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经来亨鸡雄性肝癌细胞适应的禽腺病毒4诱导的保护性免疫反应。

Protective immune response induced by Leghorn male hepatoma cell-adapted fowl adenovirus-4.

作者信息

Lee Rangyeon, Sung Haan Woo, Cheong Hee-Tae, Park Jeongho

机构信息

College of Veterinary Medicine, Kangwon National University, Chuncheon, Republic of Korea.

Institute of Veterinary Science, Kangwon National University, Chuncheon, Republic of Korea.

出版信息

Heliyon. 2024 Feb 1;10(3):e25366. doi: 10.1016/j.heliyon.2024.e25366. eCollection 2024 Feb 15.

DOI:10.1016/j.heliyon.2024.e25366
PMID:38356505
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10864904/
Abstract

Fowl adenovirus-4 (FAdV-4) is a highly contagious virus that causes acute and lethal hepatitis. It leads to substantial economic losses in the poultry industry. Among the structural proteins of FAdV-4, hexon and fiber2 are associated with immunopathogenesis. A frameshift mutation was generated in the fiber2 protein by seral passages in the Leghorn male hepatoma (LMH) cell line. Immunization using the attenuated virus (80 times passaged) before the virulent FAdV-4 challenge protected hosts from the infection and cleared the invading virus. In immunized animals, activated CD4 and CD8 T cell populations were larger during the FAdV-4 challenge. The change in the B cell population was similar. Myeloid cells were highly increased during FAdV-4 infection after the immunization, but the immunization inhibited the expansion in both liver and spleen. The functional gene expression for immune modulation was strongly associated with immune cell changes in the liver, however, this association was not strong in the spleen. The present findings imply that genetic modification by cellular adaptation regulates immune cell phenotype and function in the target organ. In addition, we suggest the attenuated virus as a protective strategy against the novel FAdV-4 strains.

摘要

禽腺病毒4型(FAdV-4)是一种高度传染性病毒,可引起急性致死性肝炎。它给家禽业造成了巨大的经济损失。在FAdV-4的结构蛋白中,六邻体和纤维2与免疫发病机制有关。通过在来航鸡雄性肝癌(LMH)细胞系中连续传代,纤维2蛋白中产生了一个移码突变。在强毒FAdV-4攻击前使用减毒病毒(传代80次)进行免疫可保护宿主免受感染并清除入侵病毒。在免疫动物中,FAdV-4攻击期间活化的CD4和CD8 T细胞群体更大。B细胞群体的变化类似。免疫后FAdV-4感染期间髓样细胞高度增加,但免疫抑制了肝脏和脾脏中的扩增。免疫调节的功能基因表达与肝脏中的免疫细胞变化密切相关,然而,这种关联在脾脏中并不强烈。目前的研究结果表明,通过细胞适应进行基因改造可调节靶器官中的免疫细胞表型和功能。此外,我们建议将减毒病毒作为针对新型FAdV-4毒株的一种保护策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c7d/10864904/492716dee27b/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c7d/10864904/13000e73b077/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c7d/10864904/8b8f7de34e7a/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c7d/10864904/c55a437bf04a/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c7d/10864904/3632ab04d633/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c7d/10864904/75a73c53efeb/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c7d/10864904/cceca97e9157/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c7d/10864904/492716dee27b/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c7d/10864904/13000e73b077/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c7d/10864904/8b8f7de34e7a/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c7d/10864904/c55a437bf04a/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c7d/10864904/3632ab04d633/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c7d/10864904/75a73c53efeb/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c7d/10864904/cceca97e9157/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c7d/10864904/492716dee27b/gr7.jpg

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