Coxsackievirus A16 infection stimulates imbalances of T cells in children

Luo, Qi; Peng, Wanjun; Chen, L I

doi:10.3892/etm.2015.2405

Cited by 8 publications

(4 citation statements)

References 26 publications

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“…It suggests that CA16 infection is unable to cause a rapid and intense immune response compared with EV71 infection, which seems to suggest an inhibiting effect during formation of the immune response to CA16 infection. These results are consistent with a report by Luo et al [47], who suggested that CA16 infection stimulates imbalances of T -cells. Notably, it is almost impossible for hosts to protect against recurrent CA16 infection due to the lack of previously characterized immune response indicators [7,8].…”

Section: Discussionsupporting

confidence: 94%

microRNA expression profiling in human diploid cells infected with enterovirus 71 or coxsackievirus A16

Li¹,

Gao²,

Zhang³

et al. 2018

SDRP-JCMP

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Background: Enterovirus 71 (EV71) and coxsackievirus A16 are the main causative agents of hand, foot and mouth disease (HFMD), but their pathogenicity has been shown to exhibit wide diversity. Methods: To illuminate the diverse pathogenicity of EV71 and CA16, microRNA (miRNA) profiles of human diploid cells infected with these two viruses were analyzed using an eukaryotic miRNA expression array. Results: Unlike EV71, directly stimulating an effective immune response, CA16 infection failed to effectively activate cytokines or the B-/T-cell immune response by repressing the expression of miRNAs. Similarly, the cytokines and antiviral-specific immune responses induced by CA16 infection were lower than those induced by EV71 in rhesus macaques. Individual miRNAs induced by EV71 and CA16 infections modulate the immune-associated target genes and lead to a distinct immune response. Conclusion: Our results provide experimental evidence focused on the miRNAs induced during EV71 and CA16 infection of human fibroblasts, which suggests some meaningful clues for explanation the wide diversity of immune responses induced by the two viruses.

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Section: Discussionsupporting

confidence: 94%

microRNA expression profiling in human diploid cells infected with enterovirus 71 or coxsackievirus A16

Li¹,

Gao²,

Zhang³

et al. 2018

SDRP-JCMP

View full text Add to dashboard Cite

show abstract

“…Next, KEGG pathway analysis further determined that these differentially expressed proteins were mainly enriched in immune- and neuro-associated pathways, such as primary immunodeficiency, cytokine‒cytokine receptor interaction, B-cell receptor signaling pathway, neuroactive ligand‒receptor interaction, GABAergic synapse, etc. It was reported that inappropriate or excessive activation of the immune reaction plays a crucial role in the regulation of the progression of CV-A16-infected HFMD, including T-cell imbalance and cytokine storm [ 37 , 38 ]. Moreover, increasing evidence has also demonstrated that CV-A16 is a neurotropic pathogen that has been associated with severe neurological forms of HFMD, such as aseptic meningitis, encephalitis, and acute flaccid paralysis [ 7 ].…”

Section: Discussionmentioning

confidence: 99%

HMGB1 is involved in viral replication and the inflammatory response in coxsackievirus A16-infected 16HBE cells via proteomic analysis and identification

Liu

Yang

et al. 2023

Virol J

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Coxsackievirus A16 (CV-A16) is still an important pathogen that causes hand, foot and mouth disease (HFMD) in young children and infants worldwide. Previous studies indicated that CV-A16 infection is usually mild or self-limiting, but it was also found that CV-A16 infection can trigger severe neurological complications and even death. However, there are currently no vaccines or antiviral compounds available to either prevent or treat CV-A16 infection. Therefore, investigation of the virus‒host interaction and identification of host proteins that play a crucial regulatory role in the pathogenesis of CV-A16 infection may provide a novel strategy to develop antiviral drugs. Here, to increase our understanding of the interaction of CV-A16 with the host cell, we analyzed changes in the proteome of 16HBE cells in response to CV-A16 using tandem mass tag (TMT) in combination with LC‒MS/MS. There were 6615 proteins quantified, and 172 proteins showed a significant alteration during CV-A16 infection. These differentially regulated proteins were involved in fundamental biological processes and signaling pathways, including metabolic processes, cytokine‒cytokine receptor interactions, B-cell receptor signaling pathways, and neuroactive ligand‒receptor interactions. Further bioinformatics analysis revealed the characteristics of the protein domains and subcellular localization of these differentially expressed proteins. Then, to validate the proteomics data, 3 randomly selected proteins exhibited consistent changes in protein expression with the TMT results using Western blotting and immunofluorescence methods. Finally, among these differentially regulated proteins, we primarily focused on HMGB1 based on its potential effects on viral replication and virus infection-induced inflammatory responses. It was demonstrated that overexpression of HMGB1 could decrease viral replication and upregulate the release of inflammatory cytokines, but deletion of HMGB1 increased viral replication and downregulated the release of inflammatory cytokines. In conclusion, the results from this study have helped further elucidate the potential molecular pathogenesis of CV-A16 based on numerous protein changes and the functions of HMGB1 Found to be involved in the processes of viral replication and inflammatory response, which may facilitate the development of new antiviral therapies as well as innovative diagnostic methods.

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“…A systematic review has demonstrated that the antibody level against EV71 or CoxA16 dramatically increased among children aged 1-4 yr (27).…”

Section: Discussionmentioning

confidence: 99%

Epidemiological Characteristics of Hand, Foot and Mouth Disease Reinfection in Guangzhou, Southern China from 2012 to 2017

Zhong¹,

Wang²,

Chen³

et al. 2022

ijph

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Background: Hand, foot and mouth disease (HFMD) reinfection is common because of the limited cross-protection from infections of different enterovirus. We aimed to investigate the epidemiological characteristics and its influential factors of HFMD reinfection in Guangzhou, China. Methods: Data on HFMD patients aged ≤5 yr from 2012 to 2017 were extracted from surveillance system. Influential factors of reinfection were assessed using the logistic regression model. Results: Of 369,054 HFMD patients, 11,321 patients (3.07%) were classified as reinfection. The reinfection rate in male was higher than in female (χ2=60.11, P<0.001). The reinfection rate in patients ≤1 yr was 3.86%, which showed a downward trend with age (Z=37.37, Ptrend<0.001). The highest reinfection rate was observed in the scattered children (3.38%), followed by nursery care children and others (χ2=514.75, P<0.001). Besides, higher risk of reinfection was detected among those who were male, lower age group, rural residence and other enteroviruses infection compared with their respective counterparts. Seasonality was illustrated according to the number of reinfections peaked from April to July. Time intervals curves revealed the number of reinfections gradually increased after 13 months from the initial infection. Conclusion: Male ≤4 yr, living rural area, especially those lived scattered and infected with other enteroviruses were more likely to be reinfection.

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Coxsackievirus A16 infection stimulates imbalances of T cells in children

Cited by 8 publications

References 26 publications

microRNA expression profiling in human diploid cells infected with enterovirus 71 or coxsackievirus A16

microRNA expression profiling in human diploid cells infected with enterovirus 71 or coxsackievirus A16

HMGB1 is involved in viral replication and the inflammatory response in coxsackievirus A16-infected 16HBE cells via proteomic analysis and identification

Epidemiological Characteristics of Hand, Foot and Mouth Disease Reinfection in Guangzhou, Southern China from 2012 to 2017

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