College of Veterinary Medicine, Shandong Agricultural University, No.61 Daizong Street, Tai'an 271018, China.
Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Shandong Agricultural University, No.61 Daizong Street, Tai'an 271018, China.
Pol J Vet Sci. 2021 Sep;24(3):439-443. doi: 10.24425/pjvs.2021.138736.
Reticuloendotheliosis virus (REV) is an avian oncogenic retrovirus that causes atrophy of immune organs, such as the spleen, thymus, and bursa of Fabricius, leading to severe immunosuppression. However, there is limited information describing the genes or microRNAs (miRNAs) that play a role in replicating REV-spleen necrosis virus (SNV). Our previous miRNA and RNA sequencing data showed that the expression of gga-miR-222b-5p was significantly upregulated in REV-SNV-infected chicken spleens of 7, 14, and 21 dpi compared to non-infected chicken spleens, but mitogen-activated protein kinase 10 (MAPK10), which is related to innate immunity, had the opposite expression pattern. To understand chicken cellular miRNA function in the virus-host interactions during REV infection, we used quantitative reverse transcription PCR (qRT-PCR) to determine whether the expression of gga-miR-222b-5p and MAPK10 in the spleen of specific-pathogen-free chickens at 28, 35, and 42 dpi was consistent with the first 3 time points, and dual-luciferase reporter assay was used to determine the targeting relationship between gga-miR-222b-5p and MAPK10. Results show that MAPK10 was downregulated at all 3 time points; however, significant difference (p⟨0.01) was noted only at 35 dpi. Moreover, the expression of gga-miR-222b-5p was upregulated; however, significant difference (p⟨0.01) was observed only at 28 and 35 dpi. A dual-luciferase reporter assay showed that MAPK10 is a direct target of gga-miR-222b-5p. This study suggests that gga-miR-222b-5p may target MAPK10 to promote the REV-SNV-induced tumorigenesis via the RLRs signaling pathway.
网状内皮组织增生症病毒 (REV) 是一种致禽类肿瘤的反转录病毒，可导致免疫器官（如脾脏、胸腺和法氏囊）萎缩，从而导致严重的免疫抑制。然而，关于在 REV-脾坏死病毒 (SNV) 复制过程中发挥作用的基因或 microRNA（miRNA）的信息有限。我们之前的 miRNA 和 RNA 测序数据表明，与非感染鸡脾脏相比，在 REV-SNV 感染鸡脾脏的 7、14 和 21 dpi 时，gga-miR-222b-5p 的表达显著上调，但与先天免疫有关的丝裂原激活蛋白激酶 10（MAPK10）的表达模式相反。为了了解鸡细胞 miRNA 在 REV 感染过程中病毒-宿主相互作用中的功能，我们使用定量逆转录 PCR（qRT-PCR）来确定在无特定病原体鸡的 28、35 和 42 dpi 时，脾脏中 gga-miR-222b-5p 和 MAPK10 的表达是否与前 3 个时间点一致，并使用双荧光素酶报告基因检测来确定 gga-miR-222b-5p 和 MAPK10 之间的靶向关系。结果表明，在所有 3 个时间点 MAPK10 的表达均下调；然而，仅在 35 dpi 时观察到显著差异（p ⟨0.01）。此外，gga-miR-222b-5p 的表达上调；然而，仅在 28 和 35 dpi 时观察到显著差异（p ⟨0.01）。双荧光素酶报告基因检测表明 MAPK10 是 gga-miR-222b-5p 的直接靶标。这项研究表明，gga-miR-222b-5p 可能通过 RLRs 信号通路靶向 MAPK10 以促进 REV-SNV 诱导的肿瘤发生。
