Differential expression analysis of mRNAs, lncRNAs, and miRNAs expression profiles and construction of ceRNA networks in PEDV infection

Shi, Xiaojie; Zhang, Qi; Wang, Jingjing; Zhang, Yuting; Yan, Yuchao; Liu, Yi; Yang, Naling; Wang, Quanqiong; Xu, Xiaoxiao

doi:10.1186/s12864-022-08805-0

Cited by 6 publications

(3 citation statements)

References 57 publications

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“…Our previous studies found that many miRNAs were significantly upregulated or downregulated after PEDV infection ( 25 ). Therefore, we explored whether there was an endogenous miRNA that specifically inhibited HNRNPA3 expression.…”

Section: Resultsmentioning

confidence: 99%

PEDV inhibits HNRNPA3 expression by miR-218-5p to enhance cellular lipid accumulation and promote viral replication

Shi,

Zhang,

Yang

et al. 2024

mBio

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Porcine epidemic diarrhea virus (PEDV) requires complete dependence on the metabolic system of the host cell to complete its life cycle. There is a strong link between efficient viral replication and cellular lipid synthesis. However, the mechanism by which PEDV interacts with host cells to hijack cellular lipid metabolism to promote its replication remains unclear. In this study, PEDV infection significantly enhanced the expression of lipid synthesis-related genes and increased cellular lipid accumulation. Furthermore, using liquid chromatography-tandem mass spectrometry, we identified heterogeneous nuclear ribonucleoprotein A3 (HNRNPA3) as the interacting molecule of PEDV NSP9. We demonstrated that the expression of HNRNPA3 was downregulated by PEDV-induced miR-218-5p through targeting its 3′ untranslated region. Interestingly, knocking down HNRNPA3 facilitated the PEDV replication by promoting cellular lipid synthesis. We next found that the knockdown of HNRNPA3 potentiated the transcriptional activity of sterol regulatory element-binding transcription factor 1 (SREBF1) through zinc finger protein 135 (ZNF135) as well as PI3K/AKT and JNK signaling pathways. In summary, we propose a model in which PEDV downregulates HNRNPA3 expression to promote the expression and activation of SREBF1 and increase cellular lipid accumulation, providing a novel mechanism by which PEDV interacts with the host to utilize cellular lipid metabolism to promote its replication. IMPORTANCE As the major components and structural basis of the viral replication complexes of positive-stranded RNA viruses, lipids play an essential role in viral replication. However, how PEDV manipulates host cell lipid metabolism to promote viral replication by interacting with cell proteins remains poorly understood. Here, we found that SREBF1 promotes cellular lipid synthesis, which is essential for PEDV replication. Moreover, HNRNPA3 negatively regulates SREBF1 activation and specifically reduces lipid accumulation, ultimately inhibiting PEDV dsRNA synthesis. Our study provides new insight into the mechanisms by which PEDV hijacks cell lipid metabolism to benefit viral replication, which can offer a potential target for therapeutics against PEDV infection.

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Section: Resultsmentioning

confidence: 99%

PEDV inhibits HNRNPA3 expression by miR-218-5p to enhance cellular lipid accumulation and promote viral replication

Shi,

Zhang,

Yang

et al. 2024

mBio

Self Cite

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“…PEDV has spread widely in swine herds over recent years, causing significant losses to the pig industry. Several studies have demonstrated that the expression profile of ncRNAs, including miRNAs [ 57 , 58 , 59 ], lncRNAs [ 58 ] and circRNAs [ 60 ], which play various roles in PEDV infection, undergoes significant changes during PEDV infection. Here, we provide an overview of recent advancements in the study of various ncRNAs during PEDV infection.…”

Section: Ncrna During Porcine Virus Infectionmentioning

confidence: 99%

Regulatory Non-Coding RNAs during Porcine Viral Infections: Potential Targets for Antiviral Therapy

Li,

Yu,

et al. 2024

Viruses

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Pigs play important roles in agriculture and bio-medicine; however, porcine viral infections have caused huge losses to the pig industry and severely affected the animal welfare and social public safety. During viral infections, many non-coding RNAs are induced or repressed by viruses and regulate viral infection. Many viruses have, therefore, developed a number of mechanisms that use ncRNAs to evade the host immune system. Understanding how ncRNAs regulate host immunity during porcine viral infections is critical for the development of antiviral therapies. In this review, we provide a summary of the classification, production and function of ncRNAs involved in regulating porcine viral infections. Additionally, we outline pathways and modes of action by which ncRNAs regulate viral infections and highlight the therapeutic potential of artificial microRNA. Our hope is that this information will aid in the development of antiviral therapies based on ncRNAs for the pig industry.

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“…Emerging evidence demonstrates that the expression pro les of host cell-encoded lncRNAs can be altered during viral infections. For instance, infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), human immunode ciency virus (HIV), hepatitis C virus (HCV), in uenza A virus (IAV), porcine epidemic diarrhea virus (PEDV), and porcine deltacoronavirus (PDCoV) has been shown to modulate the cellular lncRNA landscape [20][21][22][23][24][25]. This observation suggests that lncRNAs may participate in the reprogramming of virus-host cell interactions.…”

Section: Introductionmentioning

confidence: 99%

The long non-coding RNA lncRNA-DRNR targets the JMJD6 to enhance replication of infectious bronchitis virus（IBV） by influencing the ISG expression pathway through the JAK-STAT signaling pathway

Yan,

Fu,

Lei

et al. 2024

Preprint

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Infectious Bronchitis Virus (IBV) is the causative agent of Infectious Bronchitis (IB), a severe disease that primarily affects young chickens and poses a significant challenge to the global poultry industry. Gaining an understanding of the intricate interplay between the virus and its host is crucial for developing novel antiviral strategies. Long non-coding RNA (lncRNA) has emerged as a pivotal regulator of host antiviral immune responses, and our previous studies have indicated that IBV infection disrupts lncRNA stability in host cells, suggesting an unknown regulatory role for lncRNA in IBV pathogenesis. However, it remains unclear how lncRNA precisely modulates IBV replication. In this study, we observed down-regulation ofMSTRG.26120.58 (named lncRNA-DRNR) expression in various chicken cell lines upon IBV infection and demonstrated that silencing lncRNA-DRNR using siRNA enhances intracellular replication of IBV. Through exploration of genes encoding proteins upstream and downstream of lncRNA-DRNR within a 100kb range, we identified JMJD6 as a potential target gene negatively regulated by lncRNA-DRNR expression levels. Moreover, JMJD6 inhibits STAT1 methylation, thereby influencing induction of Interferon-Stimulated Genes (ISGs) through IFN-β-mediated JAK-STAT signaling pathway activation and ultimately promoting intracellular replication of IBV. In summary, our findings unveil the critical role played by lncRNA-DRNR during IBV infection while providing novel insights into mechanisms underlying coronavirus-induced disruption in lncRNA stability.

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Differential expression analysis of mRNAs, lncRNAs, and miRNAs expression profiles and construction of ceRNA networks in PEDV infection

Cited by 6 publications

References 57 publications

PEDV inhibits HNRNPA3 expression by miR-218-5p to enhance cellular lipid accumulation and promote viral replication

PEDV inhibits HNRNPA3 expression by miR-218-5p to enhance cellular lipid accumulation and promote viral replication

Regulatory Non-Coding RNAs during Porcine Viral Infections: Potential Targets for Antiviral Therapy

The long non-coding RNA lncRNA-DRNR targets the JMJD6 to enhance replication of infectious bronchitis virus（IBV） by influencing the ISG expression pathway through the JAK-STAT signaling pathway

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