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Evolutionary trajectory of white spot syndrome virus (WSSV) genome shrinkage during spread in Asia.

ABSTRACT: White spot syndrome virus (WSSV) is the sole member of the novel Nimaviridae family, and the source of major economic problems in shrimp aquaculture. WSSV appears to have rapidly spread worldwide after the first reported outbreak in the early 1990s. Genomic deletions of various sizes occur at two loci in the WSSV genome, the ORF14/15 and ORF23/24 variable regions, and these have been used as molecular markers to study patterns of viral spread over space and time. We describe the dynamics underlying the process of WSSV genome shrinkage using empirical data and a simple mathematical model.We genotyped new WSSV isolates from five Asian countries, and analyzed this information together with published data. Genome size appears to stabilize over time, and deletion size in the ORF23/24 variable region was significantly related to the time of the first WSSV outbreak in a particular country. Parameter estimates derived from fitting a simple mathematical model of genome shrinkage to the data support a geometric progression (k<1) of the genomic deletions, with k = 0.371 ± 0.150.The data suggest that the rate of genome shrinkage decreases over time before attenuating. Bioassay data provided support for a link between genome size and WSSV fitness in an aquaculture setting. Differences in genomic deletions between geographic WSSV isolates suggest that WSSV spread did not follow a smooth pattern of geographic radiation, suggesting spread of WSSV over long distances by commercial activities. We discuss two hypotheses for genome shrinkage, an adaptive and a neutral one. We argue in favor of the adaptive hypothesis, given that there is support for a link between WSSV genome size and fitness.

SUBMITTER: Zwart MP

PROVIDER: S-EPMC2954812 | biostudies-literature | 2010 Oct

REPOSITORIES: biostudies-literature

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Evolutionary trajectory of white spot syndrome virus (WSSV) genome shrinkage during spread in Asia.

Zwart Mark P MP Dieu Bui Thi Minh BT Hemerik Lia L Vlak Just M JM

PloS one 20101014 10

<h4>Background</h4>White spot syndrome virus (WSSV) is the sole member of the novel Nimaviridae family, and the source of major economic problems in shrimp aquaculture. WSSV appears to have rapidly spread worldwide after the first reported outbreak in the early 1990s. Genomic deletions of various sizes occur at two loci in the WSSV genome, the ORF14/15 and ORF23/24 variable regions, and these have been used as molecular markers to study patterns of viral spread over space and time. We describe t ...[more]

PMID: 20976239

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Project description:White spot syndrome virus (WSSV) is one of the most devastating pathogens of cultured shrimp, responsible for massive loss of its commercial products worldwide. The oriental river prawn Macrobrachium nipponense is an economically important species that is widely farmed in China and adult prawns can be infected by WSSV. However, the molecular mechanisms of the host pathogen interaction remain unknown. There is an urgent need to learn the host pathogen interaction between M. nipponense and WSSV which will be able to offer a solution in controlling the spread of WSSV. Next Generation Sequencing (NGS) was used in this study to determin the transcriptome differences by the comparison of control and WSSV-challenged moribund samples, control and WSSV-challenged survived samples of hepatopancreas in M. nipponense. A total of 64,049 predicted unigenes were obtained and classified into 63 functional groups. Approximately, 4,311 differential expression genes were identified with 3,308 genes were up-regulated when comparing the survived samples with the control. In the comparison of moribund samples with control, 1,960 differential expression genes were identified with 764 genes were up-regulated. In the contrast of two comparison libraries, 300 mutual DEGs with 95 up-regulated genes and 205 down-regulated genes. All the DEGs were performed GO and KEGG analysis, overall a total of 85 immune-related genes were obtained and these gene were groups into 13 functions and 4 KEGG pathways, such as protease inhibitors, heat shock proteins, oxidative stress, pathogen recognition immune receptors, PI3K/AKT/mTOR pathway, MAPK signaling pathway and Ubiquitin Proteasome Pathway. Ten genes that valuable in immune responses against WSSV were selected from those DEGs to furture discuss the response of host to WSSV. Results from this study contribute to a better understanding of the immune response of M. nipponense to WSSV, provide information for identifying novel genes in the absence of genome of M. nipponense. Furthermore, large number of transcripts obtained from this study could provide a strong basis for future genomic research on M. nipponense.

Project description:White Spot Syndrome Virus (WSSV) is the most damaging pathogen in terms of production and economic losses for the shrimp sector world-wide. Estimation of heritability for WSSV resistance was made in this study to obtain necessary parameter inputs for broadening the breeding objectives of an ongoing selective breeding programme for Whiteleg shrimp (Liptopenaeus vannamei) that has focussed exclusively on improving growth performance since 2014. The present study involved a disease challenge test experiment using a total of 15,000 shrimps from 150 full- and half-sib families (100 individuals per family). Survival rates were recorded at six different experimental periods: 1-3 days (S1), 1-5 days (S2), 1-7 days (S3), 1-9 days (S4), 1-12 days (S5), and 1-15 days (S6) and were used as measures of WSSV resistance. There was significant variation in WSSV resistance among families studied. Quantitative-real time PCR (qPCR) analysis showed that the amount of viral titer (viral load) was significantly lower in high than low resistance families. Analyses of heritability were carried out using linear mixed model (LMM) and threshold logistic generalized model (TLGM). Both linear and threshold models used showed that the heritability (h2) for WSSV resistance was moderate in the early infection phases (S1-S4), whilst a low h2 value was observed for survival after 12 and 15 days of the challenge test (S5 and S6). The transformed heritabilities for WSSV resistance ranged from 1 to 31% which were somewhat lower than those estimated on the liability scale. Genetic correlations between survival rates measured over six different days post-infection were high and positive (0.82-0.99). The phenotypic correlations ranged from 0.31 ± 0.01 to 0.97 ± 0.01. The genetic correlations between body weights and WSSV resistance were negative. Our results on the heritability and genetic correlations show that improvement of WSSV resistance can be achieved through selective breeding in this population of Whiteleg shrimp.

Dataset Information

Evolutionary trajectory of white spot syndrome virus (WSSV) genome shrinkage during spread in Asia.

Publications

Evolutionary trajectory of white spot syndrome virus (WSSV) genome shrinkage during spread in Asia.

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