Flinders Health and Medical Research Institute, and College of Medicine and Public Health, Flinders University, Adelaide, SA 5042, Australia.
Viruses. 2023 Jun 21;15(7):1410. doi: 10.3390/v15071410.
Retinopathy is a recently recognized complication of dengue, affecting up to 10% of hospitalized patients. Research on the pathogenesis has focused largely on effects of dengue virus (DENV) at the blood-retinal barrier. Involvement of retinal Müller glial cells has received little attention, although this cell population contributes to the pathology of other intraocular infections. The goal of our work was to establish the susceptibility of Müller cells to infection with DENV and to identify characteristics of the cellular antiviral, inflammatory, and immunomodulatory responses to DENV infection in vitro. Primary human Müller cell isolates and the MIO-M1 human Müller cell line were infected with the laboratory-adapted Mon601 strain and DENV serotype 1 and 2 field isolates, and cell-DENV interactions were investigated by immunolabelling and quantitative real-time polymerase chain reaction. Müller cells were susceptible to DENV infection, but experiments involving primary cell isolates indicated inter-individual variation. Viral infection induced an inflammatory response (including tumour necrosis factor-α, interleukin [IL]-1β, and IL-6) and an immunomodulatory response (including programmed death-ligand [PD-L]1 and PD-L2). The type I interferon response was muted in the Müller cell line compared to primary cell isolates. The highest infectivity and cell responses were observed in the laboratory-adapted strain, and overall, infectivity and cell responses were stronger in DENV2 strains. This work demonstrates that Müller cells mount an antiviral and immune response to DENV infection, and that this response varies across cell isolates and DENV strain. The research provides a direction for future efforts to understand the role of human retinal Müller glial cells in dengue retinopathy.
视网膜病变是登革热的一种新出现的并发症,影响高达 10%的住院患者。对发病机制的研究主要集中在登革病毒(DENV)对血视网膜屏障的影响上。视网膜 Müller 胶质细胞的参与受到的关注较少,尽管这种细胞群体对其他眼内感染的病理学有贡献。我们的工作目标是确定 Müller 细胞对 DENV 感染的易感性,并确定体外 DENV 感染时细胞抗病毒、炎症和免疫调节反应的特征。原代人 Müller 细胞分离物和 MIO-M1 人 Müller 细胞系用实验室适应的 Mon601 株和 DENV 血清型 1 和 2 野外分离株感染,并用免疫标记和定量实时聚合酶链反应研究细胞-DENV 相互作用。Müller 细胞易受 DENV 感染,但涉及原代细胞分离物的实验表明存在个体间差异。病毒感染诱导炎症反应(包括肿瘤坏死因子-α、白细胞介素[IL]-1β和 IL-6)和免疫调节反应(包括程序性死亡配体[PD-L]1 和 PD-L2)。与原代细胞分离物相比,Müller 细胞系中的 I 型干扰素反应受到抑制。在实验室适应株中观察到最高的感染性和细胞反应,总体而言,DENV2 株的感染性和细胞反应更强。这项工作表明 Müller 细胞对 DENV 感染产生抗病毒和免疫反应,并且这种反应在细胞分离物和 DENV 株之间存在差异。该研究为未来努力理解人视网膜 Müller 胶质细胞在登革热视网膜病变中的作用提供了方向。