MicroRNA‐649 promotes HSV‐1 replication by directly targeting MALT1

Zhang, Yi; Dai, Jun; Tang, Jingfeng; Zhou, Li; Zhou, Mengzhou

doi:10.1002/jmv.24728

Cited by 23 publications

(16 citation statements)

References 32 publications

(33 reference statements)

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“…MiRNAs are regulatory molecules that control the virus life cycle. Many miRNAs have been shown to promote viral replication by targeting factors involved in host antiviral activity and survival [41][42][43]. However, few reports have investigated the direct regulation of miRNAs in viral gene products that are important for viral infection.…”

Section: Discussionmentioning

confidence: 99%

MiR-155-5p modulates HSV-1 replication via the epigenetic regulation of SRSF2 gene expression

Wang

et al. 2019

Epigenetics

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A previous study reported that miR-155-5p knockout mice were more resistant to herpes simplex virus type I (HSV-1) infection. However, the exact underlying molecular mechanism remains to be elucidated. Here, we demonstrated that HSV-1 infection upregulates miR-155-5p expression. By binding to the promoter of serine/arginine-rich splicing factor 2 (SRSF2), which is an important transcriptional activator of HSV-1 genes that was previously reported by our group, and altering the histone modification located near the transcription start site (TSS) of the SRSF2 gene, miR-155-5p promotes the transcription of the SRSF2 gene, ultimately increasing viral replication and viral gene expression. Our results provide insight for an understanding of the roles and molecular mechanism of miR-155-5p in HSV-1 replication and the epigenetic control of SRSF2 gene expression.

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Section: Discussionmentioning

confidence: 99%

MiR-155-5p modulates HSV-1 replication via the epigenetic regulation of SRSF2 gene expression

Wang

et al. 2019

Epigenetics

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“…MiR-649, located within the LCRD segment of 22q11.2, targets MALT1, a component of a complex of proteins that activate NF-kB in lymphocytes. MiR-649 enhances Herpes Simplex Virus susceptibility, likely through effects on the NF-kB pathway (Zhang et al, 2017). Several miRNA target prediction programs have been applied to the 7 miRNAs encoded on chromosome 22q11.1 to identify linked pathways that relate to clinical phenotypes.…”

Section: Digeorge Syndrome Critical Region 8 and Microrna Contributiomentioning

confidence: 99%

The Genetics and Epigenetics of 22q11.2 Deletion Syndrome

Morena

Oers

2020

Front. Genet.

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Chromosome 22q11.2 deletion syndrome (22q11.2del) is a complex, multi-organ disorder noted for its varying severity and penetrance among those affected. The clinical problems comprise congenital malformations; cardiac problems including outflow tract defects, hypoplasia of the thymus, hypoparathyroidism, and/or dysmorphic facial features. Additional clinical issues that can appear over time are autoimmunity, renal insufficiency, developmental delay, malignancy and neurological manifestations such as schizophrenia. The majority of individuals with 22q11.2del have a 3 Mb deletion of DNA on chromosome 22, leading to a haploinsufficiency of~106 genes, which comprise coding RNAs, noncoding RNAs, and pseudogenes. The consequent haploinsufficiency of many of the coding genes are well described, including the key roles of T-box Transcription Factor 1 (TBX1) and DiGeorge Critical Region 8 (DGCR8) in the clinical phenotypes. However, the haploinsufficiency of these genes alone cannot account for the tremendous variation in the severity and penetrance of the clinical complications among those affected. Recent RNA and DNA sequencing approaches are uncovering novel genetic and epigenetic differences among 22q11.2del patients that can influence disease severity. In this review, the role of coding and noncoding genes, including microRNAs (miRNA) and long noncoding RNAs (lncRNAs), will be discussed in relation to their bearing on 22q11.2del with an emphasis on TBX1.

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“…This also results in the downregulation of the antiviral gene RSAD2, known to limit HSV-1 replication [ 52 ]. MiR-649 further promotes HSV-1 replication by directly targeting the mucosa associated lymphoid tissue lymphoma translocation gene 1 (MALT1) [ 53 ]. Downregulation of MALT1 results in evasion of both innate and adaptive immune responses through inhibition of the NF-κB pathway [ 54 ].…”

Section: Herpesvirusesmentioning

confidence: 99%

The Diverse Roles of microRNAs at the Host–Virus Interface

Bernier

Sagan

2018

Viruses

107

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MicroRNAs (miRNAs) are small, non-coding RNAs that regulate gene expression at the post-transcriptional level. Through this activity, they are implicated in almost every cellular process investigated to date. Hence, it is not surprising that miRNAs play diverse roles in regulation of viral infections and antiviral responses. Diverse families of DNA and RNA viruses have been shown to take advantage of cellular miRNAs or produce virally encoded miRNAs that alter host or viral gene expression. MiRNA-mediated changes in gene expression have been demonstrated to modulate viral replication, antiviral immune responses, viral latency, and pathogenesis. Interestingly, viruses mediate both canonical and non-canonical interactions with miRNAs to downregulate specific targets or to promote viral genome stability, translation, and/or RNA accumulation. In this review, we focus on recent findings elucidating several key mechanisms employed by diverse virus families, with a focus on miRNAs at the host–virus interface during herpesvirus, polyomavirus, retroviruses, pestivirus, and hepacivirus infections.

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MicroRNA‐649 promotes HSV‐1 replication by directly targeting MALT1

Cited by 23 publications

References 32 publications

MiR-155-5p modulates HSV-1 replication via the epigenetic regulation of SRSF2 gene expression

MiR-155-5p modulates HSV-1 replication via the epigenetic regulation of SRSF2 gene expression

The Genetics and Epigenetics of 22q11.2 Deletion Syndrome

The Diverse Roles of microRNAs at the Host–Virus Interface

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