Epidemiological and molecular retrospective analysis of porcine circovirus 3 in the US grower-finisher herd

IF 2.6 4区 医学 Q3 INFECTIOUS DISEASES
Molly Kroeger , Christopher James Stott , Huigang Shen , Ganwu Li , Rodger Main , Eric Bush , Margaret Parker , Dachrit Nilubo , Jean Paul Cano , Jack Creel , Pablo Piñeyro
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引用次数: 0

Abstract

Porcine circovirus type 3 (PCV3) was identified in 2016 and has since been associated with reproductive failure, multisystemic inflammation, and subclinical infection in swine. Numerous countries have retrospectively detected the presence of PCV3 before its first clinical description in 2016. The reported detection rate of PCV3 has varied from 6.5 to 84 % in pigs with various coinfections. Today, PCV3/PCV2 coinfection is commonly observed. However, the PCV3 prevalence and coinfection rate with PCV2 in the US swine industry had not been reported before 2016. The present study used serum samples from US grower finisher farms from 2000, 2006, and 2012 to determine the PCV3 and PCV3/PCV2 farm prevalence and geographical distribution, to evaluate the PCV3 evolutionary rate and selection pressure forces, and to identify structural and morphological changes in the Cap protein. Our findings revealed that PCV3 was endemic in the US swine industry before its first description in 2016. The PCV3 farm prevalence decreased from 47 % in 2000 to 22 % in 2012. The PCV3/PCV2 coinfection rate at the farm level was 47 % in 2000 and 39 % in 2006. After the introduction of PCV2 vaccines in 2006, the PCV3/PCV2 coinfection rate drastically declined to 3 % and 59 % of farms were negative for both PCV3 and PCV2 in 2012. From 13 PCV3 whole genome sequences, 12 sequences were clustered with PCV3a reference strain and one with the PCV3c subtype. From 28 PCV3 ORF2 sequences, PCV3a1 (1/28), PCV3a2 (4/28), PCV3a3 (19/28), PCV3b (2/28), and PCV3c (2/28) subtypes were obtained. ORF2 nucleotide identity ranged from 97.8 to 100 %. Diversifying selection occurred at amino acids 24 and 150 in 2006 and at amino acids 24 and 27 in 2012. Mutations A24V and R27K were common among all PCV3 subtypes in sequences identified in the present study and in reference sequences. Both the S77T and I150L mutation was common among sequences within the PCV3a2 subtype. The F104Y mutation lies within a predicted T-cell epitope and was present in sequences of the PCV3c, PCV3b, and PCV3a3 subtypes. Cap molecular modeling revealed that the structural folding of amino acids 24 and 27 changed from alpha helix to coiled in 2012 sequences. Thus, this study broadens current knowledge of PCV3's prevalence and molecular evolution in the US swine herd from 2000 to 2012.
美国种育猪群猪圆环病毒3型的流行病学和分子回顾性分析
猪圆环病毒3型(PCV3)于2016年被发现,此后与猪的生殖衰竭、多系统炎症和亚临床感染有关。在2016年首次临床描述之前,许多国家回顾性地发现了PCV3的存在。据报道,在各种合并感染的猪中,PCV3的检出率从6.5%到84%不等。今天,PCV3/PCV2合并感染是常见的。然而,在2016年之前,美国养猪业中PCV3的流行率和PCV2的合并感染率未见报道。本研究利用2000年、2006年和2012年美国育肥场的血清样本,确定了PCV3和PCV3/PCV2农场的流行情况和地理分布,评估了PCV3的进化速度和选择压力,并确定了Cap蛋白的结构和形态变化。我们的研究结果显示,在2016年首次描述之前,PCV3在美国养猪业中是地方性的。猪场PCV3流行率从2000年的47%下降到2012年的22%。2000年猪场PCV3/PCV2合并感染率为47%,2006年为39%。在2006年引入PCV2疫苗后,PCV3/PCV2合并感染率急剧下降至3%,2012年59%的农场对PCV3和PCV2均呈阴性。从13条PCV3全基因组序列中,12条序列与PCV3a参考菌株聚类,1条序列与PCV3c亚型聚类。从28个PCV3 ORF2序列中获得PCV3a1(1/28)、PCV3a2(4/28)、PCV3a3(19/28)、PCV3b(2/28)和PCV3c(2/28)亚型。ORF2核苷酸的识别范围为97.8% ~ 100%。2006年在第24和150号氨基酸上发生了多样化选择,2012年在第24和27号氨基酸上发生了多样化选择。突变A24V和R27K在本研究鉴定的序列和参考序列中所有PCV3亚型中都很常见。在PCV3a2亚型的序列中,S77T和I150L突变都很常见。F104Y突变位于预测的t细胞表位内,存在于PCV3c, PCV3b和PCV3a3亚型序列中。Cap分子模型显示,在2012年序列中,氨基酸24和27的结构折叠由α螺旋变为卷曲。因此,本研究拓宽了目前对2000年至2012年美国猪群中PCV3的流行和分子进化的认识。
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来源期刊
Infection Genetics and Evolution
Infection Genetics and Evolution 医学-传染病学
CiteScore
8.40
自引率
0.00%
发文量
215
审稿时长
82 days
期刊介绍: (aka Journal of Molecular Epidemiology and Evolutionary Genetics of Infectious Diseases -- MEEGID) Infectious diseases constitute one of the main challenges to medical science in the coming century. The impressive development of molecular megatechnologies and of bioinformatics have greatly increased our knowledge of the evolution, transmission and pathogenicity of infectious diseases. Research has shown that host susceptibility to many infectious diseases has a genetic basis. Furthermore, much is now known on the molecular epidemiology, evolution and virulence of pathogenic agents, as well as their resistance to drugs, vaccines, and antibiotics. Equally, research on the genetics of disease vectors has greatly improved our understanding of their systematics, has increased our capacity to identify target populations for control or intervention, and has provided detailed information on the mechanisms of insecticide resistance. However, the genetics and evolutionary biology of hosts, pathogens and vectors have tended to develop as three separate fields of research. This artificial compartmentalisation is of concern due to our growing appreciation of the strong co-evolutionary interactions among hosts, pathogens and vectors. Infection, Genetics and Evolution and its companion congress [MEEGID](http://www.meegidconference.com/) (for Molecular Epidemiology and Evolutionary Genetics of Infectious Diseases) are the main forum acting for the cross-fertilization between evolutionary science and biomedical research on infectious diseases. Infection, Genetics and Evolution is the only journal that welcomes articles dealing with the genetics and evolutionary biology of hosts, pathogens and vectors, and coevolution processes among them in relation to infection and disease manifestation. All infectious models enter the scope of the journal, including pathogens of humans, animals and plants, either parasites, fungi, bacteria, viruses or prions. The journal welcomes articles dealing with genetics, population genetics, genomics, postgenomics, gene expression, evolutionary biology, population dynamics, mathematical modeling and bioinformatics. We also provide many author benefits, such as free PDFs, a liberal copyright policy, special discounts on Elsevier publications and much more. Please click here for more information on our author services .
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