Human Cytomegalovirus (HCMV) is a frequent opportunistic pathogen in immunosuppressed patients, which can be involved in kidney allograft dysfunction and rejection. In order to study the pathophysiology of HCMV renal diseases, we concentrated on the impact of HCMV infection on human renal tubular epithelial HK-2 cells. Our aim was to develop a model of infection of HK-2 cells by using the viral strain TB40/E, that contains the extended cell tropism of clinical isolates and the efficient viral multiplication in cell culture of laboratory-adapted strains. We observed that HK-2 cells can be infected by HCMV and expressed viral antigens, but they do not produce extracellular viral particles. We then studied the interplay of HCMV with ciliogenesis and autophagy. Primary cilium (PC) is a stress sensor important to maintain renal tissue homeostasis that projects from the apical side into the lumen of tubule cells. PC formation and length were not modified by HCMV infection. Autophagy, another stress response process critically required for normal kidney functions, was inhibited by HCMV in HK-2 cells with a reduction in the autophagic flux. HCMV classically induces an enlargement of infected cells in vivo and in vitro, and we observed that HCMV infection led to an enlargement of the HK-2 cell volume. Our results constitute therefore an excellent starting point to further explore the role of these mechanisms in renal cells dysfunction.

人巨细胞病毒（HCMV）是免疫抑制患者中常见的机会病原体，可能与同种异体肾功能不全和排斥反应有关。为了研究HCMV肾脏疾病的病理生理学，我们集中于HCMV感染对人肾小管上皮HK-2细胞的影响。我们的目标是通过使用病毒菌株TB40 / E建立HK-2细胞感染模型，该模型包含临床分离株的扩展细胞嗜性和实验室适应菌株在细胞培养中的有效病毒繁殖。我们观察到HK-2细胞可以被HCMV感染并表达病毒抗原，但它们不产生细胞外病毒颗粒。然后，我们研究了HCMV与纤毛发生和自噬的相互作用。初级纤毛（PC）是一种应力传感器，对于维持从顶侧伸入小管细胞管腔的肾脏组织动态平衡很重要。HCMV感染不会改变PC的形成和长度。自噬是正常肾脏功能至关重要的另一个应激反应过程，它被HK-2细胞中的HCMV抑制，自噬通量减少。HCMV经典地诱导感染细胞的扩大体内 和 体外，并且我们观察到HCMV感染导致HK-2细胞体积增大。因此，我们的结果构成了进一步探索这些机制在肾细胞功能异常中作用的极佳起点。