The transcriptomic response to viral infection of two strains of shrimp (Litopenaeus vannamei)

Hollings Marine Laboratory, College of Charleston, Biology Department, Charleston, SC, USA.
Developmental and comparative immunology (Impact Factor: 3.71). 10/2010; 35(3):241-6. DOI: 10.1016/j.dci.2010.10.001
Source: PubMed

ABSTRACT The extent to which data-intensive studies of the transcriptome can provide insight into biological responses is not well defined, especially in the case of species (such as shrimp) where much physiological and biochemical knowledge is missing. In this study we took a transcriptomic approach to gain insight into the response to viral infection of two strains of the Pacific whiteleg shrimp (Litopenaeus vannamei) that differ in their resistance to Taura Syndrome Virus (TSV). Changes in gene expression in the hepatopancreas following infection with TSV and Yellow Head Virus (YHV) were assessed using a cDNA microarray containing 2469 putative unigenes. The null hypothesis tested was that significant differences between the transcriptomic responses to viral infection of resistant and sensitive strains would not be detected. This hypothesis was broadly rejected, with the most surprising observation being that the baseline (control, unchallenged) sensitive and resistant strains expressed distinguishable transcriptomic signatures. The resistant line was pre-disposed to lower expression of genes encoding viral (and host) proteins. Many of the genes differentiating resistant and sensitive lines are involved in protein metabolism, cellular trafficking, immune defense and stress response, although it was not possible to clearly identify candidate genes responsible for TSV resistance. In contrast to TSV challenge, YSV either failed to perturb the host transcriptome or created a "confused" response that was difficult to interpret.

  • Source
    • "The fact that Veloso et al. (2011) found that TSV exposure elicits a distinctive transcriptional pattern and our current work showed a distinct response at 24 h but not at 6 h indicates that there is a relatively rapid (between 6 and 24 h postinoculation) and stable (between 24 h and 14 d postexposure ) transcriptional response to TSV exposure. In addition, the results of both our research and that of Veloso et al. (2011) are largely complementary in that in both cases the different lineages are sufficiently different in the gene expression profiles elicited by exposure to TSV that they can easily be distinguished based on gene expression data and, therefore, it is highly likely that alterations in gene expression are responsible in some part for conferring resistance to TSV. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Abstract The goal of the present research was to identify the genes that are differentially expressed between two lineages of Pacific white shrimp Litopenaeus vannamei displaying different susceptibilities to Taura syndrome virus (TSV) and to understand the molecular pathways involved in resistance to the disease. An oligonucleotide microarray was constructed and used to identify several genes that were differentially expressed in the two L. vannamei lineages following infection with TSV. Individual L. vannamei from either resistant or susceptible lineages were exposed via injection to TSV. Individuals were removed at 6 and 24 h postinfection, and gene expression was assessed with the in-house microarray. The microarray data resulted in the selection of a set of 397 genes that were altered by TSV exposure between the different lineages. Significantly differentially expressed genes were subjected to hierarchical clustering and revealed a lineage-dependent clustering at 24 h postinoculation, but not at 6 h postinoculation. Discriminant analysis resulted in the identification of a set of 11 genes that were able to correctly classify Pacific white shrimp as resistant or susceptible based on gene expression data. Received June 21, 2013; accepted October 24, 2013.
    Journal of Aquatic Animal Health 09/2014; 26(3):137-143. DOI:10.1080/08997659.2013.860058 · 0.97 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Over the last decade, RNA interference pathways have emerged in eukaryotes as critical regulators of many diverse biological functions including, among others, transcriptional gene regulation, post-transcriptional gene silencing, heterochromatin remodelling, suppression of transposon activity, and antiviral defences. Although this gene silencing process has been reported to be relatively well conserved in species of different phyla, there are important discrepancies between plants, invertebrates and mammals. In penaeid shrimp, the existence of an intact and functional RNAi machinery is supported by a rapidly growing body of evidence. However, the extent to which this process participates to the host immune responses remains poorly defined in this non-model organism. This review summarizes our current knowledge of RNAi mechanisms in shrimp and focuses on their implication in antiviral activities and shrimp immune defences.
    Fish &amp Shellfish Immunology 06/2012; 34(4). DOI:10.1016/j.fsi.2012.06.008 · 3.03 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Although West Nile virus (WNV) and other arthropod-borne viruses are a major public health problem, the mechanisms of antiviral immunity in mosquitoes are poorly understood. Dicer-2, responsible for the RNAi-mediated response through the C-terminal RNase-III domain, also contains an N-terminal DExD/H-box helicase domain similar to mammalian RIG-I/MDA5 which, in Drosophila, was found to be required for activation of an antiviral gene, Vago. Here we show that the Culex orthologue of Vago (CxVago) is up-regulated in response to WNV infection in a Dicer-2-dependent manner. Further, our data show that CxVago is a secreted peptide that restricts WNV infection by activation of the Jak-STAT pathway. Thus, Vago appears to function as an IFN-like antiviral cytokine in mosquitoes.
    Proceedings of the National Academy of Sciences 10/2012; 109(46). DOI:10.1073/pnas.1205231109 · 9.81 Impact Factor
Show more