Comparative proteome analyses of host protein expression in response to Enterovirus 71 and Coxsackievirus A16 infections

Lee, Jia Jun; Seah, Joey Bing Kai; Chow, Vincent T. K.; Poh, Chit Laa; Tan, Eng Lee

doi:10.1016/j.jprot.2011.05.022

Cited by 28 publications

(28 citation statements)

References 38 publications

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“…Several hnRNPs were detected to be differentially regulated in EV-A71-and CV-A16-infected HT-29 cells, namely hnRNP L, hnRNP A/B and hnRNP A2/B1. In SK-N-MC cells, only the virulent strain EV-A71/UH1 was reported to downregulate hnRNP C [46], similar to our present findings. There are many studies of interactions of other hnRNPs with viral translational control, such as hnRNP A1, hnRNP A2 and hnRNP K; thus hnRNP C identified in our study may be involved in a similar mechanism [68].…”

Section: Discussionsupporting

confidence: 91%

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Cellular proteome alterations in response to enterovirus 71 and coxsackievirus A16 infections in neuronal and intestinal cell lines

Chan

Sam

Lai

et al. 2015

Journal of Proteomics

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Section: Discussionsupporting

confidence: 91%

“…The isoforms of HSPB1 were expressed at higher levels in the EV-A71-infected neuronal cells. In early stages of infection, HSPB1 was down-regulated, while it was up-regulated later in EV-A71 infection [46,47].…”

Section: Discussionmentioning

confidence: 94%

Cellular proteome alterations in response to enterovirus 71 and coxsackievirus A16 infections in neuronal and intestinal cell lines

Chan

Sam

Lai

et al. 2015

Journal of Proteomics

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“…On the other hand, it is intriguing that associations with immune/inflammatory function or other aspects of host defense against pathogens have been demonstrated for 8 of the top 10 genes (or their very close homologs) identified in the largest GWAS meta-analysis of MDD conducted to date (Table 2). 105, 106, 107, 108, 109, 110, 111, 112, 113, 114, 115, 116, 117, 118, 119, 120, 121, 122, 123, 124, 125, 126, 127, 128, 129, 130, 131, 132, 133, 134, 135, 136, 137, 138, 139, 140 Many other depression-relevant genes identified in earlier large GWASs (as well as meta-analyses of these studies), including PBRM1 , GNL3 , ATP6V1B2 , SP4 , AK294384 , LY86 , KSP37 , SMG7 , NFKB1 , LOC654346 , LAMC2 , ATG7 , CUGBP1 , NFE2L3 , LOC647167 , VCAN , NLGN1 , BBOX1 , ATF3 , RORA , EIF3F , CDH13 , ITGB1 and GRM8 , have also been linked to immune system and/or host defense functions (see Supplementary Table S1 for additional information/relevant references).…”

Section: Risk Alleles For Mdd and Host Defensementioning

confidence: 99%

The evolutionary significance of depression in Pathogen Host Defense (PATHOS-D)

2012

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Given the manifold ways that depression impairs Darwinian fitness, the persistence in the human genome of risk alleles for the disorder remains a much debated mystery. Evolutionary theories that view depressive symptoms as adaptive fail to provide parsimonious explanations for why even mild depressive symptoms impair fitness-relevant social functioning, whereas theories that suggest that depression is maladaptive fail to account for the high prevalence of depression risk alleles in human populations. These limitations warrant novel explanations for the origin and persistence of depression risk alleles. Accordingly, studies on risk alleles for depression were identified using PubMed and Ovid MEDLINE to examine data supporting the hypothesis that risk alleles for depression originated and have been retained in the human genome because these alleles promote pathogen host defense, which includes an integrated suite of immunological and behavioral responses to infection. Depression risk alleles identified by both candidate gene and genome-wide association study (GWAS) methodologies were found to be regularly associated with immune responses to infection that were likely to enhance survival in the ancestral environment. Moreover, data support the role of specific depressive symptoms in pathogen host defense including hyperthermia, reduced bodily iron stores, conservation/withdrawal behavior, hypervigilance and anorexia. By shifting the adaptive context of depression risk alleles from relations with conspecifics to relations with the microbial world, the Pathogen Host Defense (PATHOS-D) hypothesis provides a novel explanation for how depression can be nonadaptive in the social realm, whereas its risk alleles are nonetheless represented at prevalence rates that bespeak an adaptive function.

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“…Over the past decade, a series of sporadic cases as well as large epidemics associated with HFMD have arisen in the Asia-Pacific region; therefore HFMD has emerged as a serious threat to public health[4]. Although EV71 and CA16 share relatively high nucleotide and amino acid homologies (77% and 89% respectively), the clinical manifestations caused by the two viruses are significantly different[5, 6]. Unlike CA16, which causes milder symptoms that resolve within a few weeks, EV71 infections usually cause severe central nervous system (CNS) complications, such as poliomyelitis-like paralysis, aseptic meningitis, and encephalitis[7, 8].…”

Section: Introductionmentioning

confidence: 99%

Different microRNA profiles reveal the diverse outcomes induced by EV71 and CA16 infection in human umbilical vein endothelial cells using high-throughput sequencing

Zheng

et al. 2017

PLoS ONE

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Enterovirus 71 (EV71) and Coxsackievirus A16 (CA16) remain the predominant pathogens in hand, foot, and mouth disease (HFMD), but the factors underlying the pathogenesis of EV71 and CA16 infections have not been elucidated. Recently, the functions of microRNAs (miRNAs) in pathogen-host interactions have been highlighted. In the present study, we performed comprehensive miRNA profiling in EV71- and CA16-infected human umbilical vein endothelial cells (HUVECs) at multiple time points using high-throughput sequencing. The results showed that 135 known miRNAs exhibited remarkable differences in expression. Of these, 30 differentially expressed miRNAs presented opposite trends in EV71- and CA16-infected samples. Subsequently, we mainly focused on the 30 key differentially expressed miRNAs through further screening to predict targets. Gene ontology (GO) and pathway analysis of the predicted targets showed the enrichment of 14 biological processes, 9 molecular functions, 8 cellular components, and 85 pathways. The regulatory networks of these miRNAs with predicted targets, GOs, pathways, and co-expression genes were determined, suggesting that miRNAs display intricate regulatory mechanisms during the infection phase. Consequently, we specifically analyzed the hierarchical GO categories of the predicted targets involved in biological adhesion. The results indicated that the distinct changes induced by EV71 and CA16 infection may be partly linked to the function of the blood-brain barrier. Taken together, this is the first report describing miRNA expression profiles in HUVECs with EV71 and CA16 infections using high-throughput sequencing. Our data provide useful insights that may help to elucidate the different host-pathogen interactions following EV71 and CA16 infection and offer novel therapeutic targets for these infections.

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Comparative proteome analyses of host protein expression in response to Enterovirus 71 and Coxsackievirus A16 infections

Cited by 28 publications

References 38 publications

Cellular proteome alterations in response to enterovirus 71 and coxsackievirus A16 infections in neuronal and intestinal cell lines

Cellular proteome alterations in response to enterovirus 71 and coxsackievirus A16 infections in neuronal and intestinal cell lines

The evolutionary significance of depression in Pathogen Host Defense (PATHOS-D)

Different microRNA profiles reveal the diverse outcomes induced by EV71 and CA16 infection in human umbilical vein endothelial cells using high-throughput sequencing

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