文献类型： 外文期刊
作者： Feng, Min 1 ; Xie, Tingting 1 ; Li, Yuanfang 1 ; Zhang, Nan 1 ; Lu, Qiuyuan 1 ; Zhou, Yaohong 1 ; Shi, Meiqing 3 ; Sun, J 1 ;
作者机构： 1.South China Agr Univ, Guangdong Prov Key Lab Agroanim Genom & Mol Breed, Coll Anim Sci, Guangzhou, Guangdong, Peoples R China
2.Minist Agr, Key Lab Chicken Genet Breeding & Reprod, Guangzhou, Guangdong, Peoples R China
3.Univ Maryland, Virginia Maryland Reg Coll Vet Med, Div Immunol, College Pk, MD 20742 USA
期刊名称：VETERINARY RESEARCH （ 影响因子：3.683； 五年影响因子：4.106 ）
ISSN： 0928-4249
年卷期： 2019 年 50 卷
页码：
收录情况： SCI
摘要： Avian leukosis virus subgroup J (ALV-J) infection can cause tumors and immunosuppression in infected chickens. Macrophages play a central role in host defense against invading pathogens. In this study, we discovered an interesting phenomenon: ALV-J replication is weakened from 3hours post-infection (hpi) to 36hpi, which was verified using Western blotting and RT-PCR. To further investigate the interaction between ALV-J and macrophages, transcriptome analysis was performed to analyze the host genes' function in chicken primary monocyte-derived macrophages (MDM). Compared to the uninfected control, 624 up-regulated differentially expressed genes (DEG) and 341 down-regulated DEG at 3 hpi, and 174 up-regulated DEG and 87 down-regulated DEG at 36 hpi were identified in chicken MDM, respectively. ALV-J infection induced strong innate immune responses in chicken MDM at 3 hpi, instead of 36 hpi, according to the analysis results of Gene Ontology and KEGG pathway. Importantly, the host factors, such as up-regulated MIP-3, IL-1, iNOS, K60, IRG1, CH25H, NFKBIZ, lysozyme and OASL were involved in the host defense response during the course of ALV-J infection. On the contrary, up-regulated EX-FABP, IL4I1, COX-2, NFKBIA, TNFAIP3 and the Jak STAT pathway inhibitors including CISH, SOCS1 and SOCS3 are beneficial to ALV-J survival in chicken macrophages. We speculated that ALV-J tropism for macrophages helps to establish a latent infection in chicken MDM from 6 to 36 hpi. The present study provides a comprehensive view of the interactions between macrophages and ALV-J. It suggests the mechanisms of defense of chicken macrophages against ALV-J invasion and how ALV-J escape the host innate immune responses.
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