Microarray analyses of differentially expressed human genes and biological processes in ECV304 cells infected with rubella virus

Mo, Xiaoyang; Ma, Wenxue; Zhang, Yali; Zhao, Huabin; Deng, Yun; Yuan, Wuzhou; Wang, Yuequn; Li, Yongqin; Zhu, Chuanbing; Liu, Mingyao; Wu, Xiushan

doi:10.1002/jmv.20942

Cited by 23 publications

(27 citation statements)

References 35 publications

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“…The DDX58 gene also exhibited a 14.23-fold upregulation in rubella virus infected adult Hs888Lu cells. Likewise, the TRIM22 gene was upregulated in both rubella infected fetal/adult fibroblasts and endothelial cells [35, 36]. These observations cumulatively demonstrate how rubella virus infection alters host cells, and offer functional biologic insight into our findings.…”

Section: Discussionmentioning

confidence: 56%

“…Recently two groups [35, 36] reported the results of an analysis of gene expression in human fetal and adult fibroblasts and endothelial cells infected with rubella virus. Importantly, the retinoic acid receptor alpha (RARA), vitamin D (1.25-dihydroxyvitamin D3) receptor (VDR), DDX58 and TRIM5 genes were found to be upregulated by 3.20-, 3.16-, 19.76- and 3.37-fold, respectively, in fetal HEF cells infected with rubella virus [35].…”

Section: Discussionmentioning

confidence: 99%

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Polymorphisms in the Vitamin A Receptor and Innate Immunity Genes Influence the Antibody Response to Rubella Vaccination

et al. 2010

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Background Genetic polymorphisms play an important role in rubella vaccine-induced immunity. Methods We genotyped 714 healthy children after two age-appropriate doses of rubella-containing vaccine for 142 potential SNPs. Results Specific polymorphisms in the vitamin A receptor, RIG-I, TRIM5 and TRIM22 genes were significantly associated with rubella vaccine humoral immunity. The minor allele of the rs4416353 in the vitamin A receptor gene was associated with an allele dose-related decrease (P=.019) in rubella antibody response. The minor allele of rs6793694, in the vitamin A receptor gene, was associated with an allele dose-related antibody decrease (P=.039). The minor variant of nonsynonymous SNP rs10813831 (Arg7Cys) in the RIG-I gene was associated with an allele dose-related decrease in rubella antibody level from 37.4 IU/mL to 28.0 IU/mL (P=.035), while increased representation of the minor allele of the 5’UTR SNP (rs3824949, P=.015), in the antiretroviral TRIM5 gene, was associated with an allele dose-related increase in rubella antibody. It is of particular interest that the nonsynonymous SNP rs3740996 (His43Tyr) in the TRIM5 gene was associated with variations in rubella antibody response (P=.016) after having been previously found to have a significant functional role. Conclusions These findings further expand our immunogenetic understanding of mechanisms of rubella vaccine-induced immunity.

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Section: Discussionmentioning

confidence: 56%

Section: Discussionmentioning

confidence: 99%

Polymorphisms in the Vitamin A Receptor and Innate Immunity Genes Influence the Antibody Response to Rubella Vaccination

et al. 2010

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“…To our knowledge this is the first report demonstrating endothelial cell tropism of RV. Although other investigators reported the ability of RV to infect an endothelial cell line ECV304 [40], this cell line has been proven to be a cross-contamination with a human bladder cancer cell line T24/83, which is not of endothelial origin and thus not suited to study endothelial cell biology [41]. …”

Section: Discussionmentioning

confidence: 99%

Persistent Infection of Human Fetal Endothelial Cells with Rubella Virus

et al. 2013

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Cardiovascular abnormalities are the leading cause of neonatal death among patients with congenital rubella syndrome (CRS). Although persistence of rubella virus (RV) in fetal endothelium has been repeatedly suggested as a possible cause of cardiovascular birth defects, evidence of the permissiveness of fetal endothelial cells to RV is lacking. In this study we evaluated the ability of RV to infect and persist in primary fetal endothelial cells derived from human umbilical vein (HUVEC). We found that wild type (wt) low passage clinical RV productively infected HUVEC cultures without producing cytopathology or ultrastructural changes. RV did not inhibit host cell protein synthesis, cell proliferation, or interfere with the cell cycle. Persistently infected cultures were easily established at low and high multiplicities of infection (MOI) with both laboratory and wt clinical RV strains. However, synchronous infections of entire HUVEC monolayers were only observed with clinical RV strains. The release of infectious virions into media remained at consistently high levels for several subcultures of infected HUVEC. The results indicate that macrovascular fetal endothelial cells are highly permissive to RV and allow slow persistent RV replication. The findings provide more evidence for the suggestion that vascular pathologies in CRS are triggered by persistent rubella virus infection of the endothelium.

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“…Induction of antigen-specific Th17 cells was previously reported in hepatitis C virus infected patients, and the role of IL-17 in the pathogenesis and outcome of human immunodeficiency virus, herpes simplex virus, cytomegalovirus, rotavirus and vaccinia virus infections has been suggested [58–63]. Recent microarray gene expression studies in rubella virus stimulated human fetal/adult fibroblasts and umbilical endothelial cells have shown modulation of a number of cytokine and cytokine receptor genes such as IL-6, IL-15, IL-24 and IFNα, several IFN-stimulated genes, IL-13RA2 and IL-7R [32,33]. Taken together, the predominance of inflammatory cytokines in our population-based study and recent microarray studies (21 fold up-regulation of IL-6) [32,33] suggest that the inflammatory cytokines may play an important role in rubella-specific immunity.…”

Section: Discussionmentioning

confidence: 99%

“…Earlier studies concentrated on rubella virus-specific induction of interferons, including IFN-α and IFN-γ in cell lines and human cultures [28–31]. Recent microarray gene expression studies, when stimulated with rubella virus, revealed modulation of key cytokine and cytokine receptor genes in human cells [32,33]. Impaired cytokine production and moderate immunosuppression, including a defective lymphocyte response to mitogens, was reported in schoolgirls who received a rubella vaccination [34].…”

Section: Introductionmentioning

confidence: 99%

Predominant inflammatory cytokine secretion pattern in response to two doses of live rubella vaccine in healthy vaccinees

et al. 2010

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We conducted a population-based study on 738 schoolchildren who received two doses of rubella vaccine in order to determine cytokine secretion patterns and their associations with demographic and clinical variables. The results showed a robust rubella-specific inflammatory cytokine response characterized by high median [inter-quartile range (IQR)] secretion levels (in pg/mL) of IL-6 [3681.0 (3160.0, 4052.0)], GMCSF [28.0 (23.6, 32.6)] and TNF-α [29.7 (−7.0, 89.2)]. We also detected modest levels of rubella-specific secretion of Th1 cytokines IL-2 and IFN-γ, while IL-12p40 was undetectable. In contrast, rubella-specific Th2 responses were hardly detectable. Age at vaccination, enrollment, and time elapsed between last vaccination and enrollment was significantly associated with the outcome of IL-2, IL-6 and IFN-γ secretion. These results suggest an immune-deviation or "skewing" from Th1/Th2 cytokine patterns towards a predominant inflammatory response upon in vitro rubella virus stimulation.

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Microarray analyses of differentially expressed human genes and biological processes in ECV304 cells infected with rubella virus

Cited by 23 publications

References 35 publications

Polymorphisms in the Vitamin A Receptor and Innate Immunity Genes Influence the Antibody Response to Rubella Vaccination

Polymorphisms in the Vitamin A Receptor and Innate Immunity Genes Influence the Antibody Response to Rubella Vaccination

Persistent Infection of Human Fetal Endothelial Cells with Rubella Virus

Predominant inflammatory cytokine secretion pattern in response to two doses of live rubella vaccine in healthy vaccinees

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