Barth Heidi, Solis Morgane, Kack-Kack Wallys, Soulier Eric, Velay Aurélie, Fafi-Kremer Samira
Laboratoire de Virologie, Hôpitaux Universitaires de Strasbourg, 3 rue Koeberlé, 67000 Strasbourg, France.
Université de Strasbourg, INSERM, IRM UMR-S 1109, 4 rue Kirschleger, 67000 Strasbourg, France.
Viruses. 2016 Oct 22;8(10):292. doi: 10.3390/v8100292.
Developments of genome amplification techniques have rapidly expanded the family of human polyomaviruses (PyV). Following infection early in life, PyV persist in their hosts and are generally of no clinical consequence. High-level replication of PyV can occur in patients under immunosuppressive or immunomodulatory therapy and causes severe clinical entities, such as progressive multifocal leukoencephalopathy, polyomavirus-associated nephropathy or Merkel cell carcinoma. The characterization of known and newly-discovered human PyV, their relationship to human health, and the mechanisms underlying pathogenesis remain to be elucidated. Here, we summarize the most widely-used in vitro and in vivo models to study the PyV-host interaction, pathogenesis and anti-viral drug screening. We discuss the strengths and limitations of the different models and the lessons learned.
基因组扩增技术的发展迅速扩大了人类多瘤病毒(PyV)家族。在生命早期感染后,PyV在其宿主中持续存在,通常无临床后果。PyV的高水平复制可发生在接受免疫抑制或免疫调节治疗的患者中,并导致严重的临床病症,如进行性多灶性白质脑病、多瘤病毒相关肾病或默克尔细胞癌。已知和新发现的人类PyV的特征、它们与人类健康的关系以及发病机制仍有待阐明。在此,我们总结了用于研究PyV-宿主相互作用、发病机制和抗病毒药物筛选的最广泛使用的体外和体内模型。我们讨论了不同模型的优缺点以及从中吸取的经验教训。