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学者姓名：王松
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【目的】探究TGF-β1/Smad3在流感病毒WSN毒株感染过程中对类黏蛋白(orosomucoid,ORM)表达的调控作用。【方法】利用流感病毒WSN毒株感染或TGF-β1处理A549细胞，然后使用Smad3抑制剂处理，通过RT-PCR检测ORM的表达情况；构建过表达STAT3的细胞系与敲低STAT3的细胞系，通过RT-PCR和Western blotting方法检测STAT3在流感病毒诱导ORM表达中的作用；使用TGF-β1处理A549细胞，通过Western blotting方法检测p-STAT3表达情况；使用TGF-β1或流感病毒处理A549细胞，然后使用Smad3抑制剂处理，检测p-STAT3表达情况；构建Smad3表达敲低细胞系，通过Western blotting方法检测STAT3磷酸化水平。【结果】TGF-β1调控ORM1和ORM2的表达依赖于Smad3的活化；STAT3在流感病毒感染过程中参与了ORM1和ORM2的表达调控；TGF-β1能够诱导STAT3发生磷酸化；阻断Smad3的活化或敲低Smad3表达后，TGF-β1或WSN诱导的STAT3的磷酸化也被抑制。【结论】流感病毒WSN毒株调控ORM1和ORM2的表达依赖于TGF-β1/Smad3介导的STAT3磷酸化。
Keyword ：
STAT3 STAT3 TGF-β1/Smad3 TGF-β1/Smad3 流感病毒 流感病毒 类黏蛋白 类黏蛋白
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| GB/T 7714 | 尤冬雪 , 潘宸 , 陈玉章 et al. 流感病毒WSN毒株通过TGF-β1/Smad3介导的STAT3磷酸化调控类黏蛋白的表达 [J]. | 微生物学报 , 2025 , 65 (02) : 771-780 . |
| MLA | 尤冬雪 et al. "流感病毒WSN毒株通过TGF-β1/Smad3介导的STAT3磷酸化调控类黏蛋白的表达" . | 微生物学报 65 . 02 (2025) : 771-780 . |
| APA | 尤冬雪 , 潘宸 , 陈玉章 , 周欣霓 , 高铭 , 陈梦颖 et al. 流感病毒WSN毒株通过TGF-β1/Smad3介导的STAT3磷酸化调控类黏蛋白的表达 . | 微生物学报 , 2025 , 65 (02) , 771-780 . |
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随着翻译组测序、多肽组学和生物信息学分析等技术的快速发展，人们发现大量长链非编码RNA(long non-coding RNA, lncRNA)含有可编码功能性微肽的短开放阅读框。这些由lncRNA编码的微肽不仅参与调控骨骼肌的生理功能、胚胎发育和神经细胞发育，还对多种癌症的发生与发展、炎症反应及心血管疾病产生影响。研究这些微肽的功能对于深入理解生命活动的调控机制具有重要的科学意义，也为相关疾病的防治提供新的思路与方向。概述了鉴定lncRNA编码微肽的常用方法，以及这些微肽功能的最新研究进展，以期为后续研究提供参考。
Keyword ：
功能 功能 微肽 微肽 短开放阅读框 短开放阅读框 鉴定 鉴定 长链非编码RNA 长链非编码RNA
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| GB/T 7714 | 黄桂英 , 王李伟 , 刘嘉茵 et al. 长链非编码RNA编码微肽的鉴定和功能研究进展 [J]. | 福建农林大学学报(自然科学版) , 2025 , 54 (01) : 89-99 . |
| MLA | 黄桂英 et al. "长链非编码RNA编码微肽的鉴定和功能研究进展" . | 福建农林大学学报(自然科学版) 54 . 01 (2025) : 89-99 . |
| APA | 黄桂英 , 王李伟 , 刘嘉茵 , 王松 , 陈吉龙 , 池晓娟 . 长链非编码RNA编码微肽的鉴定和功能研究进展 . | 福建农林大学学报(自然科学版) , 2025 , 54 (01) , 89-99 . |
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本发明公开了一种由长链非编码RNA GAS5编码的微肽及其应用，所述微肽为由长链非编码RNA GAS5编码的含50个氨基酸的微肽，命名为GAS5‑P50。本方案通过血凝试验和空斑试验检测发现，与对照组相比，过表达微肽GAS5‑P50可使流感病毒HA效价和病毒载量显著升高，而敲低GAS5‑P50表达则显著降低流感病毒HA效价和病毒载量。本发明发现由长链非编码RNA编码的微肽GAS5‑P50在流感病毒感染过程中发挥了促进病毒复制的作用，可开发靶向微肽GAS5‑P50的分子作为抗流感病毒药物，为流感病毒的防治提供新的选择。
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| GB/T 7714 | 池晓娟 , 王松 , 陈吉龙 . 一种由长链非编码RNA GAS5编码的微肽及其应用 : CN202411771173.3[P]. | 2024-12-04 . |
| MLA | 池晓娟 et al. "一种由长链非编码RNA GAS5编码的微肽及其应用" : CN202411771173.3. | 2024-12-04 . |
| APA | 池晓娟 , 王松 , 陈吉龙 . 一种由长链非编码RNA GAS5编码的微肽及其应用 : CN202411771173.3. | 2024-12-04 . |
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脂滴是从内质网膜形成的一种独特的动态细胞器，主要负责细胞内中性脂质的储存。脂滴还与其它细胞器相互作用，参与脂质代谢、膜生物合成、细胞信号转导、免疫反应等生物学过程。近年来越来越多的研究表明，脂滴在病原微生物感染，尤其是病毒感染过程中发挥着重要作用。本文综述了脂滴与病毒之间的相互作用，包括脂滴对病毒复制周期的影响以及脂滴在调节抗病毒免疫反应中发挥的作用。了解脂滴在病毒感染中的功能对于深入揭示病毒的致病机制、研发新型抗病毒药物以及预防病毒传播具有重要意义。
Keyword ：
复制 复制 天然免疫 天然免疫 感染 感染 病毒 病毒 脂滴 脂滴
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| GB/T 7714 | 毛亚楠 , 高铭 , 周欣霓 et al. 脂滴在病毒感染中的功能研究进展 [J]. | 畜牧兽医学报 , 2025 , 56 (02) : 513-522 . |
| MLA | 毛亚楠 et al. "脂滴在病毒感染中的功能研究进展" . | 畜牧兽医学报 56 . 02 (2025) : 513-522 . |
| APA | 毛亚楠 , 高铭 , 周欣霓 , 尤冬雪 , 彭本群 , 王松 . 脂滴在病毒感染中的功能研究进展 . | 畜牧兽医学报 , 2025 , 56 (02) , 513-522 . |
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Long non-coding RNAs (lncRNAs) have been recognized for their crucial roles in the replication processes of various viruses. However, the specific functions and regulatory mechanisms of many lncRNAs in influenza A virus (IAV) pathogenesis remain poorly understood. In this study, we identified lncRNA THRIL and observed a significant reduction in its expression following IAV infection in A549 cells. The treatment of cells with the viral mimic poly (I:C), or with type I and type III interferons, resulted in a substantial decrease in THRIL expression. Furthermore, THRIL overexpression significantly enhanced IAV replication, while its silencing markedly reduced IAV replication. Additionally, IAV infection led to notable reductions in the expression levels of type I and type III interferons in cell lines overexpressing THRIL compared to control groups; conversely, cell lines with THRIL knockdown exhibited significantly higher interferon levels than control groups. Moreover, THRIL was found to inhibit the expression of several critical interferon-stimulated genes (ISGs), which are essential for an effective antiviral response. Notably, our findings demonstrated that THRIL impaired the activation of IRF3, a key transcription factor in the interferon signaling pathway, thereby suppressing host innate immunity. These results highlight THRIL's potential as a therapeutic target for antiviral strategies.
Keyword ：
influenza A virus influenza A virus innate immunity innate immunity IRF3 IRF3 long non-coding RNAs long non-coding RNAs THRIL THRIL
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| GB/T 7714 | Chen, Mengying , Hu, Jingyun , Zhou, Xinni et al. Long Non-Coding RNA THRIL Promotes Influenza Virus Replication by Inhibiting the Antiviral Innate Immune Response [J]. | VIRUSES-BASEL , 2025 , 17 (2) . |
| MLA | Chen, Mengying et al. "Long Non-Coding RNA THRIL Promotes Influenza Virus Replication by Inhibiting the Antiviral Innate Immune Response" . | VIRUSES-BASEL 17 . 2 (2025) . |
| APA | Chen, Mengying , Hu, Jingyun , Zhou, Xinni , Gao, Ming , Li, Ning , Yang, Guihong et al. Long Non-Coding RNA THRIL Promotes Influenza Virus Replication by Inhibiting the Antiviral Innate Immune Response . | VIRUSES-BASEL , 2025 , 17 (2) . |
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Influenza A virus (IAV) poses a significant global health threat to both humans and animals. Increasing evidence highlights long noncoding RNAs (lncRNAs) as critical regulators of various physiological and pathological processes, but their roles in virus-host interactions in chickens remain elusive. This study identified chicken lncRNAs and further investigated their functional involvement in IAV-host interactions. Transcriptome sequencing of chicken DF-1 cells revealed that 2118 lncRNAs were differentially expressed following H9N2 avian influenza virus infection. Among these, a lncRNA that we named lncRNA-up4 was significantly upregulated by H9N2 infection. LncRNA-up4 was predominantly localized in the nucleus but also detected in the cytoplasm. Furthermore, we found that the virus-induced expression of lncRNA-up4 was regulated by the pattern recognition receptor-dependent NF-kappa B signalling pathway. Functional analysis demonstrated that silencing lncRNA-up4 impaired IAV replication by upregulating the expression of several critical antiviral molecules, including IFN-beta, MX1, and OAS-1. Conversely, overexpression of lncRNA-up4 increased viral replication, as evidenced by increased viral NP protein and virus titers. Moreover, we observed that lncRNA-up4 positively regulated the expression of IL-6, TNF-alpha, and IL-1 beta but suppressed the expression of IFN-beta at the mRNA level. These results reveal that the newly identified lncRNA-up4 plays an important role in influenza virus replication through the regulation of cytokine production and antiviral gene expression in chicken cells. This study provides valuable insight into the regulatory function of chicken lncRNAs in innate immunity.
Keyword ：
Chicken Chicken IL-6 IL-6 interferon interferon LncRNA LncRNA NF-kappa B NF-kappa B
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| GB/T 7714 | Sajjad, Nelam , Maarouf, Mohamed , Wang, Yiming et al. A chicken lncRNA is identified as a critical regulator that increases influenza virus replication by impairing innate antiviral responses [J]. | VETERINARY RESEARCH , 2025 , 56 (1) . |
| MLA | Sajjad, Nelam et al. "A chicken lncRNA is identified as a critical regulator that increases influenza virus replication by impairing innate antiviral responses" . | VETERINARY RESEARCH 56 . 1 (2025) . |
| APA | Sajjad, Nelam , Maarouf, Mohamed , Wang, Yiming , Shrestha, Prasha , Rai, Kul Raj , Chi, Xiaojuan et al. A chicken lncRNA is identified as a critical regulator that increases influenza virus replication by impairing innate antiviral responses . | VETERINARY RESEARCH , 2025 , 56 (1) . |
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本发明公开了一种适合白玉菇生产的斑玉蕈菌种。本发明中，所述白玉菇菌种白玉菇87是以真姬菇‘B02’和真姬菇‘B06’为亲本进行杂交选育而成。‘B02’有菌柄粗细均匀，产量高等特点，但是菌柄偏细、偏黄等不足，‘B06’有菇帽厚实、菇柄较粗、颜色白，产量较高的特点，但易出畸形芽、均匀性稍差等缺点，白玉菇菌种‘白玉菇87’分类命名为斑玉蕈(Hypsizygus marmoreus)白玉菇87，已于2024年11月07日保藏于中国典型培养物保藏中心，保藏编号为CCTCC M 20242461，保藏地址为湖北省武汉市武昌区八一路299号。
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| GB/T 7714 | 刘新锐 , 王松 , 谢宝贵 et al. 一种适合白玉菇生产的斑玉蕈菌种 : CN202411622381.7[P]. | 2024-11-14 . |
| MLA | 刘新锐 et al. "一种适合白玉菇生产的斑玉蕈菌种" : CN202411622381.7. | 2024-11-14 . |
| APA | 刘新锐 , 王松 , 谢宝贵 , 江玉姬 , 李博 . 一种适合白玉菇生产的斑玉蕈菌种 : CN202411622381.7. | 2024-11-14 . |
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Long non-coding RNAs (lncRNAs) are critical regulators of various biological processes, yet their roles in chicken host-virus interactions remain largely unknown. This study investigated the impact of influenza A virus (IAV) H9N2 infection on the expression of two lncRNAs, Lnc9101 and Lnc8475, and the regulatory roles of these lncRNAs in the innate immune response. The results demonstrated that the expression of both lncRNAs were significantly upregulated in H9N2-infected chickens and could be induced by viral genomic RNA, poly (I:C) or LPS. Disruption of Lnc9101 expression in DF-1 cells enhanced the IAV replication, while its overexpression suppressed it. Conversely, Lnc8475 had the opposite effect on the IAV replication compared with Lnc9101. Silencing Lnc8475 expression in DF-1 cells attenuated IAV replication, while its overexpression promoted viral replication. Furthermore, we found that both lncRNAs regulated the expression of type I and type III interferons (IFNs), thereby affecting multiple interferon-stimulating genes (ISGs) expression and STAT1 activation upon IAV infection. Moreover, Lnc9101 knockdown impaired the expression of TLR7 and MDA5 and reduced IRF7 phosphorylation, whereas Lnc8475 knockdown promoted the expression of TLR3 and TLR7. In summary, Lnc9101 inhibits IAV replication by positively regulating the innate immune response, whereas Lnc8475 promotes IAV replication by suppressing it. These findings suggest that LncRNA9101 and Lnc8475 play important roles in pattern recognition receptors (PRRs)-dependent innate immune signaling and antiviral responses, advancing a better understanding of lncRNA functioning in chickens.
Keyword ：
Influenza A virus Influenza A virus Innate immune response Innate immune response Interferon Interferon Long non-coding RNA Long non-coding RNA Signaling pathway Signaling pathway
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| GB/T 7714 | Lin, Jiaqi , Hu, Pengcheng , Mei, Guiheng et al. Role of long non-coding RNA Lnc9101 and Lnc8475 in regulation of innate immune response to influenza virus infection [J]. | POULTRY SCIENCE , 2025 , 104 (12) . |
| MLA | Lin, Jiaqi et al. "Role of long non-coding RNA Lnc9101 and Lnc8475 in regulation of innate immune response to influenza virus infection" . | POULTRY SCIENCE 104 . 12 (2025) . |
| APA | Lin, Jiaqi , Hu, Pengcheng , Mei, Guiheng , Guo, Bolun , Wang, Song , Yan, Shihong et al. Role of long non-coding RNA Lnc9101 and Lnc8475 in regulation of innate immune response to influenza virus infection . | POULTRY SCIENCE , 2025 , 104 (12) . |
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Neuromedin B (NMB) and its receptor NMBR constitute a neuropeptide system implicated in various physiological processes. While previously associated with innate immunity, their precise antiviral action against influenza A virus (IAV) infection have remained poorly defined. Here, we elucidate the function of the NMB/ NMBR axis in the host defense against H9N2 influenza virus. We demonstrate that NMB treatment and NMBR overexpression potentiate IFN-beta production and restrict viral replication in H9N2-infected A549 cells and mouse lungs. Conversely, NMBR knockdown compromises the antiviral response, diminishing IFN-beta expression and enhancing viral propagation. We further show that NMB/NMBR signaling targets the viral non-structural protein 1 (NS1) by upregulating the E3 ubiquitin ligase TRIM25. Mechanistically, NMB/NMBR activation engages a positive feedback loop with the retinoic acid-inducible gene I (RIG-I) pathway, reinforcing RIG-I activation through enhanced K63-linked ubiquitination while transcriptionally repressing the deubiquitinase CYLD. Consequently, this augmented signaling potentiates the JAK-STAT1 pathway, leading to increased STAT1 phosphorylation and elevated expression of interferon-stimulated gene 15 (ISG15). Our findings establish that the NMB/NMBR axis confers protection against H9N2 IAV by amplifying RIG-I-mediated innate immunity and facilitating NS1 suppression, revealing a pivotal neuroimmune mechanism and suggesting a promising target for developing broad-spectrum, host-directed therapeutics against IAV.
Keyword ：
Innate antiviral Immunity Innate antiviral Immunity Neuromedin B Neuromedin B NMBR NMBR RIG-I RIG-I
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| GB/T 7714 | Yang, Guihong , Tian, Shimao , Yang, Jinyu et al. Neuromedin B and its receptor NMBR inhibit H9N2 infection [J]. | VETERINARY MICROBIOLOGY , 2025 , 312 . |
| MLA | Yang, Guihong et al. "Neuromedin B and its receptor NMBR inhibit H9N2 infection" . | VETERINARY MICROBIOLOGY 312 (2025) . |
| APA | Yang, Guihong , Tian, Shimao , Yang, Jinyu , Tang, Yubing , Tian, Ke , Wang, Song et al. Neuromedin B and its receptor NMBR inhibit H9N2 infection . | VETERINARY MICROBIOLOGY , 2025 , 312 . |
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Autophagy-related protein 7 (ATG7) is an essential autophagy effector enzyme. Although it is well known that autophagy plays crucial roles in the infections with various viruses including influenza A virus (IAV), function and underlying mechanism of ATG7 in infection and pathogenesis of IAV remain poorly understood. Here, in vitro studies showed that ATG7 had profound effects on replication of IAV. Depletion of ATG7 markedly attenuated the replication of IAV, whereas overexpression of ATG7 facilitated the viral replication. ATG7 conditional knockout mice were further employed and exhibited significantly resistant to viral infections, as evidenced by a lower degree of tissue injury, slower body weight loss, and better survival, than the wild type animals challenged with either IAV (RNA virus) or pseudorabies virus (DNA virus). Interestingly, we found that ATG7 promoted the replication of IAV in autophagy-dependent and -independent manners, as inhibition of autophagy failed to completely block the upregulation of IAV replication by ATG7. To determine the autophagy-independent mechanism, transcriptome analysis was utilized and demonstrated that ATG7 restrained the production of interferons (IFNs). Loss of ATG7 obviously enhanced the expression of type I and III IFNs in ATG7-depleted cells and mice, whereas overexpression of ATG7 impaired the interferon response to IAV infection. Consistently, our experiments demonstrated that ATG7 significantly suppressed IRF3 activation during the IAV infection. Furthermore, we identified long noncoding RNA (lncRNA) GAPLINC as a critical regulator involved in the promotion of IAV replication by ATG7. Importantly, both inactivation of IRF3 and inhibition of IFN response caused by ATG7 were mediated through control over GAPLINC expression, suggesting that GAPLINC contributes to the suppression of antiviral immunity by ATG7. Together, these results uncover an autophagy-independent mechanism by which ATG7 suppresses host innate immunity and establish a critical role for ATG7/GAPLINC/IRF3 axis in regulating IAV infection and pathogenesis. Influenza A virus (IAV) causes acute respiratory diseases in human and animals, posing a great threat to public health. Autophagy plays crucial roles in viral infections including IAV, but mechanisms underlying interaction between autophagy and IAV remain ambiguous. Particularly, function and underlying mechanisms of ATG7, an essential autophagy effector enzyme, in viral infections are largely unexplored, and little information is available about relationship between ATG7 and IAV pathogenesis. Here, we used in vitro and in vivo models to address ATG7 function in the IAV infection and pathogenesis. We found that forced expression of ATG7 facilitates the viral replication, while depletion of ATG7 attenuates viral replication and renders mice more resistant to IAV or pseudorabies virus (PRV) infection. Importantly, we identify that ATG7 suppresses IRF3 activation and interferon production via lncRNA GAPLINC, revealing an autophagy-independent mechanism whereby ATG7 restrains host innate immunity and unveiling a critical role of ATG7/GAPLINC/IRF3 axis in regulating IAV pathogenesis. Moreover, our observations suggest that ATG7 may positively regulate the expression of GAPLINC via suppression of NF-kappa B activation during IAV infection. Together, these results reveal that ATG7 has multiple biological roles beyond autophagy, and provide an important insight into the complicated interplay between host and IAV.
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| GB/T 7714 | Chen, Biao , Guo, Guijie , Wang, Guoqing et al. ATG7/GAPLINC/IRF3 axis plays a critical role in regulating pathogenesis of influenza A virus [J]. | PLOS PATHOGENS , 2024 , 20 (1) . |
| MLA | Chen, Biao et al. "ATG7/GAPLINC/IRF3 axis plays a critical role in regulating pathogenesis of influenza A virus" . | PLOS PATHOGENS 20 . 1 (2024) . |
| APA | Chen, Biao , Guo, Guijie , Wang, Guoqing , Zhu, Qianwen , Wang, Lulu , Shi, Wenhao et al. ATG7/GAPLINC/IRF3 axis plays a critical role in regulating pathogenesis of influenza A virus . | PLOS PATHOGENS , 2024 , 20 (1) . |
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