gga-miR-155 Enhances Type I Interferon Expression and Suppresses Infectious Burse Disease Virus Replication via Targeting SOCS1 and TANK

Wang, Bin; Fu, Mengjiao; Liu, Yanan; Wang, Yongqiang; Li, Xiaoqi; Cao, Hong; Zheng, Shijun

doi:10.3389/fcimb.2018.00055

Cited by 46 publications

(42 citation statements)

References 70 publications

(99 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recently, an increasing number of lncRNAs have been reported to play roles in innate immune response to virus infections (Ma et al, 2016;Ouyang et al, 2016). Previous studies have implicated miR-155 in host immunity against viral infections and regulation of type I IFN signalling (Harrison et al, 2017;Thounaojam et al, 2014;Wang et al, 2018;Wang, Hou, et al, 2010;Zhou et al, 2010). In this study, both in vitro and in vivo experiments demonstrated that altering lncRNA-155 expression had a profound effect on host antiviral response and IAV replication.…”

Section: Discussionmentioning

confidence: 59%

“…and S5a). miR-155 is thought to inhibit the expression of some negative regulators of type I interferon signalling (Thounaojam et al, 2014;Wang et al, 2018;Wang, Hou, et al, 2010); thus, we asked whether lncRNA-155 might also promote the antiviral immune response by inhibiting negative regulator(s) of type I IFN signalling.…”

Section: Ectopic Expression Of Lncrna-155 Promotes Type I Ifn Produmentioning

confidence: 99%

“…miR-155 is an ancient extensively studied microRNA serving several important roles in the progression of malignancy growth and virus infections (Mashima, 2015;Rodriguez et al, 2007). For example, miR-155 has been implicated in innate immunity by regulating type I interferon production and innate immune signalling pathway either through targeting the suppressor of cytokine signalling 1 (SOCS1; Staedel & Darfeuille, 2013;, Src homology 2containing inositol phosphatase 1 (SHIP1; Kim, Kim, Basu, & Jo, 2017;Thounaojam et al, 2014), or TRAF family member-associated NF-κB activator (TANK; Wang et al, 2018) during viral infection.…”

Section: Introductionmentioning

confidence: 99%

“…miR-155 is thought to inhibit the expression of some negative regulators of type I interferon signalling(Thounaojam et al, 2014;Wang et al, 2018;Wang, Hou, et al, 2010); thus, we asked whether lncRNA-155 might also promote the antiviral immune response by inhibiting negative regulator(s) of type I IFN signalling.To address this possibility, we tested the expression of several negative regulators of type I interferon signalling and found that level of PTP1B was significantly downregulated in 1.4 kb, miRDeleted, and 400 b overexpressed cells (Figure S5b). We generated 293T stable cell lines overexpressing either 1.4 kb, 1.2 kb, 400 b, or miRDeleted fragments of lncRNA-155 (Figures 6a and S3b).…”

mentioning

confidence: 99%

See 3 more Smart Citations

Identification of lncRNA‐155 encoded by MIR155HG as a novel regulator of innate immunity against influenza A virus infection

Maarouf

Chen

et al. 2019

Cellular Microbiology

View full text Add to dashboard Cite

Long noncoding RNAs (lncRNAs) are single-stranded RNA molecules longer than 200 nt that regulate many cellular processes. MicroRNA 155 host gene (MIR155HG) encodes the microRNA (miR)-155 that regulates various signalling pathways of innate and adaptive immune responses against viral infections. MIR155HG also encodes a lncRNA that we call lncRNA-155. Here, we observed that expression of lncRNA-155 was markedly upregulated during influenza A virus (IAV) infection both in vitro (several cell lines) and in vivo (mouse model). Interestingly, robust expression of lncRNA-155 was also induced by infections with several other viruses. Disruption of lncRNA-155 expression in A549 cells diminished the antiviral innate immunity against IAV. Furthermore, knockout of lncRNA-155 in mice significantly increased IAV replication and virulence in the animals. In contrast, overexpression of lncRNA-155 in human cells suppressed IAV replication, suggesting that lncRNA-155 is involved in host antiviral innate immunity induced by IAV infection. Moreover, we found that lncRNA-155 had a profound effect on expression of protein tyrosine phosphatase 1B (PTP1B) during the infection with IAV. Inhibition of PTP1B by lncRNA-155 resulted in higher production of interferon-beta (IFN-β) and several critical interferon-stimulated genes (ISGs). Together, these observations reveal that MIR155HG derived lncRNA-155 can be induced by IAV, which modulates host innate immunity during the virus infection via regulation of PTP1B-mediated interferon response. KEYWORDS influenza A virus, innate immunity, lncRNA, miR-155, MIR155HG, PTP1B List of Abbreviations: 293T, HEK293T/human embryonic kidney cells; A549, human lung epithelial cells; bic, B-cell Integration Cluster; CA/04, A/California/04/2009; DMEM, Dulbecco's modified Eagle's medium; dpi, days post infection; EV, empty vector; FBS, fetal bovine serum; HA, haemagglutination assay; h-lncRNA-155, human lncRNA-155; hpi, hours post infection; IFN, interferon; IFN-β, interferon-beta; IRF3, interferon regulatory factor 3; IRF7, interferon regulatory factor 7; ISGs, interferon-stimulated genes; KO, bic/miR-155 −/− knock out mice; LLC, mouse Lewis lung carcinoma cells; lncRNAs, long noncoding RNAs; NIH/3T3, mouse embryonic fibroblasts; MDA5, antimelanoma differentiation-associated gene 5; MDCK, Madin-Darby canine kidney cells; miR, microRNA; MIR155HG, miR-155 host gene; m-lncRNA-155, bic/mouse lncRNA-155; NP, IAV nucleoprotein; nt, nucleotide; NRAV, negative regulator of antiviral response;PFA, plaque formation assay; PR8, A/Puerto Rico/8/1934; pre-miR-155, precursor miRNA; pri-miRNA, primary-miRNA; PRRs, pattern recognition receptors; PTP1B, tyrosine-protein phosphatase nonreceptor type 1; RAW 264.7, mouse Abelson murine leukaemia virus transformed macrophages; SeV, Sendai virus; SHIP1, Src homology 2-containing inositol phosphatase 1;sh-luc, Sh-luciferase; shRNAs, short hairpin RNAs; siRNA, small interfering RNA; SOCS1, suppressor of cytokine signalling 1; SPF, specific pathogen free; STAT1, signal transducer a...

show abstract

Section: Discussionmentioning

confidence: 59%

Section: Ectopic Expression Of Lncrna-155 Promotes Type I Ifn Produmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Identification of lncRNA‐155 encoded by MIR155HG as a novel regulator of innate immunity against influenza A virus infection

Maarouf

Chen

et al. 2019

Cellular Microbiology

View full text Add to dashboard Cite

show abstract

“…Many research results have reported that some miRNAs are involved in viral life cycles by regulating the innate immune response. For example, miR-146a facilitates replication of dengue virus by dampening interferon induction by targeting TRAF6 [45], and miR-155 enhances type I interferon expression to suppress infectious burse disease virus (IBDV) replication via targeting negative regulators, SOCS1 and TANK [46]. Additionally, miRNAs can regulate downstream IFN-I-induced signalling.…”

Section: Discussionmentioning

confidence: 99%

miR-26a Inhibits Feline Herpesvirus 1 Replication by Targeting SOCS5 and Promoting Type I Interferon Signaling

Zhang

Huang

et al. 2019

Viruses

View full text Add to dashboard Cite

In response to viral infection, host cells activate various antiviral responses to inhibit virus replication. While feline herpesvirus 1 (FHV-1) manipulates the host early innate immune response in many different ways, the host could activate the antiviral response to counteract it through some unknown mechanisms. MicroRNAs (miRNAs) which serve as a class of regulatory factors in the host, participate in the regulation of the host innate immune response against virus infection. In this study, we found that the expression levels of miR-26a were significantly upregulated upon FHV-1 infection. Furthermore, FHV-1 infection induced the expression of miR-26a via a cGAS-dependent pathway, and knockdown of cellular cGAS significantly blocked the expression of miR-26a induced by poly (dA:dT) or FHV-1 infection. Next, we investigated the biological function of miR-26a during viral infection. miR-26a was able to increase the phosphorylation of STAT1 and promote type I IFN signaling, thus inhibiting viral replication. The mechanism study showed that miR-26a directly targeted host SOCS5. Knockdown of SOCS5 increased the phosphorylation of STAT1 and enhanced the type I IFN-mediated antiviral response, and overexpression of suppressor of the cytokine signalling 5 (SOCS5) decreased the phosphorylation of STAT1 and inhibited the type I IFN-mediated antiviral response. Meanwhile, with the knockdown of SOCS5, the upregulated expression of phosphorylated STAT1 and the anti-virus effect induced by miR-26a were significantly inhibited. Taken together, our data demonstrated a new strategy of host miRNAs against FHV-1 infection by enhancing IFN antiviral signaling.

show abstract

Genome-wide identification of chicken bursae of Fabricius miRNAs in response to very virulent infectious bursal disease virus

Huang

Wang

et al. 2022

Arch Virol

View full text Add to dashboard Cite

Infectious bursal disease virus (IBDV) can cause a highly contagious immunosuppressive disease in young chickens, resulting in considerable economic losses to the poultry industry. MicroRNAs (miRNAs) are crucial regulators of gene expression and are involved in the pathogenesis of IBDV infection. To investigate the roles of miRNA in chicken bursae of Fabricius in response to very virulent IBDV (vvIBDV) infection, RNA sequencing was performed. For this, we established an IBDV infection model as observed using histopathology, transmission electron microscopy (TEM), viral load detection, and cytokine expression levels. In total, 77 differentially expressed (DE) miRNAs were identified, of which 42 were upregulated and 35 were downregulated. A gene ontology analysis showed that genes associated with cellular processes, cells, and binding were enriched, and pathway analyses suggested that axon guidance, tight junctions, and endocytosis may be activated following vvIBDV infection. Moreover, we predicted the target genes of DE miRNAs and constructed an miRNA-mRNA regulatory network. In total, 189 pairs of miRNA-target genes were identified, comprising 67 DE miRNAs and 73 mRNAs. In this network, gga-miR-1684b-3p was identified with the highest fold change, and gga-miR-1788-3p and gga-miR-3530-5p showed a high degree of change, suggesting that they play vital roles in vvIBDV-host interactions. This study is the first to perform a comprehensive analysis of DE miRNAs in the bursa of Fabricius in response to vvIBDV infection, and it provides new insights into the molecular mechanisms underlying vvIBDV infection and pathogenesis. KeywordsInfectious bursal disease virus; Chicken; Bursae of Fabricius; miRNA; RNA sequencing Abbreviations: vvIBDV, very virulent infectious bursal disease virus; BF, bursa of Fabricius; miRNA, microRNA; TEM, transmission electron microscopy; DE, differentially expressed; TEM, transmission electron microscopy; PBS, phosphate-buffered saline; GO, gene ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes.

show abstract

gga-miR-155 Enhances Type I Interferon Expression and Suppresses Infectious Burse Disease Virus Replication via Targeting SOCS1 and TANK

Cited by 46 publications

References 70 publications

Identification of lncRNA‐155 encoded by MIR155HG as a novel regulator of innate immunity against influenza A virus infection

Identification of lncRNA‐155 encoded by MIR155HG as a novel regulator of innate immunity against influenza A virus infection

miR-26a Inhibits Feline Herpesvirus 1 Replication by Targeting SOCS5 and Promoting Type I Interferon Signaling

Genome-wide identification of chicken bursae of Fabricius miRNAs in response to very virulent infectious bursal disease virus

Contact Info

Product

Resources

About