Tilapia lake virus (TiLV) is a highly contagious pathogen that has detrimental effects on tilapia farming. This virus was discovered in 2014 and has received tremendous global attention from the aquaculture sector due to its association with high fish mortalities and its strong economic impact on the tilapia aquaculture industry. Currently, TiLV has been reported in 16 countries, and this number is continuing to rise due to improved diagnostic assays and surveillance activities around the world. In this review, we summarize the up-to-date knowledge of TiLV with regard to TiLV host species, the clinical signs of a TiLV infection, the affected tissues, pathogenesis and potential disease risk factors. We also describe the reported information concerning the virus itself: its morphology, genetic make-up and transmission pathways. We review the current methods for virus detection and potential control measures. We close the review of the TiLV story so far, by offering a commentary on the major TiLV research gaps, why these are delaying future TiLV research and why the TiLV field needs to come together and proceed as a more collaborative scientific community if there is any hope limiting the impact of this serious virus.
The emergence of tilapia lake virus (TiLV) has had a severely negative impact on global tilapia aquaculture. TiLV infection has been reported at different life stages of tilapia, with more emphasis on fry and fingerlings; however, the virulence and pathology of TiLV at different tilapia size remains unexplored. In this study, tilapias from a single spawning were raised to 5 g, 25 g, and 65 g, and subsequently challenged by the intraperitoneal injection and cohabitation of a virulent strain of TiLV. The cumulative mortality, viral load, and histopathology of the fish were determined until 22 days post-infection (dpi). The cumulative mortality of the 5 g, 25 g, and 65 g fish was 85% (±1.67), 55% (±2.89), and 51.67% (±7.49), respectively. At 14 dpi, the mean TiLV load in the liver of the 5 g fish was significantly higher than in the 25 g and 65 g fish. All the weight groups showed severe pathological changes in the liver, spleen, and intestine after TiLV infection, but no particular difference was otherwise noted during the study with the exception of higher pathological scores in the liver of the small fish at 14 dpi. Overall, this study indicated that small fish are more susceptible to TiLV infection than large fish. Although multiple factors, including environmental factors, farm management practices, strains of virus could contribute to different susceptibility of fish to viral infection, the present study provides the evidence to support that fish weight affects the mortality and clinical outcome during TiLV infection. More intensive measures such as strict biosecurity and disease surveillance during the susceptible weight should therefore be emphasized to reduce the impact of this virus.
Tilapia lake virus (TiLV) is a highly contagious novel orthomyxo-like RNA virus that is negatively impacting tilapia production worldwide. To prevent TiLV from spreading globally, the infection status of source farms needs to be established prior to the movement of live tilapia to minimize the risk of horizontal transmission. However, testing individual fish for TiLV requires large sample sizes, when within-farm prevalence is low and is costly, time-consuming, and labour-intensive. The objective of the present study was to evaluate the use of pool testing for TiLV detection and to estimate within-farm prevalence based on the percentage of positive pooled samples.Pooled samples of liver and spleen were prepared by diluting different numbers of positive tissue samples with negative homogenate tissue samples. A tissue pool from 5 or 10 individual fish containing at least one TiLV-positive sample was sufficient to yield a positive result except when cycle threshold (Ct) values were between 31 and the cut-off value of 34. Additionally, our study characterized viral load in two farms after TiLV outbreaks. Bayesian modelling showed that within-farm prevalence could be estimated from the percentage of positive pools of size 5 using prior information about pool sensitivity and specificity, and prevalence, and assuming random sampling of tilapia from infected ponds. Ninety-five percent posterior intervals for prevalence were slightly wider than those obtained based on the results of individual samples.Findings in the present study corroborate the use of a pooling strategy for postoutbreak surveillance of TiLV.
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