Institute of Medical Biology, Chinese Academy of Medical Science and Peking Union Medical College, Yunnan Key Laboratory of Vaccine Research and Development on Severe Infectious Disease, Kunming, China.
J Med Virol. 2016 Sep;88(9):1497-510. doi: 10.1002/jmv.24500. Epub 2016 Mar 11.
Rotavirus infection is an important cause of acute gastroenteritis in children, but the interaction between rotavirus and host cells is not completely understood. We isolated a wildtype (wt) rotavirus strain, ZTR-68(P [8] G1), which is derived from an infant with diarrhea in southwest China in 2010. In this study, we investigated host cellular miRNA expression profiles changes in response to ZTR-68 in early stage of infection to investigate the role of miRNAs upon rotavirus infection. Differentially expressed miRNAs were identified by deep sequencing and qRT-PCR and the function of their targets predicted by Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway annotation. A total of 36 candidate miRNAs were identified. Comparative analysis indicated that 29 miRNAs were significantly down-regulated and 7 were up-regulated after infection. The data were provided contrasting the types of microRNAs in two different permissive cell lines (HT29 and MA104). The target assays results showed that mml-miR-7 and mml-miR-125a are involved in anti-rotavirus and virus-host interaction in host cells. These results offer clues for identifying potential candidates in vector-based antiviral strategies. J. Med. Virol. 88:1497-1510, 2016. © 2016 Wiley Periodicals, Inc.
轮状病毒感染是儿童急性肠胃炎的一个重要病因，但轮状病毒与宿主细胞的相互作用还不完全清楚。我们分离到一株野生型（wt）轮状病毒株，ZTR-68（P [8] G1），它来源于 2010 年中国西南部一名腹泻婴儿。在这项研究中，我们研究了宿主细胞在感染早期对 ZTR-68 的 miRNA 表达谱变化，以研究 miRNA 在轮状病毒感染中的作用。通过深度测序和 qRT-PCR 鉴定差异表达的 miRNA，并通过基因本体论（GO）功能和京都基因与基因组百科全书（KEGG）通路注释预测其靶标的功能。共鉴定出 36 个候选 miRNA。比较分析表明，感染后有 29 个 miRNA 显著下调，7 个上调。该数据与两种不同允许的细胞系（HT29 和 MA104）中不同类型的 microRNAs 进行了对比分析。靶标分析结果表明，mml-miR-7 和 mml-miR-125a 参与宿主细胞中的抗轮状病毒和病毒-宿主相互作用。这些结果为基于载体的抗病毒策略中的潜在候选物提供了线索。J. Med. Virol. 88:1497-1510, 2016. © 2016 Wiley Periodicals, Inc.
