Sakai Madoka, Masuda Yoshie, Tarumoto Yusuke, Aihara Naoyuki, Tsunoda Yugo, Iwata Michiko, Kamiya Yumiko, Komorizono Ryo, Noda Takeshi, Yusa Kosuke, Tomonaga Keizo, Makino Akiko
Laboratory of RNA Viruses, Department of Virus Research, Institute for Life and Medical Sciences, Kyoto University, Kyoto 6068507, Japan.
Laboratory of Stem Cell Genetics, Department of Biosystems Science, Institute for Life and Medical Sciences, Kyoto University, Kyoto 6068507, Japan.
iScience. 2024 Jul 8;27(8):110475. doi: 10.1016/j.isci.2024.110475. eCollection 2024 Aug 16.
Although many host factors important for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection have been reported, the mechanisms by which the virus interacts with host cells remain elusive. Here, we identified tripartite motif containing (TRIM) 28, TRIM33, euchromatic histone lysine methyltransferase (EHMT) 1, and EHMT2 as proviral factors involved in SARS-CoV-2 infection by CRISPR-Cas9 screening. Our result suggested that TRIM28 may play a role in viral particle formation and that TRIM33, EHMT1, and EHMT2 may be involved in viral transcription and replication. UNC0642, a compound that specifically inhibits the methyltransferase activity of EHMT1/2, strikingly suppressed SARS-CoV-2 growth in cultured cells and reduced disease severity in a hamster infection model. This study suggests that EHMT1/2 may be a therapeutic target for SARS-CoV-2 infection.
尽管已经报道了许多对严重急性呼吸综合征冠状病毒2(SARS-CoV-2)感染至关重要的宿主因素,但病毒与宿主细胞相互作用的机制仍不清楚。在这里,我们通过CRISPR-Cas9筛选确定了含三联基序(TRIM)28、TRIM33、常染色质组蛋白赖氨酸甲基转移酶(EHMT)1和EHMT2作为参与SARS-CoV-2感染的病毒促进因子。我们的结果表明,TRIM28可能在病毒颗粒形成中起作用,而TRIM33、EHMT1和EHMT2可能参与病毒转录和复制。UNC0642是一种特异性抑制EHMT1/2甲基转移酶活性的化合物,它显著抑制了培养细胞中SARS-CoV-2的生长,并降低了仓鼠感染模型中的疾病严重程度。这项研究表明,EHMT1/2可能是SARS-CoV-2感染的治疗靶点。