Avian leukosis virus (ALV) remains a major threat to the poultry industry due to its ability to establish persistent infection, induce immunosuppression, and promote tumorigenesis. Despite progress in eradication programs, effective control is hindered by subclinical infection, vertical transmission, and rapid viral evolution. A key limitation lies in the complexity of host–virus interactions, which are governed by multi-layered regulatory processes that cannot be fully resolved by studies focusing on single genes, pathways, or omics layers. In addition, the lack of robust and dynamic phenotypic indicators further constrains the dissection of resistance mechanisms. Recent advances in multi-omics technologies provide an opportunity to overcome these challenges by capturing coordinated changes across genomic, transcriptional, proteomic, and epigenetic levels. Integrating these data with molecular phenotypes, such as expression quantitative trait loci (eQTLs) and protein quantitative trait loci (pQTLs), enables the linking of genetic variation to functional immune responses. Furthermore, CRISPR-based functional screening offers a systematic approach for validating candidate host factors and identifying key regulators of viral replication and immune modulation. In this review, we summarize the epidemiology and molecular biology of ALV, outline current understanding of host–virus interaction networks with an emphasis on innate immune responses, and highlight how integrative multi-omics combined with functional genomics can advance the identification of critical host determinants. This framework provides a systems-level perspective for deciphering ALV–host interactions and supports the development of more effective antiviral strategies.

Avian leukosis viruses (ALVs) are a group of retroviruses with immunosuppressive and tumorigenic effects, causing substantial economic losses to the poultry industry due to the lack of effective commercial vaccines and antiviral drugs. Granulocyte colony-stimulating factor 3 (CSF3) is a cytokine that regulates hematopoiesis and modulates the proliferation and differentiation of immune cells. In our previous study, we unexpectedly observed that CSF3 expression was significantly upregulated upon stimulation with interferon-α (IFN-α) and ALV, suggesting a potential role in ALV infection. In this study, we confirmed that the CSF3 promoter could be activated by ALV and polyinosinic-polycytidylic acid (poly I:C) using a CSF3 promoter-driven reporter construct, and GAS potentially serving as the response element. Phylogenetic analysis showed that avian and mammalian CSF3 genes clustered separately within the phylogenetic tree. Subsequently, we overexpressed and silenced CSF3 in DF-1 cells followed by ALV-J infection. Transcriptome analysis revealed that CSF3 overexpression significantly upregulated genes involved in antiviral and inflammatory responses, particularly those in the TLR, RIG-I, JAK/STAT, and NF-κB signaling pathways. Our results demonstrated that CSF3 induced the expression of IFNs and antiviral genes (IRF7, Mx, MDA5, OASL, and ACSL1). Furthermore, CSF3 improved the phosphorylation level of IκBα, leading to the production of pro-inflammatory cytokines and activation of the NF-κB pathway, ultimately suppressing ALV-J envelope glycoprotein expression. Notably, the pro-inflammatory and antiviral effects of CSF3 were abolished upon treatment with a STAT3 inhibitor, suggesting that CSF3 exerts its antiviral function through STAT3 phosphorylation. A similar effect of CSF3 was observed in primary fibroblasts derived from chicken embryos. Collectively, our findings indicate that CSF3 may function as an atypical interferon-stimulated gene (ISG), enhancing the immune response against ALV-J by activating the NF-κB signaling pathway and interferon-mediated antiviral mechanisms. These results not only reveal the antiviral role of CSF3 but also provide new insights into the host's innate immune response to ALV. Furthermore, they highlight the potential of CSF3 as a candidate resistance gene for breeding programs or as a vaccine adjuvant for disease prevention.

Hyperpigmentation of the visceral peritoneum (HVP) is a pigmentation abnormality in chickens that adversely affects carcass appearance, consumer acceptance, and poultry production. However, the genetic basis of HVP remains unclear. To investigate the causes and regulatory mechanisms of HVP, we employed high-performance liquid chromatography (HPLC), bulk RNA sequencing (RNA-seq), qRT-PCR, Western blotting, and siRNA interference. Additionally, single-cell RNA sequencing (scRNA-seq) was used to examine gene expression at the cellular level. Anatomical examination and hematoxylin and eosin (HE) staining revealed melanin deposition in the peritoneum of HVP-affected chickens. Spectrophotometric analysis at 500 nm showed significantly higher absorbance in the HVP group (p < 0.05), which correlated with the degree of pigmentation. HPLC confirmed the pigmentation as eumelanin, based on the pyrrole-2,3,5-tricarboxylic acid (PTCA) peak. RNA-seq identified 61 differentially expressed genes. Functional studies showed that dopachrome tautomerase (DCT) overexpression, combined with L-tyrosine (L-Tyr) supplementation, significantly increased melanin content (p < 0.05) and promoted melanocyte proliferation. In contrast, DCT silencing reduced melanin secretion and inhibited cell growth. ScRNA-seq analysis of over 9700 high-quality cells identified distinct melanocyte clusters, with DCT expression approximately 2.5-fold higher in melanocytes from the HVP group compared to the normal group. Furthermore, a DCT polymorphism (g.147917398 C > T) was identified as a potential marker for genetic selection (p-values = 0.033). These findings demonstrate that HVP is driven by DCT overexpression and excessive eumelanin deposition. DCT could serve as a molecular marker for genomic selection to improve poultry carcass quality and reduce economic losses in the poultry industry.

Avian leukosis virus Subgroup J (ALVJ) exhibits high morbidity and pathogenicity, affecting approximately 20% of poultry farms. It induces neoplastic diseases and immunosuppression. Phorbol-12-myristate-13-acetate-induced protein 1 ( PMAIP1 ), a proapoptotic mitochondrial protein in the B-cell lymphoma-2 (Bcl-2) family, plays a role in apoptosis in cancer cells. However, the connection between the PMAIP1 gene and ALV -J pathogenicity remains unexplored. This study investigates the potential impact of the PMAIP1 gene on ALV -J replication and its regulatory mechanisms. Initially, we examined PMAIP1 expression using quantitative real -time PCR (qRT-PCR) in vitro and in vivo. Furthermore, we manipulated PMAIP1 expression in chicken fibroblast cells (DF-1) and assessed its effects on ALV -J infection through qRTPCR, immunofluorescence assay (IFA), and western blotting (WB). Our findings reveal a significant downregulation of PMAIP1 in the spleen, lung, and kidney, coupled with an up-regulation in the bursa and liver of ALV -J infected chickens compared to uninfected ones. Additionally, DF-1 cells infected with ALV -J displayed a notable up-regulation of PMAIP1 at 6, 12, 24, 48, 74, and 108 h. Over-expression of PMAIP1 enhanced ALVJ replication, interferon expression, and proinflammatory factors. Conversely, interference led to contrasting results. Furthermore, we observed that PMAIP1 promotes virus replication by modulating mitochondrial function. In conclusion, the PMAIP1 gene facilitates virus replication by regulating mitochondrial function, thereby enriching our understanding of mitochondriarelated genes and their involvement in ALV -J infection, offering valuable insights for avian leukosis disease resistance strategies.

Growth hormone (GH) plays a crucial role in growth, sexual maturity, and immunity in chickens. Avian leukosis virus subgroup J (ALV-J) is an exogenous tumorigenic retrovirus that primarily induces immunosuppression, growth retardation, decreased egg production, tumors formation, and even death in chickens. Previous studies have suggested that GH is involved in the regulation of innate immunity and inflammation. However, the specific role of GH in response to ALV-J remains unclear. In this study, we observed a significant upregulation of GH protein expression in the plasma of ALV infected chickens, and a marked increase in GH mRNA in ALV-J infected cells. We found that lower gp85 expression correlated with higher GH expression in immune tissues, suggesting that GH may inhibit gp85 expression. Additionally, GH overexpression enhanced the expression of interferons (IFN-α, IFN-β), interferon-stimulating genes (Mx1, ASCL1, CH25H), and pro-inflammatory factors (Mx1, ASCL1, CH25H) in DF-1 cells infected with ALV-J. GH also affected the cell cycle by regulating the expression of cell proliferation-related genes (p21, PCNA, Cyclin B2, Cyclin D1, Cyclin D2) and cell apoptosis-related genes (p53, Fas, Cyct, Caspase-1, Caspase-3, Caspase-8). More importantly, we found that GH restricted cell proliferation and apoptosis, and inhibited the replication of ALV-J by activating the PI3K/Akt signaling pathway in DF-1 cells. In conclusion, these results indicate GH plays a role in the antiviral response against the replication of ALV-J, providing evidence of an interaction between GH and the innate immunity in chickens.

Myoblast differentiation requires metabolic reprogramming driven by increased mitochondrial biogenesis and oxidative phosphorylation. The canonical GH-GHR-IGFs axis in liver exhibits a great complexity in response to somatic growth. However, the underlying mechanism of whether local GHR acts as a control valve to regulate mitochondrial function through mitochondrial biogenesis during myoblast differentiation remains unknown. We manipulated the GHR expression in chicken primary myoblast to investigate its roles in mitochondrial biogenesis and function during myoblast differentiation. We reported that GHR is induced during myoblast differentiation. Local GHR promoted mitochondrial biogenesis during myoblast differentiation, as determined by the fluorescence intensity of Mito-Tracker Green staining and MitoTimer reporter system, the expression of mitochondrial biogenesis markers (PGC1α, NRF1, TFAM) and mtDNA encoded gene (ND1, CYTB, COX1, ATP6), as well as mtDNA content. Consistently, local GHR enhanced mitochondrial function during myoblast differentiation, as determined by the oxygen consumption rate, mitochondrial membrane potential, ATP level and ROS production. We next revealed that the regulation of mitochondrial biogenesis and function by GHR depends on IGF1. In terms of the underlying mechanism, we demonstrated that IGF1 regulates mitochondrial biogenesis via PI3K/AKT/CREB pathway. Additionally, GHR knockdown repressed myoblast differentiation. In conclusion, our data corroborate that local GHR acts as a control valve to enhance mitochondrial function by promoting mitochondrial biogenesis via IGF1-PI3K/AKT/CREB pathway during myoblast differentiation.

Autophagy plays an important role in host antiviral defense. The avian leukosis virus subgroup J (ALV-J) has been shown to inhibit autophagy while promoting viral replication. The underlying autophagic mechanisms, however, are unknown. Cholesterol 25-hydroxylase (CH25H) is a conserved interferon-stimulated gene, which converts cholesterol to a soluble antiviral factor, 25-hydroxycholesterol (25HC). In this study, we further investigated the autophagic mechanism of CH25H resistance to ALV-J in chicken embryonic fibroblast cell lines (DF1). Our results found that overexpression of CH25H and treatment with 25HC promoted the autophagic markers microtubule-associated protein 1 light chain 3 II (LC3II) and autophagy-related gene 5(ATG5), while decreased autophagy substrate p62/SQSTM1 (p62) expression in ALV-J infection DF-1 cells. Induction of cellular autophagy also reduces the levels of ALV-J gp85 and p27. ALV-J infection, on the other hand, suppresses autophagic marker protein LC3II expression. These findings suggest that CH25H-induced autophagy is a host defense mechanism that aids in ALV-J replication inhibition. In particular, CH25H interacts with CHMP4B and inhibits ALV-J infection in DF-1 cells by promoting autophagy, revealing a novel mechanism by which CH25H inhibits ALV-J infection. Although the underlying mechanisms are not completely understood, CH25H and 25HC are the first to show inhibiting ALV-J infection via autophagy.

本试验旨在研究益生菌(丁酸梭菌和粪肠球菌)对惠阳胡须鸡的生产性能和屠宰性能的影响.选取6 000只健康、体重均匀的70日龄的胡须鸡仔鸡,随机分成4组,分别为对照组、粪肠球菌组、丁酸梭菌组、粪肠球菌和丁酸梭菌混合组.试验鸡饲养于同一鸡舍中,所有试验肉鸡均采用相同饲养管理方法,在相同环境下进行饲养,自由饮水和采食.试验结果表明:与对照组相比,丁酸梭菌组平均总增重有所增加,混合组在12、13和15周龄的体重显著提高(P＜0.05),平均总增重高于其他组,饲料转化率有较大提高;在屠宰性能方面,丁酸梭菌组的宰前体重、半净膛重和胸肌重显著提高(P＜0.05),混合组胡须鸡的宰前体重、屠体重和半净体重有极显著提高(P＜0.01),而全净膛重、胸肌重和脚重有显著提高(P＜0.05).由此可见,在胡须鸡的日常饮水中添加丁酸梭菌制剂和粪肠球菌制剂对胡须鸡的生长性能和屠宰性能具有良好的改善作用.

Endogenous retroviruses (ERVs) are viral sequences that have integrated into the genomes of vertebrates. Our preliminary transcriptome sequencing analysis revealed that chERV3 is active and is located on chromosome 1:32602284–32615631. We hypothesized that chERV3 may have a role in the host innate immune response to viral infection. In this study, using reverse genetics, we constructed the puc57-chERV3 full-length reverse cloning plasmid in vitro. We measured the p27 content in culture supernatant by enzyme-linked immunosorbent assay (ELISA). Finally, transcriptome analysis was performed to analyze the function of chERV3 in innate immunity. The results showed that chERV3 may generate p27 viral particles. We found that compared to the negative control (NC) group (transfected with pMD18T-EGFP), the chERV3 group exhibited 2538 up-regulated differentially expressed genes (DEGs) and 1828 down-regulated DEGs at 24 hours (h) and 1752 up-regulated DEGs and 1282 down-regulated DEGs at 48 h. Based on Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses, the down-regulated DEGs were enriched mainly in immune-related processes such as the inflammatory response, innate immune response, and Toll-like receptor signaling pathway. GSEA showed that the Toll-like receptor signaling pathway was suppressed by chERV3 at both time points. We hypothesized that chERV3 can influence the activation of the innate immune pathway by blocking the Toll-like receptor signaling pathway to achieve immune evasion.

Prolactin (PRL) and growth hormone (GH) exhibit important roles in the immune system maintenance. In poultry, PRL mainly plays its roles in nesting, hatching, and reproduction, while GH is primarily responding to body weight, fat formation and feed conversion. In this review, we attempt to provide a critical overview of the relationship between PRL and GH, PRLR and GHR, and the immune response of poultry. We also propose a hypothesis that PRL, GH and their receptors might be used by viruses as viral receptors. This may provide new insights into the pathogenesis of viral infection and host immune response.

为探讨发酵桂闽引象草替代部分日粮对鸡肠道菌群的影响,试验选定30日龄的东兰乌鸡4羽,随机分成4组,每组1羽.使用发酵桂闽引象草分别替代5％(1组)、10％(2组)、15％(3组)及0％(K组)的日粮;以1、2、3组为试验组,K组为对照组,进行饲养试验.采集鸡大肠内容物,对其细菌16S rDNA扩增子V3～V4区进行二代高通量测序,分析菌群的物种组成及相对丰度差异.结果表明:Chao1指数,2组(813.500)>3组(782.892)>1组(765.444)>K组(751.243);Shannon指数,K组(7.386)>2组(7.327)>3组(7.098)>1组(6.968).从chao1指数来看,物种丰富度最高的是2组,最低的是K组;三个试验组的物种丰富度均高于对照组.从Shannon指数来看,对照组的菌群多样性高于试验组;三个试验组的菌群多样性以2组最高,以1组最低.拟杆菌门和厚壁菌门在1、2、3、K组的相对丰度分别为43.59％、55.33％、56.84％、56.01％和49.89％、40.32％、38.79％、39.95％,在各组中占比分别为93.48％、95.65％、95.63％、95.96％,是四组中的优势门,试验组和对照组中的相对丰度差异不明显.变形菌门在1、2、3组中的相对丰度(4.08％、1.41％、2.05％)高于对照组(0.97％),分别为对照组的4.2、1.45、2.11倍.互养菌门在1、2、3组中的相对丰度(0.72％、0.9％、0.49％)高于对照组(0.32％),分别为对照组的2.25、2.81、1.53倍.相对丰度前10位的属隶属于两个门(拟杆菌门和厚壁菌门).多形杆状菌属在各组中的相对丰度分别为28.4％、29.4％、31.84％、28.23％,是四组中的优势属;其相对丰度在试验组和对照组中差异不明显.瘤胃球菌属和巨单胞菌属在1、2、3组中的相对丰度(8.03％、5.21％、3.97％和5.44％、2.05％、2.06％)高于对照组(2.44％和0.15％),分别是对照组的3.29、2.19、2.20倍和36.26、13.66、13.73倍.用发酵桂闽引象草替代部分日粮,鸡肠道菌群丰富度增高,多样性降低,对鸡肠道优势菌影响不明显,最主要的影响是变形菌门、互养菌门的数量增多及厚壁菌门中的瘤胃球菌属、巨单胞菌属的数量增多.

The birth weight of chickens does not significantly affect the weight at slaughter, while the different growth rate after birth was one of the important reasons for the difference in slaughter weight. Also, the increase in chickens' postnatal skeletal muscle weight is the main cause of the slaughter weight gain, but which genes are involved in this biological process is still unclear. In this study, by integrating four transcriptome datasets containing chicken muscles at different developmental times or different chicken tissues in public databases, a total of nine candidate genes that may be related to postnatal muscle development in chickens were obtained, including RPL3L, FBP2, ASB4, ASB15, CKMT2, PGAM1, YIPF7, PFKM, and LDHA. One of these candidate genes is RPL3L, whose 42 bp insertion/deletion (indel) mutation significantly correlated with multiple carcass traits in the F2 resource population from Xinghua chickens crossing with White Recessive Rock (WRR) chickens, including live weight, carcass weight, half eviscerated weight, eviscerated weight, breast meat weight, wing weight, leg muscle shear force, and breast muscle shear force. Also, there was a very significant difference between different genotypes of the RPL3L 42 bp indel mutation in these trains. Further experiments showed that RPL3L was highly expressed in chicken skeletal muscle, and its overexpression could promote the proliferation and inhibit the differentiation of chicken myoblasts by regulating ASB4 and ASB15 expression. Our findings demonstrated that the RPL3L 42 bp indel may be one of the molecular markers of chicken weight-related traits.

Avian leukosis (AL) is a general term for a variety of neoplastic diseases in avian caused by avian leukosis virus (ALV). No vaccine or drug is currently available for the disease. Therefore, the disease can result in severe economic losses in poultry flocks. Increasing the resistance of poultry to ALV may be one effective strategy. In this review, we provide an overview of the roles of genes associated with ALV infection in the poultry genome, including endogenous retroviruses, virus receptors, interferon-stimulated genes, and other immune-related genes. Furthermore, some methods and techniques that can improve ALV resistance in poultry are discussed. The objectives are willing to provide some valuable references for disease resistance breeding in poultry.

试验旨在探究多个地方品种快慢羽鸡的内源性病毒基因21(ev21)以及SPEF2基因与PRLR基因的部分重复序列(JS序列)分布对羽速基因(Kk)表型的影响.采用PCR扩增、HaeⅢ限制性内切酶酶切的方法检测不同地方品种快慢羽鸡性染色体上OR区域(ev21占据片段)、UR区域(URa、URb(ev21未占据片段))以及JS序列分布情况.结果表明:国内的一些地方品种部分慢羽鸡个体OR区域ev21基因缺失以及部分快羽鸡的URb区域存在ev21基因插入;可通过JS序列扩增对快慢羽表型进行准确鉴定.研究结果显示JS序列可作为快慢羽鉴定候选基因,该方法可广泛应用于国内快慢羽鸡种的鉴定.

为了研究使用不同益生菌制剂对东兰乌鸡的生长性能、免疫功能和血清生化指标的影响,选用1日龄东兰乌鸡360只,随机分成4组,每组3个重复,每个重复30只.对照组只喂养基础日粮(不含抗生素),试验组在基础日粮中按产品说明书添加益生菌制剂,拌匀后饲喂.结果表明:益生菌B组的耗料量比对照组低9.13％,但增重提高1.15％;添加益生菌后能够提高脾脏指数和胸腺指数,并且能够提高机体的免疫抗体水平,降低血清中的超氧化物岐化酶、碱性磷酸酶、总胆固醇含量.结论:在基础日粮中添加益生菌,能够在一定程度上提高东兰乌鸡的生长性能、免疫器官指数和免疫抗体水平,并且能够影响血清中一些生化指标.

J subgroup avian leukosis virus (ALV-J) infection causes serious immunosuppression problems, leading to hematopoietic malignancy tumors in chicken. It has been demonstrated that interferon-stimulated genes (ISGs) could limit ALV-J replication; nevertheless, the underlying mechanisms remain obscure. Here, we demonstrate that Long-chain Acyl-CoA synthetase 1 (ACSL1) is an interferon (IFN)-stimulated gene that specifically restricts the replication of ALV-J due to the higher IFN-I production. More importantly, ACSL1 induces primary monocyte-derived macrophages (MDMs) to pro-inflammatory phenotypic states during ALV-J infection, and ACSL1 mediates apoptosis through the PI3K/Akt signaling pathway in ALV-J-infected primary monocyte-derived macrophages (MDMs). Overall, these results provide evidence that ACSL1 contributes to the antiviral response against ALV-J.

Based on the RNA-seq data of chicken spleen tissues infected with J subgroup avian leukosis virus (ALV-J), we found that prolactin (PRL) gene was one of differentially expressed gene. We measured ALV-J viremia and PRL levels in the plasma of two groups of ALV-J-infected adult chickens. Furthermore, recombinant chicken PRL (cPRL) was used to assess how cPRL affects ALV-J virus replication both in vivo and in vitro. The results showed that PRL levels in the plasma of adult chickens infected with ALV-J were lower than those of uninfected chickens, and that the difference was more significant in the avian leukemia pathological apparent changes. Notably, the fluctuations in PRL levels might influence the disappearance of ALV-J viremia in chickens. The in vitro results showed that preincubating DF-1 cells with cPRL before ALV-J infection elicited the best antiviral effects. Moreover, these effects were not dose-dependent. in vivo, injection of cPRL into ALV-J-infected chicks could reduce the levels of viremia at the 14 days post infection (dpi). Additionally, the expression of the interferon-stimulated genes oligoadenylate synthetase-like (OSAL) and vasoactive intestinal peptide (VIP) increased, and that of the proinflammatory cytokine-encoding TNTα, IL-1β, and IL-6 genes decreased in the spleens of ALV-J-infected chicks injected with cPRL, leading to inhibition of viral replication at the 7 dpi. Collectively, our data demonstrated that PRL plays an important antiviral role in the immune response to ALV-J infection. This is the first report of the relationship between ALV-J infection and PRL. It is of great significance for the prevention and control of ALV-J.

The aim of this study was to better understand the sequence characteristics and immune responses in avian leukosis virus subgroup J (ALV-J) infected yellow chicken flocks in South China. We isolated four strains of ALV-J virus from these flocks, which were then identified by several methods, including subtype-specific polymerase chain reaction (PCR), enzyme-linked immunosorbent assay (ELISA), and immunofluorescence assay (IFA). All four viruses were sequenced for their complete genomes and named GD19GZ01, GD19GZ02, GD19GZ03, and GD19GZ04. In comparison with the reference sequence, the homology analysis showed that the gag and pol genes were relatively conserved, whereas env contained much variation. Both GD19GZ01 and GD19GZ02 almost entirely lacked the rTM region and E element, while the latter was retained in GD19GZ03 and GD19GZ04. Moreover, the virus replication levels in GD19GZ03 and GD19GZ04were much higher than those in GD19GZ01 and GD19GZ02. And three virus recombination events in GD19GZ01 and GD19GZ02 were revealed by the results of PDR5 and SimPlot software analysis. Additionally, we found that some interferon-stimulating genes (CH25H, MX, PKR, OAS, and ZAP) and inflammatory mediators (IL-4, IL-6, IL-10, IL-12, 1L-18, and TNF-α) were significantly upregulated in the immune system organs of clinical chickens. Taken together, these findings clarify and reveal the sequence characteristics and trends in the variation of ALV-J infection in yellow chicken flocks of South China.

试验旨在分析GSTA2基因的SNPs和杏花鸡与隐性白洛克鸡F2群体的肉质、生长和屠体性状的相关性.试验采用Sanger测序从359个杏花鸡与隐性白洛克鸡F2群体的基因组序列中筛选到4个GSTA2基因的SNPs,均位于5'UTR区域.利用SPSS 22.0软件对4个SNPs与杏花鸡和隐性白洛克鸡F2群体的经济性状进行了关联分析.结果显示:4个SNPs与杏花鸡和隐性白洛克鸡F2群体的体重、胫长、肤色等性状显著相关.对4个SNPs进行单倍型分析发现SNP1、SNP3、SNP4组成的单倍型AGAGTT与鸡的翅重有显著相关性,SNP2、SNP4组成的单倍型GGTT与鸡的胫长有显著相关性.结果表明GSTA2基因的SNPs显著影响鸡的经济性状,可以作为鸡经济性状选育的候选分子标记.

Cytokine-inducible Srchomology2 (SH2)-containing protein (CIS) belongs to the suppressors of cytokine signaling (SOCS) protein family function as a negative feedback loop inhibiting cytokine signal transduction. J subgroup avian leukosis virus (ALV-J), a commonly-seen avian virus with a feature of immunosuppression, poses an unmeasurable threat to the poultry industry across the world. However, commercial medicines or vaccines are still no available for this virus. This study aims to evaluate the potential effect of chicken CIS in antiviral response and its role on ALV-J replication. The results showed that ALV-J strain SCAU-HN06 infection induced CIS expression in DF-1 cells, which was derived from chicken embryo free of endogenous avian sarcoma-leukosis virus (ASLV) like sequences. By overexpressing CIS, the expression of chicken type I interferon (IFN-I) and interferon-stimulated genes (ISGs; PKR, ZAP, CH25H, CCL4, IFIT5, and ISG12) were both suppressed. Meanwhile, data showed that CIS overexpression also increased viral yield. Interestingly, knockdown of CIS enhanced induction of IFN-I and ISGs and inhibited viral replication. Collectively, we proved that modulation of CIS expression not only affected SCAU-HN06 replication in vitro but also altered the expression of IFN-I and ISGs that act as an essential part of antiviral innate immune system. Our data provide a potential target for developing antiviral agents for ALV-J.