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Avian leukosis virus usurps the cellular SERBP1 protein to enhance its transcription and promote productive infections in avian cells

文献类型： 外文期刊

作者： Cui, Ning 1 ; Han, Xiaoxia 1 ; Yang, Xiao 1 ; Zhao, Xiaoran 1 ; Huang, Qinghua 1 ; Xu, Chuantian 1 ; Su, Shuai 4 ;

作者机构： 1.Shandong Acad Agr Sci, Shandong Key Lab Anim Dis Control & Breeding, Jinan, Peoples R China

2.Shandong Acad Agr Sci, Inst Anim Sci & Vet Med, Jinan, Peoples R China

3.Key Lab Livestock & Poultry Multiom MARA, Jinan, Peoples R China

4.Shandong Agr Univ, Shandong Prov Key Lab Anim Biotechnol & Dis Contro, Tai An, Peoples R China

5.Shandong Agr Univ, Coll Vet Med, Tai An, Peoples R China

6.Shandong Normal Univ, Coll Life Sci, Jinan, Peoples R China

关键词： avian leukosis virus; U3; mutation; SERBP1; interaction

期刊名称：POULTRY SCIENCE （ 影响因子：4.4； 五年影响因子：4.4 ）

ISSN： 0032-5791

年卷期： 2024 年 103 卷 6 期

页码：

收录情况： SCI

摘要： Avian leukosis virus subgroup K (ALV-K) is composed of newly emerging isolates, which cluster separately from the well -characterized subgroups A, B, C, D, E, and J in sequence analysis, and exhibits a speci fic host range and a unique pattern of superinfection interference. Avian leukosis virus subgroup K replicate more slowly in avian cells than other ALV strains, leading to escaped detection during ALV eradication, but the underlying mechanism are largely unknown. In our previous study, we have reported that JS11C1 and most of other suspected ALV-K strains possessed unique mutations in the U3 region. Here, we selected 5 mutations in some important transcriptional regulation elements to explore the possible factor contributing for the lower activity of LTR, including CATG mutation in the CAAT box, 21 nt deletion in the CAAT box, A -G and A -T mutations in the CArG boxes, 11 nt insertion in the PRE boxes, and C -T mutation in the TATA box. On the basis of infectious clone of JS11C1, we demonstrated that the 11 nt fragment in the PRE boxes was associated with the transcription activity of LTR, the enhancer ability of U3, and the replication capacity of the virus. Notably, we determined the differential U3 -protein interaction profile of ALVs and found that the 11 nt fragment speci fi- cally binds to cellular SERPINE1 mRNA binding protein 1 (SERBP1) to increase the LTR activity and enhance virus replication. Collectively, these findings reveal that a 11 nt fragment in the U3 gene contributed to its binding ability to the cellular SERBP1 to enhance its transcription and the infectious virus productions in avian cells. This study highlighted the vital role of host factor in retrovirus replication and thus provides a new perspective to elucidate the interaction between retrovirus and its host and a molecular basis to develop ef fi- cient strategies against retroviruses.

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