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兔乙型肝炎病毒慢性感染中高度表达的新型枢纽基因特征:生物信息学和实验分析。

Characterization of highly expressed novel hub genes in hepatitis E virus chronicity in rabbits: a bioinformatics and experimental analysis.

机构信息

Division I of In Vitro Diagnostics for Infectious Diseases, Institute for In Vitro Diagnostics Control, National Institutes for Food and Drug Control, 2 Tiantanxili Rd, Dongcheng District, 100050, Beijing, China.

First Clinical Medical College, Shanxi Medical University, Taiyuan, China.

出版信息

BMC Vet Res. 2022 Jun 23;18(1):239. doi: 10.1186/s12917-022-03337-x.

DOI:10.1186/s12917-022-03337-x
PMID:35739587
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9219159/
Abstract

BACKGROUND

Hepatitis E virus (HEV), which is the leading cause of acute viral hepatitis worldwide, usually causes self-limited infections in common individuals. However, it can lead to chronic infection in immunocompromised individuals and its mechanisms remain unclear. Rabbits are the natural host of HEV, and chronic HEV infections have been observed in rabbits. Therefore, we aimed to investigate potential key genes in HEV chronicity process in rabbits. In this study, both bioinformatics and experimental analysis were performed to deepen the understanding of hub genes in HEV chronic infection in rabbits.

RESULTS

Ninety-four candidate differentially expressed genes (DEGs) and the pathways they enriched were identified to be related with HEV chronicity. A total of 10 hub genes were found by protein-protein interaction (PPI) network construction. Rabbits of group P (n = 4) which showed symptoms of chronic HEV infection were selected to be compared with HEV negative rabbits (group N, n = 6). By detecting the identified hub genes in groups P and N by real-time PCR, we found that the expressions of MX1, OAS2 and IFI44 were significantly higher in group P (P < 0.05).

CONCLUSIONS

In this work, we presented that MX1, OAS2 and IFI44 were significantly upregulated in HEV chronic infected rabbits, indicating that they may be involved in the pathogenesis of HEV chronicity.

摘要

背景

戊型肝炎病毒(HEV)是全球急性病毒性肝炎的主要病因,通常在普通个体中引起自限性感染。然而,它可在免疫功能低下的个体中导致慢性感染,其机制尚不清楚。兔是 HEV 的天然宿主,并且已在兔中观察到慢性 HEV 感染。因此,我们旨在研究兔 HEV 慢性感染过程中的潜在关键基因。在这项研究中,我们同时进行了生物信息学和实验分析,以加深对兔 HEV 慢性感染中关键基因的理解。

结果

鉴定出 94 个候选差异表达基因(DEGs)及其相关的途径,这些基因与 HEV 慢性性有关。通过构建蛋白质-蛋白质相互作用(PPI)网络,共发现 10 个枢纽基因。选择出现慢性 HEV 感染症状的 P 组(n=4)的兔子与 HEV 阴性兔子(N 组,n=6)进行比较。通过实时 PCR 检测 P 组和 N 组中鉴定出的枢纽基因,我们发现 P 组中 MX1、OAS2 和 IFI44 的表达明显升高(P<0.05)。

结论

在这项工作中,我们发现 MX1、OAS2 和 IFI44 在慢性 HEV 感染的兔子中明显上调,表明它们可能参与了 HEV 慢性性的发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0788/9219159/ab3a8c986d6b/12917_2022_3337_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0788/9219159/b08a3f6300f4/12917_2022_3337_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0788/9219159/f4387aa5b442/12917_2022_3337_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0788/9219159/3743defce26a/12917_2022_3337_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0788/9219159/d52b0d7161f3/12917_2022_3337_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0788/9219159/ab3a8c986d6b/12917_2022_3337_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0788/9219159/b08a3f6300f4/12917_2022_3337_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0788/9219159/f4387aa5b442/12917_2022_3337_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0788/9219159/3743defce26a/12917_2022_3337_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0788/9219159/d52b0d7161f3/12917_2022_3337_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0788/9219159/ab3a8c986d6b/12917_2022_3337_Fig5_HTML.jpg

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