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An animal body's immune response to viruses might vary depending on various factors. The relationship between 2'-5'-oligoadenylate synthetase like (OASL), interferon alpha (IFN-α), and duck hepatitis A virus type 3 (DHAV-3) virus genome copy number in duck embryo tissues was studied to investigate duck's natural antiviral immunity mechanism. 15-day-old SPF duck embryos were infected with DHAV-3 and their organs and tissues were collected at various times after inoculation. RT real-time PCR was used to determine OASL and IFNA mRNA expression levels and the DHAV-3 copy number. Compared with that at 0 hours, liver OASL transcription increased significantly at 24 hours, and extremely significantly in the liver, heart, gizzard, small intestine, and muscle at 48 hours. The heart had the highest expression level, followed by the liver, with lower expression in the other tissues. There was no significant difference in IFNA expression between the heart and liver at 12 hours, but it started to rise at 24 hours, reaching its maximum at 48 hours. Although IFNA expression increased in the gizzards, small intestines, and muscles, its relative expression levels were lower than those in the heart and liver. In the tissues, the virus genome copy number peaked at 24 hours, and then decreased. The liver had the highest virus genome copy number, followed by the heart. The results implied that the differences in OASL transcription in the tested tissues were similar to those of IFNA. Thus, the immune response (OASL and IFN-α levels) of duck embryos to DHAV-3 shows tissue differences, especially in the liver and heart.
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http://dx.doi.org/10.24425/pjvs.2025.154010 | DOI Listing |
Mol Genet Genomic Med
September 2025
Department of Maternal-Fetal Medicine, Augusta University, Augusta, Georgia, USA.
Introduction: Spinal muscular atrophy (SMA), caused by pathogenic variants in the survival motor neuron (SMN) gene, is the most common genetic cause of mortality in children under the age of two. Prior reports of obstetric sonograms performed in pregnancies with severe forms of fetal SMA have discrepant findings that may stem from a failure to account for the SMN2 copy number.
Methods: We present a neonate diagnosed with SMA type 0 postnatally (0SMN1/1SMN2 genotype).
JDS Commun
September 2025
Livestock Improvement Corporation Ltd., Newstead, Hamilton 3240, New Zealand.
SLICK1 is an allelic variant of the prolactin receptor () that is found in Senepol beef cattle. The presence of a single copy of this allele produces a short hair coat and confers heat tolerance. We aimed to determine the effect of 2 copies of this allele on milking performance of dairy cattle.
View Article and Find Full Text PDFBioimpacts
August 2025
Department of Surgery, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran.
Introduction: Mitochondrial DNA (mtDNA) copy number variations have been reported in multiple human cancers. Previous studies indicate that mitochondrial retrograde signaling regulates , which plays a key role in tumorigenesis, including regulating apoptosis antagonizing transcription factor (). This study investigates the expression of and in relation to mtDNA copy number in invasive ductal carcinoma (IDC) of the breast.
View Article and Find Full Text PDFMol Ecol Resour
September 2025
College of Life Sciences, Henan Normal University, Xinxiang, China.
Miniature inverted-repeat transposable elements (MITEs) are short, non-autonomous class II transposable elements prevalent in eukaryotic genomes, contributing to various genomic and genic functions in plants. However, research on MITEs mainly targets a few species, limiting a comprehensive understanding and systematic comparison of MITEs in plants. Here, we developed a highly sensitive MITE annotation pipeline with a low false positive rate and applied it to 207 high-quality plant genomes.
View Article and Find Full Text PDFMedicine (Baltimore)
September 2025
Diagnosis and Treatment Center for Children, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, Jilin Province, China.
Rationale: Phelan-McDermid syndrome, also known as chromosome 22q13.3 deletion syndrome, is a genetic disorder primarily caused by a chromosome 22q13.3 deletion or mutation.
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