Zoladek Jim, Cannac Marion, Seite Maël, Davies Emma, Quellec Jordan, Barthelemy Jonathan, Gorna Kamila, Desgraupes Sophie, Bribes Ines, Salinas Sara, Coulpier Muriel, Arhel Nathalie J, Palmarini Massimo, Simonin Yannick, Wilson Sam J, Nisole Sébastien
Viral Trafficking, Restriction and Innate Signaling, CNRS UMR 9004, Institut de Recherche en Infectiologie de Montpellier, Université de Montpellier, Montpellier 34090, France.
Pathogenesis and Control of Chronic and Emerging Infections, INSERM, Établissement français du sang (EFS), Université de Montpellier, Montpellier 34394, France.
Proc Natl Acad Sci U S A. 2025 Mar 25;122(12):e2502064122. doi: 10.1073/pnas.2502064122. Epub 2025 Mar 20.
West Nile virus (WNV) and Usutu virus (USUV) are closely related mosquito-borne neurotropic flaviviruses that share common transmission cycle and can infect humans. However, while human infections by WNV are widespread, infections by USUV are comparatively less frequent, less severe, and currently limited to Africa and Europe. To identify human host factors that contribute to the pathogenic signatures of these two flaviviruses, we carried out an arrayed expression screen of over 1,300 interferon-stimulated genes (ISGs). Several ISGs known to target flaviviruses, including IFI6, SHFL, and RTP4 were among the strongest hits. Interestingly, we also found MITD1, an ISG with no previously reported antiviral activity, among the strongest hits. We demonstrated that the antiviral activity of MITD1 was not limited to USUV and WNV, since it also inhibited Zika and dengue virus replication. We found MITD1 to interfere with viral RNA replication by sequestering specific endosomal sorting complexes required for transport-III (ESCRT-III) proteins involved in the formation of viral replication factories. MITD1 expression was not increased by type I interferon (IFN-I) in most human cells and mouse tissues that we examined, although WNV and USUV replication was strongly inhibited by IFN-I. Strikingly, MITD1 was induced in the brain of USUV-infected mice and importantly, in human monocyte-derived microglia. Using human microglial-like cells, we confirmed that MITD1 is an essential mediator of the anti-flavivirus activity of IFN-I in these cells. We conclude that MITD1 plays a key role in the cellular defenses against neurotropic flaviviruses.
西尼罗河病毒(WNV)和乌苏图病毒(USUV)是密切相关的蚊媒嗜神经性黄病毒,它们具有共同的传播周期,且都能感染人类。然而,虽然WNV引起的人类感染很普遍,但USUV引起的感染相对较少见,症状也较轻,目前仅限于非洲和欧洲。为了确定促成这两种黄病毒致病特征的人类宿主因子,我们对1300多个干扰素刺激基因(ISG)进行了阵列表达筛选。几个已知靶向黄病毒的ISG,包括IFI6、SHFL和RTP4,是筛选结果中最强的命中基因。有趣的是,我们还在最强的命中基因中发现了MITD1,这是一个以前没有报道过抗病毒活性的ISG。我们证明,MITD1的抗病毒活性不仅限于USUV和WNV,因为它也抑制寨卡病毒和登革病毒的复制。我们发现MITD1通过隔离参与病毒复制工厂形成的特定转运所需的内体分选复合物III(ESCRT-III)蛋白来干扰病毒RNA复制。在我们检测的大多数人类细胞和小鼠组织中,I型干扰素(IFN-I)不会增加MITD1的表达,尽管WNV和USUV的复制受到IFN-I的强烈抑制。引人注目的是,MITD1在感染USUV的小鼠大脑中被诱导,重要的是,在人单核细胞衍生的小胶质细胞中也被诱导。使用人小胶质细胞样细胞,我们证实MITD1是IFN-I在这些细胞中抗黄病毒活性的重要介质。我们得出结论,MITD1在细胞对抗嗜神经性黄病毒的防御中起关键作用。