ArticleJournal of genomics2017
CNV Analysis of Host Responses to Porcine Reproductive and Respiratory Syndrome Virus Infection.
Article in Journal of genomics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Copy number variant-based genome wide association study reveals immune-related genes associated with parasite resistance in a heritage sheep breed from the United States.Parasite immunology · 2022Article
- Classical, Molecular, and Genomic Cytogenetics of the Pig, a Clinical Perspective.Animals : an open access journal from MDPI · 2021Review
- CNV analysis of Meishan pig by next-generation sequencing and effects ofJournal of animal science and biotechnology · 2020Article
- Porcine Interferon Complex and Co-Evolution with Increasing Viral Pressure after Domestication.Viruses · 2019Review
- A Survey of Copy Number Variation in the Porcine Genome Detected From Whole-Genome Sequence.Frontiers in genetics · 2019Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Porcine reproductive and respiratory syndrome (PRRS) is a devastating disease with a significant impact on the swine industry causing major economic losses. The objective of this study is to examine copy number variations (CNVs) associated with the group-specific host responses to PRRS virus infection. We performed a genome-wide CNV analysis using 660 animals genotyped with on the porcine SNP60 BeadChip and discovered 7097 CNVs and 271 CNV regions (CNVRs). For this study, we used two established traits related to host response to the virus, i.e. viral load (VL, area under the curve of log-transformed serum viremia from 0 to 21 days post infection) and weight gain (WG42 from 0 to 42 days post infection). To investigate the effects of CNVs on differential host responses to PRRS, we compared groups of animals with extreme high and low estimated breeding values (EBVs) for both traits using a case-control study design. For VL, we identified 163 CNVRs (84 Mb) from the high group and 159 CNVRs (76 Mb) from the low group. For WG42, we detected 126 (68 Mb) and 156 (79 Mb) CNVRs for high and low groups, respectively. Based on gene annotation within group-specific CNVRs, we performed network analyses and observed some potential candidate genes. Our results revealed these group-specific genes are involved in regulating innate and acquired immune response pathways. Specifically, molecules like interferons and interleukins are closely related to host responses to PRRS virus infection.
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Registered trials
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