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学者姓名：郭桂杰
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Abstract ：
H3N3 avian influenza viruses (AIVs) are less prevalent in poultry than H3N8 viruses. However, although relatively rare, reassortant H3N3 viruses have been known to appear in both domestic poultry and wild birds. In this study, we isolated the H3N3 virus in chickens sourced from a live poultry market in China. A comprehensive genomic analysis revealed that the virus possessed a single basic amino acid in the cleavage site of the hemagglutinin (HA) gene. Phylogenetic analysis indicated that eight genes in the H3N3 virus belong to the Eurasian lineage. Specifically, the HA and NA genes were clustered with H3N2 and H11N3, respectively, while the internal genes were closely related to the H3N8 and H9N2 viruses. Furthermore, the H3N3 virus exhibited high and moderate stability in thermal and acidic conditions and efficient replication capabilities in mammalian cells. The H3N3 virus demonstrated that it could infect and replicate in the upper and lower respiratory tract of BALB/c mice without prior adaptation, triggering hemagglutination inhibition (HI) antibody titres ranging from 80 to 160; notably, the H3N3 virus replicated vigorously within the chicken respiratory and digestive tracts. The virus also transmitted efficiently and swiftly among chickens through direct contact, leading to higher levels of HI antibodies in both the inoculated and contact birds. These findings suggest that the H3N3 virus may be a novel reassortant originating from viruses circulating in domestic poultry, thus demonstrating an increased pathogenicity and transmissibility in chickens. Our study determines that H3N3 AIV potentially threatens the poultry industry and public health, highlighting the importance of active surveillance of AIVs.
Keyword ：
avian influenza virus avian influenza virus evolution evolution pathogenicity pathogenicity transmissibility transmissibility Zoonoses Zoonoses
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| GB/T 7714 | Zhang, Chunping , Zhao, Conghui , Huang, Jiacheng et al. Emergence of a novel reassortant H3N3 avian influenza virus with enhanced pathogenicity and transmissibility in chickens in China [J]. | VETERINARY RESEARCH , 2025 , 56 (1) . |
| MLA | Zhang, Chunping et al. "Emergence of a novel reassortant H3N3 avian influenza virus with enhanced pathogenicity and transmissibility in chickens in China" . | VETERINARY RESEARCH 56 . 1 (2025) . |
| APA | Zhang, Chunping , Zhao, Conghui , Huang, Jiacheng , Wang, Yang , Jiang, Bo , Zheng, Hangyu et al. Emergence of a novel reassortant H3N3 avian influenza virus with enhanced pathogenicity and transmissibility in chickens in China . | VETERINARY RESEARCH , 2025 , 56 (1) . |
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本发明公开了RAD51抑制剂在制备抗伪狂犬病病毒药物中的应用，本方案属于生物医药技术领域，具体公开了小分子化合物RAD51抑制剂B02、DIDS在制备抗伪狂犬病病毒药物中的新应用；本方案所提供的一类小分子化合物具有抗伪狂犬病病毒的活性，该类小分子化合物均可降低PRV在A549细胞中的复制，同时其中一个小分子化合物B02也能够显著抑制PRV在PK‑15细胞中的复制，该类化合物可以为筛选和开发抗伪狂犬病病毒的药物提供理论依据和创新方向，在开发抗PRV药物研发领域中具有重要的科学意义与潜在应用价值。
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| GB/T 7714 | 郭桂杰 , 李凤 , 杨灵恩 et al. RAD51抑制剂在制备抗伪狂犬病病毒药物中的应用 : CN202510797898.8[P]. | 2025-06-16 . |
| MLA | 郭桂杰 et al. "RAD51抑制剂在制备抗伪狂犬病病毒药物中的应用" : CN202510797898.8. | 2025-06-16 . |
| APA | 郭桂杰 , 李凤 , 杨灵恩 , 黄攀锋 . RAD51抑制剂在制备抗伪狂犬病病毒药物中的应用 : CN202510797898.8. | 2025-06-16 . |
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Lactylation, a novel form of post-translational modifications (PTMs) of protein, particularly within histone proteins, has recently gained attention for its role in regulating gene expression and cellular processes. In recent years, lactylation has been widely studied in cancer, immune diseases, neurological diseases, cardiovascular diseases, metabolic diseases, etc. Increasing evidence now suggests that lactylation also plays a significant role in the host's innate immune response to viruses. Lactylation influences fundamental cellular functions, including transcriptional regulation, signal transduction, cell proliferation and differentiation. It affects protein behavior by modulating their function, stability, subcellular localization and interactions. Studies have shown that many viral infections promote lactate production through enhanced glycolysis, a process that facilitates viral replication. Given that innate immunity serves as the host's first line of defense against pathogenic invasion, understanding how lactylation regulates antiviral responses offers promising avenues for the development of diagnostic tools and therapeutic strategies against viral diseases. In this review, we provide a comprehensive overview of recent research on the role of lactylation in viral-host interactions.
Keyword ：
innate immunity innate immunity lactylation lactylation post-translational modifications (PTMs) post-translational modifications (PTMs) viral infection viral infection virus virus
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| GB/T 7714 | Zhao, Gejie , Zhou, Jia , He, Shutong et al. The Role of Lactylation in Virus-Host Interactions [J]. | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES , 2025 , 26 (14) . |
| MLA | Zhao, Gejie et al. "The Role of Lactylation in Virus-Host Interactions" . | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES 26 . 14 (2025) . |
| APA | Zhao, Gejie , Zhou, Jia , He, Shutong , Fei, Xiao , Guo, Guijie . The Role of Lactylation in Virus-Host Interactions . | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES , 2025 , 26 (14) . |
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Porcine epidemic diarrhoea virus (PEDV) has caused substantial economic losses to the global swine industry. The PEDV spike (S) protein mediates viral entry by interacting with host receptors. However, the molecular mechanisms underlying PEDV entry remain incompletely understood. In this study, we identified the L-type calcium channel Cav1.2 as a critical host factor for PEDV entry. Depletion of Cav1.2 significantly suppressed PEDV replication. Additionally, treatment with the FDA-approved Cav1.2 blocker diltiazem inhibited PEDV replication and disrupted early infection events. Mechanistically, we found that Cav1.2 interacts with the PEDV S1 subunit. Both Cav1.2 knockdown and diltiazem treatment substantially reduced the binding and internalisation of PEDV. These findings reveal that Cav1.2 is a key host factor for PEDV binding and internalisation via interaction with the viral S protein, and suggest that Cav1.2 may serve as a promising target for antiviral drug development against PEDV.
Keyword ：
Cav1.2 Cav1.2 entry factor entry factor internalisation internalisation PEDV PEDV viral binding viral binding
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| GB/T 7714 | Wang, Xinxin , Guo, Guilan , He, Shutong et al. Cav1.2 facilitates the binding and internalisation of porcine epidemic diarrhoea virus [J]. | VETERINARY RESEARCH , 2025 , 56 (1) . |
| MLA | Wang, Xinxin et al. "Cav1.2 facilitates the binding and internalisation of porcine epidemic diarrhoea virus" . | VETERINARY RESEARCH 56 . 1 (2025) . |
| APA | Wang, Xinxin , Guo, Guilan , He, Shutong , Wang, Kaili , Chen, Jianing , Guo, Guijie . Cav1.2 facilitates the binding and internalisation of porcine epidemic diarrhoea virus . | VETERINARY RESEARCH , 2025 , 56 (1) . |
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为了解福建地区致猪腹泻病病毒的流行现状和猪流行性腹泻病毒(PEDV)的变异情况，2023—2024年从福州市某疑似感染腹泻病毒的规模化猪场采集发病仔猪样品，经RT-PCR进行PEDV、猪传染性胃肠炎病毒(TGEV)和猪轮状病毒(PoRV)核酸检测，并对PEDV阳性病料进行纤突蛋白(S)基因序列扩增和测序，进行遗传演化分析。结果：PEDV、TGEV和PoRV检出率分别为32.29%(31/96)、30.21%(29/96)和4.17%(4/96),其中PEDV和TGEV混合感染17份(17.71%),TGEV和PoRV混合感染1份(1.04%),PEDV、TGEV和PoRV三重混合感染1份(1.04%)。从10份PEDV阳性猪肠道组织样品中获得10株PEDV的S基因序列，全长3 753～4 179 bp,编码1 250～1 392 aa, 10株PEDV的S基因核苷酸及氨基酸序列同源性分别为94.9%～99.8%和83.8%～99.7%。S基因系统发育进化树结果表明，6株属于GⅠb亚型，4株属于GⅡb亚型，且4株PEDV的S基因为独立的一小分支。与经典毒株CV777的S基因序列相比，10株PEDV的S基因核苷酸及氨基酸序列同源性分别为93.6%～96.9%和83.9%～95.9%,存在23个保守氨基酸位点突变，在162 aa处缺失1个氨基酸(R),GⅠb亚型的6株PEDV S蛋白存在10个保守氨基酸位点突变；GⅡb亚型的4株PEDV S蛋白存在45个保守氨基酸位点突变，在59～62 aa处有4个氨基酸(QGVN)插入，163 aa处缺失1个氨基酸(D)。综上，福建某规模化猪场PEDV流行率较高，流行毒株基因型呈现多样性，说明流行株持续变异，临床上应予以高度重视。
Keyword ：
序列分析 序列分析 猪传染性胃肠炎病毒 猪传染性胃肠炎病毒 猪流行性腹泻病毒 猪流行性腹泻病毒 猪轮状病毒 猪轮状病毒 福州 福州 鉴定 鉴定
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| GB/T 7714 | 郭桂兰 , 王凯莉 , 王鑫鑫 et al. 福州市某规模化猪场3种腹泻病毒流行情况调查及猪流行性腹泻病毒S基因序列遗传变异分析 [J]. | 畜牧与兽医 , 2025 , 57 (07) : 131-138 . |
| MLA | 郭桂兰 et al. "福州市某规模化猪场3种腹泻病毒流行情况调查及猪流行性腹泻病毒S基因序列遗传变异分析" . | 畜牧与兽医 57 . 07 (2025) : 131-138 . |
| APA | 郭桂兰 , 王凯莉 , 王鑫鑫 , 郭桂杰 . 福州市某规模化猪场3种腹泻病毒流行情况调查及猪流行性腹泻病毒S基因序列遗传变异分析 . | 畜牧与兽医 , 2025 , 57 (07) , 131-138 . |
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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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African swine fever (ASF) is an infectious disease with high mortality caused by African swine fever virus (ASFV), which poses a great threat to the global swine industry. ASFV has evolved multiple strategies to evade host antiviral innate immunity by perturbing inflammatory responses and interferon production. However, the molecular mechanisms underlying manipulation of inflammatory responses by ASFV proteins are not fully understood. Here, we report that A137R protein of ASFV is a key suppressor of host inflammatory responses. Ectopic expression of ASFV A137R in HEK293T cells significantly inhibited the activation of IL -8 and NF- kappa B promoters triggered by Sendai virus (SeV), influenza A virus (IAV), or vesicular stomatitis virus (VSV). Accordingly, forced A137R expression caused a significant decrease in the production of several inflammatory cytokines such as IL -8, IL -6 and TNF- alpha in the cells infected with SeV or IAV. Similar results were obtained from experiments using A137R overexpressing PK15 and 3D4/21 cells infected with SeV or VSV. Furthermore, we observed that A137R impaired the activation of MAPK and NF- kappa B signaling pathways, as enhanced expression of A137R significantly decreased the phosphorylation of JNK, p38 and p65 respectively upon viral infection (SeV or IAV) and IL-1 beta treatment. Mechanistically, we found that A137R interacted with MyD88, and dampened MyD88-mediated activation of MAPK and NF- kappa B signaling. Together, these findings uncover a critical role of A137R in restraining host inflammatory responses, and improve our understanding of complicated mechanisms whereby ASFV evades innate immunity.
Keyword ：
A137R A137R ASFV ASFV Inflammatory response Inflammatory response MyD88 MyD88 NF-kappa B NF-kappa B
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| GB/T 7714 | Xu, Yang , Wu, Lei , Hong, Jinxuan et al. African swine fever virus A137R protein inhibits NF- κB activation via suppression of MyD88 signaling in PK15 and 3D4/21 cells in vitro [J]. | VETERINARY MICROBIOLOGY , 2024 , 292 . |
| MLA | Xu, Yang et al. "African swine fever virus A137R protein inhibits NF- κB activation via suppression of MyD88 signaling in PK15 and 3D4/21 cells in vitro" . | VETERINARY MICROBIOLOGY 292 (2024) . |
| APA | Xu, Yang , Wu, Lei , Hong, Jinxuan , Chi, Xiaojuan , Zheng, Meichun , Wang, Liwei et al. African swine fever virus A137R protein inhibits NF- κB activation via suppression of MyD88 signaling in PK15 and 3D4/21 cells in vitro . | VETERINARY MICROBIOLOGY , 2024 , 292 . |
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Many annotated long noncoding RNAs (lncRNAs) contain small open reading frames (sORFs), some of which have been demonstrated to encode small proteins or micropeptides with fundamental biological importance. However, functions of lncRNAs-encoded small proteins or micropeptides in viral pathogenesis remain largely unexplored. Here, we identified a 110-amino acid small protein as a key regulator of influenza A virus (IAV) replication. This small protein that we call PESP was encoded by the putative lncRNA PCBP1-AS1. It was observed that both PCBP1-AS1 and PESP were significantly upregulated by IAV infection. Furthermore, they were markedly induced by treatment with either type I or type III interferon. Overexpression of either PCBP1-AS1 or PESP alone significantly enhanced IAV replication. In contrast, shRNA-mediated knockdown of PCBP1-AS1 or CRISPR/Cas9-mediated knockout of PESP markedly inhibited the viral production. Moreover, the targeted deletion or mutation of the sORF within the PCBP1-AS1 transcript, which resulted in the disruption of PESP expression, significantly diminished the capacity of PCBP1-AS1 to enhance IAV replication, underscoring the indispensable role of PESP in the facilitation of IAV replication by PCBP1-AS1. Interestingly, overexpression of PESP enhanced the IAV-induced autophagy by increasing the expression of ATG7, an essential autophagy effector enzyme. We also found that the 7-22 amino acids at the N-terminus of PESP were crucial for its functionality in modulating ATG7 expression and action as an enhancer of IAV replication. Additionally, HSP90AA1, a protein identified previously as a facilitator of autophagy, was found to interact with PESP, resulting in the stabilization of PESP and consequently an increase in the production of IAV. These data reveal a critical lncRNA-encoded small protein that is induced and exploited by IAV during its infection, and provide a significant insight into IAV-host interaction network. Emerging evidence has shown that some lncRNAs encode biologically active small proteins or micropeptides involved in diverse cellular processes. Here, we identified a previously unrecognized small protein derived from the lncRNA PCBP1-AS1 and established a role for this protein in influenza A virus (IAV) infection. We named it as PCBP1-AS1-encoded small protein (PESP) and found it to be crucially implicated in replication of IAV. Expression of both PESP and PCBP1-AS1 were significantly increased in response to IAV infection or upon interferon treatment. By overexpressing PESP, we observed a substantial enhancement in IAV replication, which was counteracted by reducing PESP level. We further demonstrated that PESP coding sequences were essential for PCBP1-AS1 to facilitate IAV replication, as evidenced by significantly reduced functionality of PCBP1-AS1 with deletion of the sequences. Intriguingly, PESP appeared to promote viral replication by modulating autophagy. This was achieved by significant upregulation of ATG7, a key enzyme in autophagy. Additionally, we revealed that interaction of PESP with HSP90AA1, a protein known to support autophagy, contributed to the protein's stability of PESP and consequently to increased IAV replication. This study sheds light on the intricate interplay between host factors and viral pathogens, offering potential targets for antiviral strategies.
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| GB/T 7714 | Chi, Xiaojuan , Huang, Guiying , Wang, Liwei et al. A small protein encoded by PCBP1-AS1 is identified as a key regulator of influenza virus replication via enhancing autophagy [J]. | PLOS PATHOGENS , 2024 , 20 (8) . |
| MLA | Chi, Xiaojuan et al. "A small protein encoded by PCBP1-AS1 is identified as a key regulator of influenza virus replication via enhancing autophagy" . | PLOS PATHOGENS 20 . 8 (2024) . |
| APA | Chi, Xiaojuan , Huang, Guiying , Wang, Liwei , Zhang, Xinge , Liu, Jiayin , Yin, Zhihui et al. A small protein encoded by PCBP1-AS1 is identified as a key regulator of influenza virus replication via enhancing autophagy . | PLOS PATHOGENS , 2024 , 20 (8) . |
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Circular RNAs (circRNAs) are an important subclass of noncoding RNAs implicated in the regulation of multiple biological processes. However, the functional involvement of circRNAs in the pathogenesis of influenza A viruses (IAVs) remains largely unknown. Here, we employed RNA sequencing (RNA-Seq) to examine the differentially expressed circRNAs in mouse lung tissues challenged or not challenged with IAV to evaluate the impact of viral infection on circRNAs in vivo. We observed that 413 circRNAs exhibited significantly altered levels following IAV infection. Among these, circMerTK, the derivative of myeloid-epithelial-reproductive tyrosine kinase (MerTK) pre-mRNA, was highly induced by IAV. Interestingly, circMerTK expression was also increased upon infection with multiple DNA and RNA viruses in human and animal cell lines, and thus it was selected for further studies. Poly(I:C) and interferon beta (IFN-beta) stimulated circMerTK expression, while RIG-I knockout and IFNAR1 knockout cell lines failed to elevate circMerTK levels after IAV infection, demonstrating that circMerTK is regulated by IFN signaling. Furthermore, circMerTK overexpression or silencing accelerated or impeded IAV and Sendai virus replication, respectively. Silencing circMerTK enhanced the production of type I IFNs and interferon-stimulating genes (ISGs), whereas circMerTK overexpression suppressed their expression at both the mRNA and protein levels. Notably, altering circMerTK expression had no effect on the MerTK mRNA level in cells infected or not infected with IAV, and vice versa. In addition, human circMerTK and mouse homologs functioned similarly in antiviral responses. Together, these results identify circMerTK as an enhancer of IAV replication through suppression of antiviral immunity.IMPORTANCE CircRNAs are an important class of noncoding RNAs characterized by a covalently closed circular structure. CircRNAs have been proven to impact numerous cellular processes, where they conduct specialized biological activities. In addition, circRNAs are believed to play a crucial role in regulating immune responses. Nevertheless, the functions of circRNAs in the innate immunity against IAV infection remain obscure. In this study, we employed transcriptomic analysis to investigate the alterations in circRNAs expression following IAV infection in vivo. It was found that expression of 413 circRNAs was significantly altered, of which 171 were upregulated, and 242 were downregulated following the IAV infection. Interestingly, circMerTK was identified as a positive regulator of IAV replication in both human and mouse hosts. CircMerTK was shown to influence IFN-beta production and its downstream signaling, enhancing IAV replication. This finding provides new insights into the critical roles of circRNAs in regulating antiviral immunity. CircRNAs are an important class of noncoding RNAs characterized by a covalently closed circular structure. CircRNAs have been proven to impact numerous cellular processes, where they conduct specialized biological activities.
Keyword ：
circular RNA circular RNA influenza A virus influenza A virus innate immune response innate immune response interferon-stimulating genes interferon-stimulating genes MerTK MerTK
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| GB/T 7714 | Qiu, Haori , Yang, Bincai , Chen, Yuhai et al. Influenza A Virus-Induced circRNA circMerTK Negatively Regulates Innate Antiviral Responses [J]. | MICROBIOLOGY SPECTRUM , 2023 , 11 (2) . |
| MLA | Qiu, Haori et al. "Influenza A Virus-Induced circRNA circMerTK Negatively Regulates Innate Antiviral Responses" . | MICROBIOLOGY SPECTRUM 11 . 2 (2023) . |
| APA | Qiu, Haori , Yang, Bincai , Chen, Yuhai , Zhu, Qianwen , Wen, Faxin , Peng, Min et al. Influenza A Virus-Induced circRNA circMerTK Negatively Regulates Innate Antiviral Responses . | MICROBIOLOGY SPECTRUM , 2023 , 11 (2) . |
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This study identifies interleukin-6 (IL-6)-independent phosphorylation of STAT3 Y705 at the early stage of infec-tion with several viruses, including influenza A virus (IAV). Such activation of STAT3 is dependent on the retinoic acid-induced gene I/mitochondrial antiviral-signaling protein/spleen tyrosine kinase (RIG-I/MAVS/Syk) axis and critical for antiviral immunity. We generate STAT3Y705F/1" knockin mice that display a remarkably suppressed antiviral response to IAV infection, as evidenced by impaired expression of several antiviral genes, severe lung tissue injury, and poor survival compared with wild-type animals. Mechanistically, STAT3 Y705 phosphor-ylation restrains IAV pathogenesis by repressing excessive production of interferons (IFNs). Blocking phosphor-ylation significantly augments the expression of type I and III IFNs, potentiating the virulence of IAV in mice. Importantly, knockout of IFNAR1 or IFNLR1 in STAT3Y705F/1" mice protects the animals from lung injury and re-duces viral load. The results indicate that activation of STAT3 by Y705 phosphorylation is vital for establishment of effective antiviral immunity by suppressing excessive IFN signaling induced by viral infection.
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| GB/T 7714 | Liu, Shasha , Liu, Siya , Yu, Ziding et al. STAT3 regulates antiviral immunity by suppressing excessive interferon signaling [J]. | CELL REPORTS , 2023 , 42 (7) . |
| MLA | Liu, Shasha et al. "STAT3 regulates antiviral immunity by suppressing excessive interferon signaling" . | CELL REPORTS 42 . 7 (2023) . |
| APA | Liu, Shasha , Liu, Siya , Yu, Ziding , Zhou, Wenzhuo , Zheng, Meichun , Gu, Rongrong et al. STAT3 regulates antiviral immunity by suppressing excessive interferon signaling . | CELL REPORTS , 2023 , 42 (7) . |
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