Tilapia lake virus (TiLV) causes high mortality and high economic losses in tilapines. We describe an experimental challenge study focusing on early post challenge innate immune responses. Nile tilapia (Oreochromis niloticus) were infected with 10⁵ TCID₅₀/mL TiLV intraperitoneally, followed by virus quantification, histopathology and gene expression analysis in target (brain/liver) and lymphoid (spleen/headkidney) organs at 3, 7, 12, 17, and 34 days post challenge (dpc). Onset of mortality was from 21 dpc, and cumulative mortality was 38.5% by 34 dpc. Liver and kidney histopathology developed over the period 3–17 dpc, characterized by anisocytosis, anisokaryocytosis, and formation of multinucleated hepatocytes. Viral loads were highest at early time (3 dpc) in liver, spleen and kidney, declining towards 34 dpc. In brain, viral titer peaked 17 dpc. Innate sensors, TLRs 3/7 were inversely correlated with virus titer in brain and headkidney, and IFN-ß and Mx showed a similar pattern. All organs showed increased mRNA IgM expression over the course of infection. Overall, high virus titers downplay innate responses, and an increase is seen when viral titers decline. In silico modeling found that TiLV segments 4, 5 and 10 carry nucleolar localization signals. Anti-viral effects of TiLV facilitate production of virus at early stage of infection.

罗非鱼湖病毒（TiLV）在提拉平斯造成高死亡率和高经济损失。我们描述了一项集中于早期挑战后先天免疫反应的实验性挑战研究。尼罗罗非鱼（Oreochromis niloticus）被感染10 ⁵ TCID ₅₀/ mL腹腔内TiLV，然后在攻击（dpc）后3、7、12、17和34天对目标（脑/肝）和淋巴样（脾/头肾）器官中的病毒进行定量，组织病理学和基因表达分析。死亡率为21 dpc，累积死亡率为34 dpc，为38.5％。肝和肾脏的组织病理学发展期为3-17 dpc，其特征为异吞，异核细胞增多和多核肝细胞的形成。肝脏，脾脏和肾脏中的病毒载量在早期（3 dpc）最高，下降到34 dpc。在大脑中，病毒滴度达到峰值17 dpc。先天性传感器TLRs 3/7与脑和头肾中的病毒滴度呈负相关，IFN-ß和Mx表现出相似的模式。在感染过程中，所有器官均显示出增加的mRNA IgM表达。总体，高病毒滴度会淡化先天反应，而病毒滴度下降时则会增加。在计算机模拟中发现，TiLV片段4、5和10携带核仁定位信号。TiLV的抗病毒作用可促进感染初期的病毒生产。