yang

2016

Viruses

View full text Add to dashboard Cite

There are no currently available specific antiviral therapies for non-polio Enterovirus infections. Although several vaccines have entered clinical trials, the efficacy requires further evaluation, particularly for cross-strain protective activity. Curing patients with viral infections is a public health problem due to antigen alterations and drug resistance caused by the high genomic mutation rate. To conquer these limits in the development of anti-Enterovirus treatments, a comprehensive understanding of the interactions between Enterovirus and host cells is urgently needed. MicroRNA (miRNA) constitutes the biggest family of gene regulators in mammalian cells and regulates almost a half of all human genes. The roles of miRNAs in Enterovirus pathogenesis have recently begun to be noted. In this review, we shed light on recent advances in the understanding of Enterovirus infection-modulated miRNAs. The impacts of altered host miRNAs on cellular processes, including immune escape, apoptosis, signal transduction, shutdown of host protein synthesis and viral replication, are discussed. Finally, miRNA-based medication provides a promising strategy for the development of antiviral therapy.

show abstract

miR‐466 is putative negative regulator of Coxsackie virus and Adenovirus Receptor

Cited by 13 publications

References 60 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

Coxsackievirus B4 Can Infect Human Peripheral Blood-Derived Macrophages

MicroRNA and Pathogenesis of Enterovirus Infection

Contact Info

Product

Resources

About