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DOCK11 和 DENND2A 在宿主细胞中维持乙型肝炎病毒方面发挥着关键作用。

DOCK11 and DENND2A play pivotal roles in the maintenance of hepatitis B virus in host cells.

机构信息

Department of Molecular Pathophysiology, Institute of Advanced Medicine, Wakayama Medical University, Wakayama, Japan.

Japan Science and Technology Agency, CREST, Tokyo, Japan.

出版信息

PLoS One. 2021 Feb 4;16(2):e0246313. doi: 10.1371/journal.pone.0246313. eCollection 2021.

Abstract

Human hepatitis B virus (HBV) infection remains a serious health problem worldwide. However, the mechanism for the maintenance of HBV in a latent state within host cells remains unclear. Here, using single-cell RNA sequencing analysis, we identified four genes linked to the maintenance of HBV in a liver cell line expressing HBV RNA at a low frequency. These genes included DOCK11 and DENND2A, which encode small GTPase regulators. In primary human hepatocytes infected with HBV, knockdown of these two genes decreased the amount of both HBV DNA and covalently closed circular DNA to below the limit of detection. Our findings reveal a role for DOCK11 and DENND2A in the maintenance of HBV.

摘要

乙型肝炎病毒(HBV)感染仍然是全球范围内的一个严重健康问题。然而,HBV 在宿主细胞内处于潜伏状态的维持机制仍不清楚。在这里,我们使用单细胞 RNA 测序分析,鉴定出四个与在低频率表达 HBV RNA 的肝细胞系中维持 HBV 相关的基因。这些基因包括编码小 GTPase 调节剂的 DOCK11 和 DENND2A。在感染 HBV 的原代人肝细胞中,这两个基因的敲低使 HBV DNA 和共价闭合环状 DNA 的量均降至检测限以下。我们的研究结果揭示了 DOCK11 和 DENND2A 在维持 HBV 中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/907a/7861363/38683d955946/pone.0246313.g001.jpg

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