Wargo Andrew R, Scott Robert J, Kerr Benjamin, Kurath Gael
Virginia Institute of Marine Science, College of William and Mary, PO Box 1346, Gloucester Point, VA 23062, United States.
USGS Western Fisheries Research Center, 6505 NE 65th St., Seattle, WA 98115, United States.
Virus Res. 2017 Jan 2;227:200-211. doi: 10.1016/j.virusres.2016.10.011. Epub 2016 Oct 19.
Viral replication and shedding are key components of transmission and fitness, the kinetics of which are heavily dependent on virus, host, and environmental factors. To date, no studies have quantified the shedding kinetics of infectious hematopoietic necrosis virus (IHNV) in rainbow trout (Oncorhynchus mykiss), or how they are associated with replication, making it difficult to ascertain the transmission dynamics of this pathogen of high agricultural and conservation importance. Here, the replication and shedding kinetics of two M genogroup IHNV genotypes were examined in their naturally co-evolved rainbow trout host. Within host virus replication began rapidly, approaching maximum values by day 3 post-infection, after which viral load was maintained or gradually dropped through day 7. Host innate immune response measured as stimulation of Mx-1 gene expression generally followed within host viral loads. Shedding also began very quickly and peaked within 2days, defining a generally uniform early peak period of shedding from 1 to 4days after exposure to virus. This was followed by a post-peak period where shedding declined, such that the majority of fish were no longer shedding by day 12 post-infection. Despite similar kinetics, the average shedding rate over the course of infection was significantly lower in mixed compared to single genotype infections, suggesting a competition effect, however, this did not significantly impact the total amount of virus shed. The data also indicated that the duration of shedding, rather than peak amount of virus shed, was correlated with fish mortality. Generally, the majority of virus produced during infection appeared to be shed into the environment rather than maintained in the host, although there was more retention of within host virus during the post-peak period. Viral virulence was correlated with shedding, such that the more virulent of the two genotypes shed more total virus. This fundamental understanding of IHNV shedding kinetics and variation at the individual fish level could assist with management decisions about how to respond to disease outbreaks when they occur.
病毒复制和释放是传播和适应性的关键组成部分,其动力学在很大程度上取决于病毒、宿主和环境因素。迄今为止,尚无研究对虹鳟(Oncorhynchus mykiss)中传染性造血坏死病毒(IHNV)的释放动力学进行量化,也未研究其与复制的关联,因此难以确定这种具有高度农业和保护重要性的病原体的传播动态。在此,研究了两种M基因群IHNV基因型在与其自然共同进化的虹鳟宿主中的复制和释放动力学。在宿主体内,病毒复制迅速开始,感染后第3天接近最大值,此后病毒载量在第7天保持稳定或逐渐下降。以Mx-1基因表达刺激来衡量的宿主先天免疫反应通常与宿主体内病毒载量变化趋势一致。释放也很快开始,并在2天内达到峰值,确定了从接触病毒后1至4天的一个总体均匀的早期释放高峰期。随后是峰值后阶段,释放量下降,以至于大多数鱼在感染后第12天不再释放病毒。尽管动力学相似,但与单一基因型感染相比,混合基因型感染在感染过程中的平均释放率显著较低,表明存在竞争效应,然而,这并未显著影响病毒的总释放量。数据还表明,释放持续时间而非病毒释放峰值量与鱼类死亡率相关。一般来说,感染期间产生的大多数病毒似乎释放到环境中,而不是保留在宿主体内,尽管在峰值后阶段宿主体内病毒的保留量更多。病毒毒力与释放相关,两种基因型中致病性更强的基因型释放的病毒总量更多。对IHNV在个体鱼水平上的释放动力学和变异的这种基本理解,有助于在疾病爆发时做出如何应对的管理决策。