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INTRODUCTION: The Environmental Determinants of Islet Autoimmunity (ENDIA) Study is an ongoing Australian prospective cohort study investigating how modifiable prenatal and early-life exposures drive the development of islet autoimmunity and type 1 diabetes (T1D) in children. In this profile, we describe the cohort's parental demographics, maternal and neonatal outcomes and human leukocyte antigen (HLA) genotypes. RESEARCH DESIGN AND METHODS: Inclusion criteria were an unborn child, or infant aged less than 6 months, with a first-degree relative (FDR) with T1D. The primary outcome was persistent islet autoimmunity, with children followed until a T1D diagnosis or 10 years of age. Demographic data were collected at enrollment. Lifestyle, clinical and anthropometric data were collected at each visit during pregnancy and clinical pregnancy and birth data were verified against medical case notes. Data were compared between mothers with and without T1D. HLA genotyping was performed on the ENDIA child and all available FDRs. RESULTS: The final cohort comprised 1473 infants born to 1214 gestational mothers across 1453 pregnancies, with 80% enrolled during pregnancy. The distribution of familial T1D probands was 62% maternal, 28% paternal and 11% sibling. The frequency of high-risk HLA genotypes was highest in T1D probands, followed by ENDIA infants, and lowest among unaffected family members. Mothers with T1D had higher rates of pregnancy complications and perinatal intervention, and larger babies of shorter gestation. Parent demographics were comparable to the Australian population for age, parity and obesity. A greater percentage of ENDIA parents were Australian born, lived in a major city and had higher socioeconomic advantage and education. CONCLUSIONS: This comprehensive profile provides the context for understanding ENDIA's scope, methodology, unique strengths and limitations. Now fully recruited, ENDIA will provide unique insights into the roles of early-life factors

AIMS: Studies of the gut microbiome have focused on its bacterial composition. We aimed to characterize the gut fungal microbiome (mycobiome) across pregnancy in women with and without type 1 diabetes. METHODS: Faecal samples (n = 162) were collected from 70 pregnant women (45 with and 25 without type 1 diabetes) across all trimesters. Fungi were analysed by internal transcribed spacer 1 amplicon sequencing. Markers of intestinal inflammation (faecal calprotectin) and intestinal epithelial integrity (serum intestinal fatty acid binding protein; I-FABP), and serum antibodies to Saccharomyces cerevisiae (ASCA) were measured. RESULTS: Women with type 1 diabetes had decreased fungal alpha diversity by the third trimester, associated with an increased abundance of Saccharomyces cerevisiae that was inversely related to the abundance of the anti-inflammatory butyrate-producing bacterium Faecalibacterium prausnitzii. Women with type 1 diabetes had higher concentrations of calprotectin, I-FABP and ASCA. CONCLUSIONS: Women with type 1 diabetes exhibit a shift in the gut mycobiome across pregnancy associated with evidence of gut inflammation and impaired intestinal barrier function. The relevance of these findings to the higher rate of pregnancy complications in type 1 diabetes warrants further study.

Introduction: We aimed to compare the mental health of mothers, with and without type 1 diabetes (T1D), during pregnancy and postpartum, and to examine the relationship between glycaemic control and mental health in T1D. Objective(s): We hypothesised that mental health in trimester 3 (T3) and post-partum is less favourable in mothers with T1D, and that poorer mental health scores relate directly to glycaemic control. Method(s): Participants were 800/946 women enrolled in the Environmental Determinants of Islet Autoimmunity (ENDIA) study, an Australiawide pregnancy-birth prospective cohort following children with a first-degree relative with T1D, from 2016-2020.Women with and without T1D (n=518, 282) completed the Edinburgh Postnatal Depression Scale (EPDS) and Perceived Stress Scale (PSS) during T3, (median [IQR], 34 [32, 36] weeks) and early post-partum (median 14 [13, 16] weeks). Linear mixed regression models were adjusted for parity. Result(s): Women without T1D were aged mean (SD) 33.1 (4.4) years; 31.9 (4.4) years with T1D. Pre-existing mental health issues requiring psychotropic medications were of similar number in non-T1D n=17 [6%] and T1D n=41 [8%]. EPDS and PSS scores did not differ between non-T1D and T1D mothers at T3 or post-partum (all p>=0.5; Table 1). EPDS scores were less favourable at T3 compared with postpartum (p=0.01), independent of T1D status, and by post-partum 12/47 women had improved to below the threshold (=12) recommended for intervention. HbA1c during pregnancy in 398/518 women (76.8%) with T1D did not relate to EPDS (r2=0.01, p=0.2) or PSS (r2=0.02, p=0.4) scores. Median [IQR] HbA1c was 6.3% [5.8-6.9]. Conclusion(s): Overall, mental health in late pregnancy and postpartum was not adversely impacted by T1D. Glycaemic control did not relate to mental health scores in mothers with T1D. A generalised improvement in mental health between T3 and post-partum was independent of T1D status.

Background: The gut microbiome changes in response to a range of environmental conditions, life events and disease states. Pregnancy is a natural life event that involves major physiological adaptation yet studies of the microbiome in pregnancy are limited and their findings inconsistent. Pregnancy with type 1 diabetes (T1D) is associated with increased maternal and fetal risks but the gut microbiome in this context has not been characterized. By whole metagenome sequencing (WMS), we defined the taxonomic composition and function of the gut bacterial microbiome across 70 pregnancies, 36 in women with T1D. Result(s): Women with and without T1D exhibited compositional and functional changes in the gut microbiome across pregnancy. Profiles in women with T1D were distinct, with an increase in bacteria that produce lipopolysaccharides and a decrease in those that produce short-chain fatty acids, especially in the third trimester. In addition, women with T1D had elevated concentrations of fecal calprotectin, a marker of intestinal inflammation, and serum intestinal fatty acid-binding protein (I-FABP), a marker of intestinal epithelial damage. Conclusion(s): Women with T1D exhibit a shift towards a more pro-inflammatory gut microbiome during pregnancy, associated with evidence of intestinal inflammation. These changes could contribute to the increased risk of pregnancy complications in women with T1D and are potentially modifiable by dietary means. [MediaObject not available: see fulltext.]Copyright © 2021, The Author(s).

Introduction: We aimed to compare the mental health of mothers, with and without type 1 diabetes (T1D), during pregnancy and postpartum, and to examine the relationship between glycaemic control and mental health in T1D. Objective(s): We hypothesised that mental health in trimester 3 (T3) and post-partum is less favourable in mothers with T1D, and that poorer mental health scores relate directly to glycaemic control. Method(s): Participants were 800/946 women enrolled in the Environmental Determinants of Islet Autoimmunity (ENDIA) study, an Australiawide pregnancy-birth prospective cohort following children with a first-degree relative with T1D, from 2016-2020.Women with and without T1D (n=518, 282) completed the Edinburgh Postnatal Depression Scale (EPDS) and Perceived Stress Scale (PSS) during T3, (median [IQR], 34 [32, 36] weeks) and early post-partum (median 14 [13, 16] weeks). Linear mixed regression models were adjusted for parity. Result(s): Women without T1D were aged mean (SD) 33.1 (4.4) years; 31.9 (4.4) years with T1D. Pre-existing mental health issues requiring psychotropic medications were of similar number in non-T1D n=17 [6%] and T1D n=41 [8%]. EPDS and PSS scores did not differ between non-T1D and T1D mothers at T3 or post-partum (all p>=0.5; Table 1). EPDS scores were less favourable at T3 compared with postpartum (p=0.01), independent of T1D status, and by post-partum 12/47 women had improved to below the threshold (=12) recommended for intervention. HbA1c during pregnancy in 398/518 women (76.8%) with T1D did not relate to EPDS (r2=0.01, p=0.2) or PSS (r2=0.02, p=0.4) scores. Median [IQR] HbA1c was 6.3% [5.8-6.9]. Conclusion(s): Overall, mental health in late pregnancy and postpartum was not adversely impacted by T1D. Glycaemic control did not relate to mental health scores in mothers with T1D. A generalised improvement in mental health between T3 and post-partum was independent of T1D status.

Background: The gut microbiome changes in response to a range of environmental conditions, life events and disease states. Pregnancy is a natural life event that involves major physiological adaptation yet studies of the microbiome in pregnancy are limited and their findings inconsistent. Pregnancy with type 1 diabetes (T1D) is associated with increased maternal and fetal risks but the gut microbiome in this context has not been characterized. By whole metagenome sequencing (WMS), we defined the taxonomic composition and function of the gut bacterial microbiome across 70 pregnancies, 36 in women with T1D. Result(s): Women with and without T1D exhibited compositional and functional changes in the gut microbiome across pregnancy. Profiles in women with T1D were distinct, with an increase in bacteria that produce lipopolysaccharides and a decrease in those that produce short-chain fatty acids, especially in the third trimester. In addition, women with T1D had elevated concentrations of fecal calprotectin, a marker of intestinal inflammation, and serum intestinal fatty acid-binding protein (I-FABP), a marker of intestinal epithelial damage. Conclusion(s): Women with T1D exhibit a shift towards a more pro-inflammatory gut microbiome during pregnancy, associated with evidence of intestinal inflammation. These changes could contribute to the increased risk of pregnancy complications in women with T1D and are potentially modifiable by dietary means. [MediaObject not available: see fulltext.]Copyright © 2021, The Author(s).

BACKGROUND: The gut microbiome changes in response to a range of environmental conditions, life events and disease states. Pregnancy is a natural life event that involves major physiological adaptation yet studies of the microbiome in pregnancy are limited and their findings inconsistent. Pregnancy with type 1 diabetes (T1D) is associated with increased maternal and fetal risks but the gut microbiome in this context has not been characterized. By whole metagenome sequencing (WMS), we defined the taxonomic composition and function of the gut bacterial microbiome across 70 pregnancies, 36 in women with T1D. RESULTS: Women with and without T1D exhibited compositional and functional changes in the gut microbiome across pregnancy. Profiles in women with T1D were distinct, with an increase in bacteria that produce lipopolysaccharides and a decrease in those that produce short-chain fatty acids, especially in the third trimester. In addition, women with T1D had elevated concentrations of fecal calprotectin, a marker of intestinal inflammation, and serum intestinal fatty acid-binding protein (I-FABP), a marker of intestinal epithelial damage. CONCLUSIONS: Women with T1D exhibit a shift towards a more pro-inflammatory gut microbiome during pregnancy, associated with evidence of intestinal inflammation. These changes could contribute to the increased risk of pregnancy complications in women with T1D and are potentially modifiable by dietary means. Video abstract.

Backgrounds: We aimed to monitor pancreatic exocrine function longitudinally in relation to the development of islet autoimmunity (IA) and type 1 diabetes (T1D) in at-risk children with a first-degree relative with T1D, who were followed prospectively in the Environmental Determinants of Islet Autoimmunity (ENDIA) study. Method(s): Fecal elastase-1 (FE-1) concentration was measured longitudinally in 85 ENDIA children from median age 1.0 (IQR 0.7,1.3) year. Twenty-eight of 85 children (progressors) developed persistent islet autoantibodies at median age of 1.5 (IQR 1.1,2.5) years, of whom 11 went on to develop clinical diabetes. The other 57 islet autoantibody-negative children (non-progressors) followed similarly were age and gender-matched with the progressors. An adjusted linear mixed model compared FE-1 concentrations in progressors and non-progressors. Result(s): Baseline FE-1 did not differ between progressors and non-progressors, or by HLA DR type or proband status. FE-1 decreased over time in progressors in comparison to non-progressors (Wald statistic 5.46, P =.02); in some progressors the fall in FE-1 preceded the onset of IA. Conclusion(s): Pancreatic exocrine function decreases in the majority of young at-risk children who progress to IA and T1D.Copyright © 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd

Backgrounds: We aimed to monitor pancreatic exocrine function longitudinally in relation to the development of islet autoimmunity (IA) and type 1 diabetes (T1D) in at-risk children with a first-degree relative with T1D, who were followed prospectively in the Environmental Determinants of Islet Autoimmunity (ENDIA) study. Method(s): Fecal elastase-1 (FE-1) concentration was measured longitudinally in 85 ENDIA children from median age 1.0 (IQR 0.7,1.3) year. Twenty-eight of 85 children (progressors) developed persistent islet autoantibodies at median age of 1.5 (IQR 1.1,2.5) years, of whom 11 went on to develop clinical diabetes. The other 57 islet autoantibody-negative children (non-progressors) followed similarly were age and gender-matched with the progressors. An adjusted linear mixed model compared FE-1 concentrations in progressors and non-progressors. Result(s): Baseline FE-1 did not differ between progressors and non-progressors, or by HLA DR type or proband status. FE-1 decreased over time in progressors in comparison to non-progressors (Wald statistic 5.46, P =.02); in some progressors the fall in FE-1 preceded the onset of IA. Conclusion(s): Pancreatic exocrine function decreases in the majority of young at-risk children who progress to IA and T1D.Copyright © 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd

BACKGROUNDS: We aimed to monitor pancreatic exocrine function longitudinally in relation to the development of islet autoimmunity (IA) and type 1 diabetes (T1D) in at-risk children with a first-degree relative with T1D, who were followed prospectively in the Environmental Determinants of Islet Autoimmunity (ENDIA) study. METHODS: Fecal elastase-1 (FE-1) concentration was measured longitudinally in 85 ENDIA children from median age 1.0 (IQR 0.7,1.3) year. Twenty-eight of 85 children (progressors) developed persistent islet autoantibodies at median age of 1.5 (IQR 1.1,2.5) years, of whom 11 went on to develop clinical diabetes. The other 57 islet autoantibody-negative children (non-progressors) followed similarly were age and gender-matched with the progressors. An adjusted linear mixed model compared FE-1 concentrations in progressors and non-progressors. RESULTS: Baseline FE-1 did not differ between progressors and non-progressors, or by HLA DR type or proband status. FE-1 decreased over time in progressors in comparison to non-progressors (Wald statistic 5.46, P = .02); in some progressors the fall in FE-1 preceded the onset of IA. CONCLUSIONS: Pancreatic exocrine function decreases in the majority of young at-risk children who progress to IA and T1D.

To optimize shoot growth and structure of cereals, we need to understand the genetic components controlling initiation and elongation. While measuring total shoot growth at high throughput using 2D imaging has progressed, recovering the 3D shoot structure of small grain cereals at a large scale is still challenging. Here, we present a method for measuring defined individual leaves of cereals, such as wheat and barley, using few images. Plant shoot modelling over time was used to measure the initiation and elongation of leaves in a bi-parental barley mapping population under low and high soil salinity. We detected quantitative trait loci (QTL) related to shoot growth per se, using both simple 2D total shoot measurements and our approach of measuring individual leaves. In addition, we detected QTL specific to leaf elongation and not to total shoot size. Of particular importance was the detection of a QTL on chromosome 3H specific to the early responses of leaf elongation to salt stress, a locus that could not be detected without the computer vision tools developed in this study.

White spot disease is a serious viral panzootic affecting prawn aquaculture. The causative agent is white spot syndrome virus (WSSV), a large double-stranded circular DNA virus. In November 2016, WSSV was identified following the onset of disease in a prawn farm near Brisbane, Queensland, Australia (previously free of white spot disease). The prawn farming industry in Queensland is valued at approximately AU$87 million annually, and the potential impact of establishment of endemic WSD would be severe. We report the complete genome sequence of the Australian WSSV (WSSV-AU) and the analysis of previously described genomic markers that have been reported to show variation among WSSV strains. WSSV-AU genome length was 285,973 bp, shorter than most but within the previously reported size range of 281 kbp to 312 kbp. There are high levels of homology (91–97%) between the WSSV-AU and other reported genomes sequences. The WSSV-AU genome sequence has a number of substantial deletions, most significantly in regions that were previously reported as genomic markers (regions known to contain variable numbers of tandem repeats and regions with deletions of variable length). Additionally, several deletions of regions reported to encode envelope proteins were deleted. It may be that some of the envelope proteins needed for an ancestral natural host infection are redundant, and therefore expendable, with respect to infection of penaeids. Hence, that deletion of redundant regions may show homoplasy and be an unreliable epidemiological tool. In light of the undetermined epidemiological relevance of deletions, including those associated with long tandem repeats, it is concluded that the comparison of reported complete genome sequences cannot identify the source of the virus in Queensland and an alternative genotyping method is required.

White spot disease is a serious viral panzootic affecting prawn aquaculture. The causative agent is white spot syndrome virus (WSSV), a large double-stranded circular DNA virus. In November 2016, WSSV was identified following the onset of disease in a prawn farm near Brisbane, Queensland, Australia (previously free of white spot disease). The prawn farming industry in Queensland is valued at approximately AU$87 million annually, and the potential impact of establishment of endemic WSD would be severe. We report the complete genome sequence of the Australian WSSV (WSSV-AU) and the analysis of previously described genomic markers that have been reported to show variation among WSSV strains. WSSV-AU genome length was 285,973 bp, shorter than most but within the previously reported size range of 281 kbp to 312 kbp. There are high levels of homology (91–97%) between the WSSV-AU and other reported genomes sequences. The WSSV-AU genome sequence has a number of substantial deletions, most significantly in regions that were previously reported as genomic markers (regions known to contain variable numbers of tandem repeats and regions with deletions of variable length). Additionally, several deletions of regions reported to encode envelope proteins were deleted. It may be that some of the envelope proteins needed for an ancestral natural host infection are redundant, and therefore expendable, with respect to infection of penaeids. Hence, that deletion of redundant regions may show homoplasy and be an unreliable epidemiological tool. In light of the undetermined epidemiological relevance of deletions, including those associated with long tandem repeats, it is concluded that the comparison of reported complete genome sequences cannot identify the source of the virus in Queensland and an alternative genotyping method is required.

White spot disease is a serious viral panzootic affecting prawn aquaculture. The causative agent is white spot syndrome virus (WSSV), a large double-stranded circular DNA virus. In November 2016, WSSV was identified following the onset of disease in a prawn farm near Brisbane, Queensland, Australia (previously free of white spot disease). The prawn farming industry in Queensland is valued at approximately AU$87 million annually, and the potential impact of establishment of endemic WSD would be severe. We report the complete genome sequence of the Australian WSSV (WSSV-AU) and the analysis of previously described genomic markers that have been reported to show variation among WSSV strains. WSSV-AU genome length was 285,973 bp, shorter than most but within the previously reported size range of 281 kbp to 312 kbp. There are high levels of homology (91–97%) between the WSSV-AU and other reported genomes sequences. The WSSV-AU genome sequence has a number of substantial deletions, most significantly in regions that were previously reported as genomic markers (regions known to contain variable numbers of tandem repeats and regions with deletions of variable length). Additionally, several deletions of regions reported to encode envelope proteins were deleted. It may be that some of the envelope proteins needed for an ancestral natural host infection are redundant, and therefore expendable, with respect to infection of penaeids. Hence, that deletion of redundant regions may show homoplasy and be an unreliable epidemiological tool. In light of the undetermined epidemiological relevance of deletions, including those associated with long tandem repeats, it is concluded that the comparison of reported complete genome sequences cannot identify the source of the virus in Queensland and an alternative genotyping method is required.

White spot disease is a serious viral panzootic affecting prawn aquaculture. The causative agent is white spot syndrome virus (WSSV), a large double-stranded circular DNA virus. In November 2016, WSSV was identified following the onset of disease in a prawn farm near Brisbane, Queensland, Australia (previously free of white spot disease). The prawn farming industry in Queensland is valued at approximately AU$87 million annually, and the potential impact of establishment of endemic WSD would be severe. We report the complete genome sequence of the Australian WSSV (WSSV-AU) and the analysis of previously described genomic markers that have been reported to show variation among WSSV strains. WSSV-AU genome length was 285,973 bp, shorter than most but within the previously reported size range of 281 kbp to 312 kbp. There are high levels of homology (91–97%) between the WSSV-AU and other reported genomes sequences. The WSSV-AU genome sequence has a number of substantial deletions, most significantly in regions that were previously reported as genomic markers (regions known to contain variable numbers of tandem repeats and regions with deletions of variable length). Additionally, several deletions of regions reported to encode envelope proteins were deleted. It may be that some of the envelope proteins needed for an ancestral natural host infection are redundant, and therefore expendable, with respect to infection of penaeids. Hence, that deletion of redundant regions may show homoplasy and be an unreliable epidemiological tool. In light of the undetermined epidemiological relevance of deletions, including those associated with long tandem repeats, it is concluded that the comparison of reported complete genome sequences cannot identify the source of the virus in Queensland and an alternative genotyping method is required.

White spot disease is a serious viral panzootic affecting prawn aquaculture. The causative agent is white spot syndrome virus (WSSV), a large double-stranded circular DNA virus. In November 2016, WSSV was identified following the onset of disease in a prawn farm near Brisbane, Queensland, Australia (previously free of white spot disease). The prawn farming industry in Queensland is valued at approximately AU$87 million annually, and the potential impact of establishment of endemic WSD would be severe. We report the complete genome sequence of the Australian WSSV (WSSV-AU) and the analysis of previously described genomic markers that have been reported to show variation among WSSV strains. WSSV-AU genome length was 285,973 bp, shorter than most but within the previously reported size range of 281 kbp to 312 kbp. There are high levels of homology (91–97%) between the WSSV-AU and other reported genomes sequences. The WSSV-AU genome sequence has a number of substantial deletions, most significantly in regions that were previously reported as genomic markers (regions known to contain variable numbers of tandem repeats and regions with deletions of variable length). Additionally, several deletions of regions reported to encode envelope proteins were deleted. It may be that some of the envelope proteins needed for an ancestral natural host infection are redundant, and therefore expendable, with respect to infection of penaeids. Hence, that deletion of redundant regions may show homoplasy and be an unreliable epidemiological tool. In light of the undetermined epidemiological relevance of deletions, including those associated with long tandem repeats, it is concluded that the comparison of reported complete genome sequences cannot identify the source of the virus in Queensland and an alternative genotyping method is required.

White spot disease is a serious viral panzootic affecting prawn aquaculture. The causative agent is white spot syndrome virus (WSSV), a large double-stranded circular DNA virus. In November 2016, WSSV was identified following the onset of disease in a prawn farm near Brisbane, Queensland, Australia (previously free of white spot disease). The prawn farming industry in Queensland is valued at approximately AU$87 million annually, and the potential impact of establishment of endemic WSD would be severe. We report the complete genome sequence of the Australian WSSV (WSSV-AU) and the analysis of previously described genomic markers that have been reported to show variation among WSSV strains. WSSV-AU genome length was 285,973 bp, shorter than most but within the previously reported size range of 281 kbp to 312 kbp. There are high levels of homology (91–97%) between the WSSV-AU and other reported genomes sequences. The WSSV-AU genome sequence has a number of substantial deletions, most significantly in regions that were previously reported as genomic markers (regions known to contain variable numbers of tandem repeats and regions with deletions of variable length). Additionally, several deletions of regions reported to encode envelope proteins were deleted. It may be that some of the envelope proteins needed for an ancestral natural host infection are redundant, and therefore expendable, with respect to infection of penaeids. Hence, that deletion of redundant regions may show homoplasy and be an unreliable epidemiological tool. In light of the undetermined epidemiological relevance of deletions, including those associated with long tandem repeats, it is concluded that the comparison of reported complete genome sequences cannot identify the source of the virus in Queensland and an alternative genotyping method is required.

White spot disease is a serious viral panzootic affecting prawn aquaculture. The causative agent is white spot syndrome virus (WSSV), a large double-stranded circular DNA virus. In November 2016, WSSV was identified following the onset of disease in a prawn farm near Brisbane, Queensland, Australia (previously free of white spot disease). The prawn farming industry in Queensland is valued at approximately AU$87 million annually, and the potential impact of establishment of endemic WSD would be severe. We report the complete genome sequence of the Australian WSSV (WSSV-AU) and the analysis of previously described genomic markers that have been reported to show variation among WSSV strains. WSSV-AU genome length was 285,973 bp, shorter than most but within the previously reported size range of 281 kbp to 312 kbp. There are high levels of homology (91–97%) between the WSSV-AU and other reported genomes sequences. The WSSV-AU genome sequence has a number of substantial deletions, most significantly in regions that were previously reported as genomic markers (regions known to contain variable numbers of tandem repeats and regions with deletions of variable length). Additionally, several deletions of regions reported to encode envelope proteins were deleted. It may be that some of the envelope proteins needed for an ancestral natural host infection are redundant, and therefore expendable, with respect to infection of penaeids. Hence, that deletion of redundant regions may show homoplasy and be an unreliable epidemiological tool. In light of the undetermined epidemiological relevance of deletions, including those associated with long tandem repeats, it is concluded that the comparison of reported complete genome sequences cannot identify the source of the virus in Queensland and an alternative genotyping method is required.

White spot disease is a serious viral panzootic affecting prawn aquaculture. The causative agent is white spot syndrome virus (WSSV), a large double-stranded circular DNA virus. In November 2016, WSSV was identified following the onset of disease in a prawn farm near Brisbane, Queensland, Australia (previously free of white spot disease). The prawn farming industry in Queensland is valued at approximately AU$87 million annually, and the potential impact of establishment of endemic WSD would be severe. We report the complete genome sequence of the Australian WSSV (WSSV-AU) and the analysis of previously described genomic markers that have been reported to show variation among WSSV strains. WSSV-AU genome length was 285,973 bp, shorter than most but within the previously reported size range of 281 kbp to 312 kbp. There are high levels of homology (91–97%) between the WSSV-AU and other reported genomes sequences. The WSSV-AU genome sequence has a number of substantial deletions, most significantly in regions that were previously reported as genomic markers (regions known to contain variable numbers of tandem repeats and regions with deletions of variable length). Additionally, several deletions of regions reported to encode envelope proteins were deleted. It may be that some of the envelope proteins needed for an ancestral natural host infection are redundant, and therefore expendable, with respect to infection of penaeids. Hence, that deletion of redundant regions may show homoplasy and be an unreliable epidemiological tool. In light of the undetermined epidemiological relevance of deletions, including those associated with long tandem repeats, it is concluded that the comparison of reported complete genome sequences cannot identify the source of the virus in Queensland and an alternative genotyping method is required.

White spot disease is a serious viral panzootic affecting prawn aquaculture. The causative agent is white spot syndrome virus (WSSV), a large double-stranded circular DNA virus. In November 2016, WSSV was identified following the onset of disease in a prawn farm near Brisbane, Queensland, Australia (previously free of white spot disease). The prawn farming industry in Queensland is valued at approximately AU$87 million annually, and the potential impact of establishment of endemic WSD would be severe. We report the complete genome sequence of the Australian WSSV (WSSV-AU) and the analysis of previously described genomic markers that have been reported to show variation among WSSV strains. WSSV-AU genome length was 285,973 bp, shorter than most but within the previously reported size range of 281 kbp to 312 kbp. There are high levels of homology (91–97%) between the WSSV-AU and other reported genomes sequences. The WSSV-AU genome sequence has a number of substantial deletions, most significantly in regions that were previously reported as genomic markers (regions known to contain variable numbers of tandem repeats and regions with deletions of variable length). Additionally, several deletions of regions reported to encode envelope proteins were deleted. It may be that some of the envelope proteins needed for an ancestral natural host infection are redundant, and therefore expendable, with respect to infection of penaeids. Hence, that deletion of redundant regions may show homoplasy and be an unreliable epidemiological tool. In light of the undetermined epidemiological relevance of deletions, including those associated with long tandem repeats, it is concluded that the comparison of reported complete genome sequences cannot identify the source of the virus in Queensland and an alternative genotyping method is required.

White spot disease is a serious viral panzootic affecting prawn aquaculture. The causative agent is white spot syndrome virus (WSSV), a large double-stranded circular DNA virus. In November 2016, WSSV was identified following the onset of disease in a prawn farm near Brisbane, Queensland, Australia (previously free of white spot disease). The prawn farming industry in Queensland is valued at approximately AU$87 million annually, and the potential impact of establishment of endemic WSD would be severe. We report the complete genome sequence of the Australian WSSV (WSSV-AU) and the analysis of previously described genomic markers that have been reported to show variation among WSSV strains. WSSV-AU genome length was 285,973 bp, shorter than most but within the previously reported size range of 281 kbp to 312 kbp. There are high levels of homology (91–97%) between the WSSV-AU and other reported genomes sequences. The WSSV-AU genome sequence has a number of substantial deletions, most significantly in regions that were previously reported as genomic markers (regions known to contain variable numbers of tandem repeats and regions with deletions of variable length). Additionally, several deletions of regions reported to encode envelope proteins were deleted. It may be that some of the envelope proteins needed for an ancestral natural host infection are redundant, and therefore expendable, with respect to infection of penaeids. Hence, that deletion of redundant regions may show homoplasy and be an unreliable epidemiological tool. In light of the undetermined epidemiological relevance of deletions, including those associated with long tandem repeats, it is concluded that the comparison of reported complete genome sequences cannot identify the source of the virus in Queensland and an alternative genotyping method is required.

White spot disease is a serious viral panzootic affecting prawn aquaculture. The causative agent is white spot syndrome virus (WSSV), a large double-stranded circular DNA virus. In November 2016, WSSV was identified following the onset of disease in a prawn farm near Brisbane, Queensland, Australia (previously free of white spot disease). The prawn farming industry in Queensland is valued at approximately AU$87 million annually, and the potential impact of establishment of endemic WSD would be severe. We report the complete genome sequence of the Australian WSSV (WSSV-AU) and the analysis of previously described genomic markers that have been reported to show variation among WSSV strains. WSSV-AU genome length was 285,973 bp, shorter than most but within the previously reported size range of 281 kbp to 312 kbp. There are high levels of homology (91–97%) between the WSSV-AU and other reported genomes sequences. The WSSV-AU genome sequence has a number of substantial deletions, most significantly in regions that were previously reported as genomic markers (regions known to contain variable numbers of tandem repeats and regions with deletions of variable length). Additionally, several deletions of regions reported to encode envelope proteins were deleted. It may be that some of the envelope proteins needed for an ancestral natural host infection are redundant, and therefore expendable, with respect to infection of penaeids. Hence, that deletion of redundant regions may show homoplasy and be an unreliable epidemiological tool. In light of the undetermined epidemiological relevance of deletions, including those associated with long tandem repeats, it is concluded that the comparison of reported complete genome sequences cannot identify the source of the virus in Queensland and an alternative genotyping method is required.

White spot disease is a serious viral panzootic affecting prawn aquaculture. The causative agent is white spot syndrome virus (WSSV), a large double-stranded circular DNA virus. In November 2016, WSSV was identified following the onset of disease in a prawn farm near Brisbane, Queensland, Australia (previously free of white spot disease). The prawn farming industry in Queensland is valued at approximately AU$87 million annually, and the potential impact of establishment of endemic WSD would be severe. We report the complete genome sequence of the Australian WSSV (WSSV-AU) and the analysis of previously described genomic markers that have been reported to show variation among WSSV strains. WSSV-AU genome length was 285,973 bp, shorter than most but within the previously reported size range of 281 kbp to 312 kbp. There are high levels of homology (91–97%) between the WSSV-AU and other reported genomes sequences. The WSSV-AU genome sequence has a number of substantial deletions, most significantly in regions that were previously reported as genomic markers (regions known to contain variable numbers of tandem repeats and regions with deletions of variable length). Additionally, several deletions of regions reported to encode envelope proteins were deleted. It may be that some of the envelope proteins needed for an ancestral natural host infection are redundant, and therefore expendable, with respect to infection of penaeids. Hence, that deletion of redundant regions may show homoplasy and be an unreliable epidemiological tool. In light of the undetermined epidemiological relevance of deletions, including those associated with long tandem repeats, it is concluded that the comparison of reported complete genome sequences cannot identify the source of the virus in Queensland and an alternative genotyping method is required.

White spot disease is a serious viral panzootic affecting prawn aquaculture. The causative agent is white spot syndrome virus (WSSV), a large double-stranded circular DNA virus. In November 2016, WSSV was identified following the onset of disease in a prawn farm near Brisbane, Queensland, Australia (previously free of white spot disease). The prawn farming industry in Queensland is valued at approximately AU$87 million annually, and the potential impact of establishment of endemic WSD would be severe. We report the complete genome sequence of the Australian WSSV (WSSV-AU) and the analysis of previously described genomic markers that have been reported to show variation among WSSV strains. WSSV-AU genome length was 285,973 bp, shorter than most but within the previously reported size range of 281 kbp to 312 kbp. There are high levels of homology (91–97%) between the WSSV-AU and other reported genomes sequences. The WSSV-AU genome sequence has a number of substantial deletions, most significantly in regions that were previously reported as genomic markers (regions known to contain variable numbers of tandem repeats and regions with deletions of variable length). Additionally, several deletions of regions reported to encode envelope proteins were deleted. It may be that some of the envelope proteins needed for an ancestral natural host infection are redundant, and therefore expendable, with respect to infection of penaeids. Hence, that deletion of redundant regions may show homoplasy and be an unreliable epidemiological tool. In light of the undetermined epidemiological relevance of deletions, including those associated with long tandem repeats, it is concluded that the comparison of reported complete genome sequences cannot identify the source of the virus in Queensland and an alternative genotyping method is required.

White spot disease is a serious viral panzootic affecting prawn aquaculture. The causative agent is white spot syndrome virus (WSSV), a large double-stranded circular DNA virus. In November 2016, WSSV was identified following the onset of disease in a prawn farm near Brisbane, Queensland, Australia (previously free of white spot disease). The prawn farming industry in Queensland is valued at approximately AU$87 million annually, and the potential impact of establishment of endemic WSD would be severe. We report the complete genome sequence of the Australian WSSV (WSSV-AU) and the analysis of previously described genomic markers that have been reported to show variation among WSSV strains. WSSV-AU genome length was 285,973 bp, shorter than most but within the previously reported size range of 281 kbp to 312 kbp. There are high levels of homology (91–97%) between the WSSV-AU and other reported genomes sequences. The WSSV-AU genome sequence has a number of substantial deletions, most significantly in regions that were previously reported as genomic markers (regions known to contain variable numbers of tandem repeats and regions with deletions of variable length). Additionally, several deletions of regions reported to encode envelope proteins were deleted. It may be that some of the envelope proteins needed for an ancestral natural host infection are redundant, and therefore expendable, with respect to infection of penaeids. Hence, that deletion of redundant regions may show homoplasy and be an unreliable epidemiological tool. In light of the undetermined epidemiological relevance of deletions, including those associated with long tandem repeats, it is concluded that the comparison of reported complete genome sequences cannot identify the source of the virus in Queensland and an alternative genotyping method is required.

White spot disease is a serious viral panzootic affecting prawn aquaculture. The causative agent is white spot syndrome virus (WSSV), a large double-stranded circular DNA virus. In November 2016, WSSV was identified following the onset of disease in a prawn farm near Brisbane, Queensland, Australia (previously free of white spot disease). The prawn farming industry in Queensland is valued at approximately AU$87 million annually, and the potential impact of establishment of endemic WSD would be severe. We report the complete genome sequence of the Australian WSSV (WSSV-AU) and the analysis of previously described genomic markers that have been reported to show variation among WSSV strains. WSSV-AU genome length was 285,973 bp, shorter than most but within the previously reported size range of 281 kbp to 312 kbp. There are high levels of homology (91–97%) between the WSSV-AU and other reported genomes sequences. The WSSV-AU genome sequence has a number of substantial deletions, most significantly in regions that were previously reported as genomic markers (regions known to contain variable numbers of tandem repeats and regions with deletions of variable length). Additionally, several deletions of regions reported to encode envelope proteins were deleted. It may be that some of the envelope proteins needed for an ancestral natural host infection are redundant, and therefore expendable, with respect to infection of penaeids. Hence, that deletion of redundant regions may show homoplasy and be an unreliable epidemiological tool. In light of the undetermined epidemiological relevance of deletions, including those associated with long tandem repeats, it is concluded that the comparison of reported complete genome sequences cannot identify the source of the virus in Queensland and an alternative genotyping method is required.

The impacts of wild dogs (Canis lupus dingo and their hybrids) are increasingly being felt by producers and residents throughout the fragmented landscapes of peri-urban areas of north-eastern Australia. Management options are limited in such environs, and confounded by a lack of knowledge of wild dog ecology. Genetics of wild dog populations has been studied generally, but limited information is available from the peri-urban areas. Tissue samples (n=812) were collected from wild dogs euthanised from control or research programs conducted in peri-urban and more rural areas. DNA was extracted, seventeen microsatellite loci examined, and allelic data analysed using methods including the Average 3Q score, Paetkau assignment, and Cavalli-Sforza Distance and Nei’s standard distance matrices. Collectively, these results were used to determine the degree of hybridisation of dog populations, and compare the genetic profile of geographically-distinct dog populations. We use the hybridisation distribution of dingoes, hybrid wild dogs, and domestic dogs to determine whether domestic dogs are a major contributor to peri-urban wild dog populations. The genetic profile of geographically distinct populations were compared to determine if a region is likely to be a single/multiple demographic management unit, hypothesise patterns of movement between subpopulations, and examine the potential for any source/sink populations. More importantly, defining subpopulations is useful to determine the appropriate scale and location of management units, to improve the long-term effectiveness of control. Finally, in a novel approach, we examined the identity of the species, genotype, individual, and number of individuals responsible for predation events on wildlife species. Determining the ‘identity’ of individuals preying on wildlife is an increasingly available means to define the problem and thus develop more targeted solutions. This study is part of an Invasive Animals CRC research project

The impacts of wild dogs (Canis lupus dingo and their hybrids) are increasingly being felt by producers and residents throughout the fragmented landscapes of peri-urban areas of north-eastern Australia. Management options are limited in such environs, and confounded by a lack of knowledge of wild dog ecology. Genetics of wild dog populations has been studied generally, but limited information is available from the peri-urban areas. Tissue samples (n=812) were collected from wild dogs euthanised from control or research programs conducted in peri-urban and more rural areas. DNA was extracted, seventeen microsatellite loci examined, and allelic data analysed using methods including the Average 3Q score, Paetkau assignment, and Cavalli-Sforza Distance and Nei’s standard distance matrices. Collectively, these results were used to determine the degree of hybridisation of dog populations, and compare the genetic profile of geographically-distinct dog populations. We use the hybridisation distribution of dingoes, hybrid wild dogs, and domestic dogs to determine whether domestic dogs are a major contributor to peri-urban wild dog populations. The genetic profile of geographically distinct populations were compared to determine if a region is likely to be a single/multiple demographic management unit, hypothesise patterns of movement between subpopulations, and examine the potential for any source/sink populations. More importantly, defining subpopulations is useful to determine the appropriate scale and location of management units, to improve the long-term effectiveness of control. Finally, in a novel approach, we examined the identity of the species, genotype, individual, and number of individuals responsible for predation events on wildlife species. Determining the ‘identity’ of individuals preying on wildlife is an increasingly available means to define the problem and thus develop more targeted solutions. This study is part of an Invasive Animals CRC research project

The impacts of wild dogs (Canis lupus dingo and their hybrids) are increasingly being felt by producers and residents throughout the fragmented landscapes of peri-urban areas of north-eastern Australia. Management options are limited in such environs, and confounded by a lack of knowledge of wild dog ecology. Genetics of wild dog populations has been studied generally, but limited information is available from the peri-urban areas. Tissue samples (n=812) were collected from wild dogs euthanised from control or research programs conducted in peri-urban and more rural areas. DNA was extracted, seventeen microsatellite loci examined, and allelic data analysed using methods including the Average 3Q score, Paetkau assignment, and Cavalli-Sforza Distance and Nei’s standard distance matrices. Collectively, these results were used to determine the degree of hybridisation of dog populations, and compare the genetic profile of geographically-distinct dog populations. We use the hybridisation distribution of dingoes, hybrid wild dogs, and domestic dogs to determine whether domestic dogs are a major contributor to peri-urban wild dog populations. The genetic profile of geographically distinct populations were compared to determine if a region is likely to be a single/multiple demographic management unit, hypothesise patterns of movement between subpopulations, and examine the potential for any source/sink populations. More importantly, defining subpopulations is useful to determine the appropriate scale and location of management units, to improve the long-term effectiveness of control. Finally, in a novel approach, we examined the identity of the species, genotype, individual, and number of individuals responsible for predation events on wildlife species. Determining the ‘identity’ of individuals preying on wildlife is an increasingly available means to define the problem and thus develop more targeted solutions. This study is part of an Invasive Animals CRC research project

The impacts of wild dogs (Canis lupus dingo and their hybrids) are increasingly being felt by producers and residents throughout the fragmented landscapes of peri-urban areas of north-eastern Australia. Management options are limited in such environs, and confounded by a lack of knowledge of wild dog ecology. Genetics of wild dog populations has been studied generally, but limited information is available from the peri-urban areas. Tissue samples (n=812) were collected from wild dogs euthanised from control or research programs conducted in peri-urban and more rural areas. DNA was extracted, seventeen microsatellite loci examined, and allelic data analysed using methods including the Average 3Q score, Paetkau assignment, and Cavalli-Sforza Distance and Nei’s standard distance matrices. Collectively, these results were used to determine the degree of hybridisation of dog populations, and compare the genetic profile of geographically-distinct dog populations. We use the hybridisation distribution of dingoes, hybrid wild dogs, and domestic dogs to determine whether domestic dogs are a major contributor to peri-urban wild dog populations. The genetic profile of geographically distinct populations were compared to determine if a region is likely to be a single/multiple demographic management unit, hypothesise patterns of movement between subpopulations, and examine the potential for any source/sink populations. More importantly, defining subpopulations is useful to determine the appropriate scale and location of management units, to improve the long-term effectiveness of control. Finally, in a novel approach, we examined the identity of the species, genotype, individual, and number of individuals responsible for predation events on wildlife species. Determining the ‘identity’ of individuals preying on wildlife is an increasingly available means to define the problem and thus develop more targeted solutions. This study is part of an Invasive Animals CRC research project

The impacts of wild dogs (Canis lupus dingo and their hybrids) are increasingly being felt by producers and residents throughout the fragmented landscapes of peri-urban areas of north-eastern Australia. Management options are limited in such environs, and confounded by a lack of knowledge of wild dog ecology. Genetics of wild dog populations has been studied generally, but limited information is available from the peri-urban areas. Tissue samples (n=812) were collected from wild dogs euthanised from control or research programs conducted in peri-urban and more rural areas. DNA was extracted, seventeen microsatellite loci examined, and allelic data analysed using methods including the Average 3Q score, Paetkau assignment, and Cavalli-Sforza Distance and Nei’s standard distance matrices. Collectively, these results were used to determine the degree of hybridisation of dog populations, and compare the genetic profile of geographically-distinct dog populations. We use the hybridisation distribution of dingoes, hybrid wild dogs, and domestic dogs to determine whether domestic dogs are a major contributor to peri-urban wild dog populations. The genetic profile of geographically distinct populations were compared to determine if a region is likely to be a single/multiple demographic management unit, hypothesise patterns of movement between subpopulations, and examine the potential for any source/sink populations. More importantly, defining subpopulations is useful to determine the appropriate scale and location of management units, to improve the long-term effectiveness of control. Finally, in a novel approach, we examined the identity of the species, genotype, individual, and number of individuals responsible for predation events on wildlife species. Determining the ‘identity’ of individuals preying on wildlife is an increasingly available means to define the problem and thus develop more targeted solutions. This study is part of an Invasive Animals CRC research project