Profiling of EBV-Encoded microRNAs in EBV-Associated Hemophagocytic Lymphohistiocytosis

Zhou, Chen; Xie, Zhengde; Gao, Li; Liu, Chunyan; Ai, Junhong; Zhang, Li; Shen, Kunling

doi:10.1620/tjem.237.117

Cited by 17 publications

(22 citation statements)

References 40 publications

(47 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Interestingly, the inhibition of NK cell cytotoxicity following severe influenza virus infections was related to the viral load, suggestive of a dose-dependent effect of this immunoevasive mechanism ( 66 ). In EBV-associated HLH, surprisingly higher viral loads are detected when compared to other EBV-associated diseases like infectious mononucleosis ( 33 , 81 ), indicating that EBV-encoded immunoevasion strategies may exert a more pronounced effect in EBV-HLH as well. Supporting this hypothesis, decreased perforin levels and reduced cytotoxicity were uniquely detected in infected T cells from patients with EBV-associated secondary HLH, not in infected NK cells from patients with chronic active EBV disease ( 82 ).…”

Section: Discussionmentioning

confidence: 99%

“…More highly elevated levels of EBV-encoded microRNAs (miRNAs) (BamHI A rightward transcripts miRNAs, another class of immunoevasins) were reported in patients with EBV-HLH compared to patients with EBV-associated infectious mononucleosis, urging the authors to speculate a role for these miRNAs in HLH pathogenesis. Levels of one specific miRNA, the antiapoptotic BART16-1 ( 83 ), even correlated with disease activity and remission ( 81 ). In this light, virus-encoded evasins may constitute novel biomarkers to track disease severity, evaluate treatment responses, or predict progression from acute infection to virus-associated HLH.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

How Viruses Contribute to the Pathogenesis of Hemophagocytic Lymphohistiocytosis

et al. 2017

View full text Add to dashboard Cite

Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening, hyperinflammatory syndrome, characterized by the uncontrolled activation of macrophages and T cells, eliciting key symptoms such as persistent fever, hepatosplenomegaly, pancytopenia, hemophagocytosis, hyperferritinemia, and coagulopathy. Viral infections are frequently implicated in the onset of active HLH episodes, both in primary, genetic HLH as in the secondary, acquired form. Infections with herpesviruses such as Epstein–Barr virus and cytomegalovirus are the most common. In autoimmune diseases, a link between viral infections and autoreactive immune responses has been recognized for a considerable time. However, the mechanisms by which viruses contribute to HLH pathogenesis remain to be clarified. In this viewpoint, different factors that may come into play are discussed. Viruses, particularly larger DNA viruses such as herpesviruses, are potent modulators of the immune response. By evading immune recognition, interfering with cytokine balances and inhibiting apoptotic pathways, viruses may increase the host’s susceptibility to HLH development. In particular cases, a direct connection between the viral infection and inhibition of natural killer cell or T cell cytotoxicity was reported, indicating that viruses may create immunological deficiencies reminiscent of primary HLH.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

How Viruses Contribute to the Pathogenesis of Hemophagocytic Lymphohistiocytosis

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Kawano et al [ 24 ] pointed out that the levels of miR-BART2-5p, 13, and 15 in plasma correlated with the severity and prognosis of CAEBV. Zhou et al [ 25 ] found that levels of several EBV-miRNAs (miR-BART3-3p, 3-5p, 1-3p, 1-5p, 15–1, 5-3p, and 16–1 et al) in Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis (EBV-HLH) were higher than in IM and healthy controls, and suggested that plasma miR-BART16-1 could be a potential biomarker for monitoring EBV-HLH progression.…”

Section: Discussionmentioning

confidence: 99%

Dynamic expression of viral and cellular microRNAs in infectious mononucleosis caused by primary Epstein-Barr virus infection in children

Gao

Xie

et al. 2015

Virol J

Self Cite

View full text Add to dashboard Cite

BackgroundEpstein-Barr virus (EBV) was the first virus identified to encode microRNAs (miRNAs). Both of viral and human cellular miRNAs are important in EBV infection. However, the dynamic expression profile of miRNAs during primary EBV infection was unknown. This study aimed to investigate the dynamic expression profile of viral and cellular miRNAs in infectious mononucleosis (IM) caused by primary EBV infection.MethodsThe levels of viral and cellular miRNAs were measured in fifteen pediatric IM patients at three different time-points. Fifteen healthy children who were seropositive for EBV were enrolled in the control group. Relative expression levels of miRNAs were detected by quantitative real-time PCR (qPCR) assay.ResultsEBV-miR-BHRF1-1, 1-2-3P, miR-BART13-1, 19-3p, 11-3P, 12–1, and 16–1 in IM patients of early phase were significantly higher than in healthy children. Most cellular miRNAs of B cells, such as hsa-miR-155-5p, −34a-5p, −18b-5p, −181a-5p, and −142-5p were up-regulated; while most of cellular miRNAs of CD8 + T cells, such as hsa-miR-223, −29c-3p, −181a, −200a-3p, miR-155-5p, −146a, and −142-5p were down-regulated in IM patients. With disease progression, nearly all of EBV-miRNAs decreased, especially miR-BHRF1, but at a slower rate than EBV DNA loads. Most of the cellular miRNAs of B cells, including hsa-miR-134-5p, −18b-5p, −34a-5p, and -196a-5p increased with time. However, most of the cellular miRNAs of CD8 + T cells, including hsa-let-7a-5p, −142-3p, −142-5p, and −155-5p decreased with time. Additionally, hsa-miR-155-5p of B cells and hsa-miR-18b-5p of CD8+ T cells exhibited a positive correlation with miR-BHRF1-2-5P and miR-BART2-5P (0.96 ≤ r ≤ 0.99, P < 0.05). Finally, hsa-miR-181a-5p of B cells had positive correlation with miR-BART4-3p, 4-5P, 16–1, and 22 (0.97 ≤ r ≤ 0.99, P < 0.05).ConclusionsOur study is the first to describe the expression profile of viral and cellular miRNAs in IM caused by primary EBV infection. These results might be the basis of investigating the pathogenic mechanism of EBV-related diseases and bring new insights into their diagnosis and treatment.

show abstract

“…Primary infection with EBV in adolescence frequently results in acute infectious mononucleosis (IM) [2]. In some cases, EBV can infect T cells and NK cells and induce chronic active EBV infection (CAEBV) [3], EBV-associated hemophagocytic lymphohistiocytosis (EBV-HLH) [4], and EBV-associated T/NK cell lymphoproliferative diseases [5]. CAEBV is classified as a lymphoproliferative disorder in the 2016 World Health Organization lymphoma classification [6].…”

Section: Introductionmentioning

confidence: 99%

The Oncogenic Role of miR-BART19-3p in Epstein-Barr Virus-Associated Diseases

Zhang

Luo

Xie

et al. 2020

BioMed Research International

Self Cite

View full text Add to dashboard Cite

Accumulating evidence so far has shown that EBV’s miRNAs have been found to be involved in cancer progression. However, the comprehensive EBV miRNA expression profiles and their biological significance in EBV-associated diseases are not well documented. A comprehensive profiling of EBV-encoded miRNAs expressed in CAEBV, EBV-HLH, and nasopharyngeal carcinoma (NPC) patients was constructed, and the results showed that miR-BART19-3p was upregulated in all these diseases. Ectopic expression of miR-BART19-3p induced EBV-negative cell proliferation and suppressed cell apoptosis. Molecularly, adenomatous polyposis coli (APC) was identified to be a direct target of miR-BART19-3p, and APC mRNA expression was inversely correlated with miR-BART19-3p in CAEBV samples. Our results demonstrated that miR-BART19-3p contributes to the tumorigenesis of EBV-associated diseases and may be a potential therapeutic target.

show abstract

Profiling of EBV-Encoded microRNAs in EBV-Associated Hemophagocytic Lymphohistiocytosis

Cited by 17 publications

References 40 publications

How Viruses Contribute to the Pathogenesis of Hemophagocytic Lymphohistiocytosis

How Viruses Contribute to the Pathogenesis of Hemophagocytic Lymphohistiocytosis

Dynamic expression of viral and cellular microRNAs in infectious mononucleosis caused by primary Epstein-Barr virus infection in children

The Oncogenic Role of miR-BART19-3p in Epstein-Barr Virus-Associated Diseases

Contact Info

Product

Resources

About