Macrophages et Développement de l'Immunité, Institut Pasteur, Paris, France.
PLoS Pathog. 2011 Feb 3;7(2):e1001269. doi: 10.1371/journal.ppat.1001269.
The progression of viral infections is notoriously difficult to follow in whole organisms. The small, transparent zebrafish larva constitutes a valuable system to study how pathogens spread. We describe here the course of infection of zebrafish early larvae with a heat-adapted variant of the Infectious Hematopoietic Necrosis Virus (IHNV), a rhabdovirus that represents an important threat to the salmonid culture industry. When incubated at 24 °C, a permissive temperature for virus replication, larvae infected by intravenous injection died within three to four days. Macroscopic signs of infection followed a highly predictable course, with a slowdown then arrest of blood flow despite continuing heartbeat, followed by a loss of reactivity to touch and ultimately by death. Using whole-mount in situ hybridization, patterns of infection were imaged in whole larvae. The first infected cells were detectable as early as 6 hours post infection, and a steady increase in infected cell number and staining intensity occurred with time. Venous endothelium appeared as a primary target of infection, as could be confirmed in fli1:GFP transgenic larvae by live imaging and immunohistochemistry. Disruption of the first vessels took place before arrest of blood circulation, and hemorrhages could be observed in various places. Our data suggest that infection spread from the damaged vessels to underlying tissue. By shifting infected fish to a temperature of 28 °C that is non-permissive for viral propagation, it was possible to establish when virus-generated damage became irreversible. This stage was reached many hours before any detectable induction of the host response. Zebrafish larvae infected with IHNV constitute a vertebrate model of an hemorrhagic viral disease. This tractable system will allow the in vivo dissection of host-virus interactions at the whole organism scale, a feature unrivalled by other vertebrate models.
病毒感染的进程在整个生物体中很难被跟踪。微小透明的斑马鱼幼虫是研究病原体如何传播的有价值的系统。我们在这里描述了经静脉注射感染具有热适应变体的传染性造血坏死病毒 (IHNV) 的早期斑马鱼幼虫的过程,该病毒是对鲑鱼养殖业的重要威胁。在 24°C 下孵育时,病毒复制的允许温度,感染的幼虫会在三到四天内死亡。感染的宏观迹象遵循高度可预测的过程,尽管心跳持续,但血流缓慢然后停止,随后对触摸失去反应,最终死亡。通过全胚胎原位杂交,对整个幼虫的感染模式进行了成像。感染的第一个细胞早在感染后 6 小时即可检测到,并且随着时间的推移,感染细胞数量和染色强度稳步增加。静脉内皮似乎是感染的主要靶标,可以通过活体成像和免疫组织化学在 fli1:GFP 转基因幼虫中得到证实。血液循环停止之前,第一批血管被破坏,并且可以在不同部位观察到出血。我们的数据表明,感染从受损的血管扩散到下面的组织。通过将感染的鱼转移到不允许病毒繁殖的 28°C 温度下,可以确定病毒产生的损伤何时变得不可逆。在宿主反应被检测到之前的许多小时,就达到了这个阶段。感染 IHNV 的斑马鱼幼虫构成了一种出血性病毒性疾病的脊椎动物模型。这种易于处理的系统将允许在整个生物体范围内对宿主-病毒相互作用进行体内剖析,这是其他脊椎动物模型所无法比拟的。