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感染 A 型和 C 型轮状病毒后猪回肠类器官的差异转录组反应。

Differential transcriptome response following infection of porcine ileal enteroids with species A and C rotaviruses.

机构信息

Center for Food Animal Health Research Program, Department of Veterinary Preventive Medicine, College of Veterinary Medicine, Department of Animal Sciences, College of Food Agricultural and Environmental Sciences, The Ohio State University, Wooster, OH, 44677, USA.

出版信息

Virol J. 2023 Oct 17;20(1):238. doi: 10.1186/s12985-023-02207-8.

DOI:10.1186/s12985-023-02207-8
PMID:37848925
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10580564/
Abstract

BACKGROUND

Rotavirus C (RVC) is the major causative agent of acute gastroenteritis in suckling piglets, while most RVAs mostly affect weaned animals. Besides, while most RVA strains can be propagated in MA-104 and other continuous cell lines, attempts to isolate and culture RVC strains remain largely unsuccessful. The host factors associated with these unique RVC characteristics remain unknown.

METHODS

In this study, we have comparatively evaluated transcriptome responses of porcine ileal enteroids infected with RVC G1P[1] and two RVA strains (G9P[13] and G5P[7]) with a focus on innate immunity and virus-host receptor interactions.

RESULTS

The analysis of differentially expressed genes regulating antiviral immune response indicated that in contrast to RVA, RVC infection resulted in robust upregulation of expression of the genes encoding pattern recognition receptors including RIG1-like receptors and melanoma differentiation-associated gene-5. RVC infection was associated with a prominent upregulation of the most of glycosyltransferase-encoding genes except for the sialyltransferase-encoding genes which were downregulated similar to the effects observed for G9P[13].

CONCLUSIONS

Our results provide novel data highlighting the unique aspects of the RVC-associated host cellular signalling and suggest that increased upregulation of the key antiviral factors maybe one of the mechanisms responsible for RVC age-specific characteristics and its inability to replicate in most cell cultures.

摘要

背景

轮状病毒 C(RVC)是引起仔猪急性胃肠炎的主要病原体,而大多数 RVAs 主要影响断奶动物。此外,虽然大多数 RVA 株可以在 MA-104 和其他连续细胞系中繁殖,但分离和培养 RVC 株的尝试仍然基本不成功。与这些独特的 RVC 特征相关的宿主因素尚不清楚。

方法

在这项研究中,我们比较评估了感染 RVC G1P[1]和两种 RVA 株(G9P[13]和 G5P[7])的猪回肠肠上皮细胞的转录组反应,重点关注先天免疫和病毒-宿主受体相互作用。

结果

抗病毒免疫反应调节差异表达基因的分析表明,与 RVA 相反,RVC 感染导致包括 RIG1 样受体和黑色素瘤分化相关基因 5 在内的模式识别受体的基因表达强烈上调。RVC 感染与大多数糖基转移酶编码基因的显著上调有关,但除了唾液酸转移酶编码基因下调外,其作用类似于 G9P[13]观察到的作用。

结论

我们的研究结果提供了新的数据,突出了 RVC 相关宿主细胞信号的独特方面,并表明关键抗病毒因子的上调增加可能是 RVC 年龄特异性特征及其在大多数细胞培养物中无法复制的原因之一。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c585/10580564/4e52047912a4/12985_2023_2207_Fig10_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c585/10580564/7c3a907bafdf/12985_2023_2207_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c585/10580564/0acc6a3cb989/12985_2023_2207_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c585/10580564/4e52047912a4/12985_2023_2207_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c585/10580564/511b1321f287/12985_2023_2207_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c585/10580564/68f5e6b63a7c/12985_2023_2207_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c585/10580564/dbf6bd8087c0/12985_2023_2207_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c585/10580564/ba3cf41fafee/12985_2023_2207_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c585/10580564/546aafb02cab/12985_2023_2207_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c585/10580564/d8849c805c3e/12985_2023_2207_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c585/10580564/6f4e0234e5ef/12985_2023_2207_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c585/10580564/7c3a907bafdf/12985_2023_2207_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c585/10580564/0acc6a3cb989/12985_2023_2207_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c585/10580564/4e52047912a4/12985_2023_2207_Fig10_HTML.jpg

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