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Hydropericardium syndrome (HPS) is one of the important emerging diseases causing huge losses to the poultry industry. It affects mainly 3- to 6-week-old broiler chickens and rarely occurs in breeding and laying flocks. Recently, an HPS case was recorded with a sudden heavy mortality in a 100-day-old laying flock. A fowl adenovirus serotype 4 (FAdV-4), named as GDMZ strain, was isolated and identified using polymerase chain reaction coupled with electron microscopy. The animal experiment showed that a mortality of 100% was recorded with hydropericardium as a conspicuous lesion throughout the course of infection. Microscopically, vacuolar changes and intranuclear inclusion bodies were observed in the liver and vacuolar changes were observed in the heart. The complete genome sequence of GDMZ strain was determined to investigate the molecular properties of GDMZ strain. The comparative analysis revealed that the novel Chinese FAdV-4 isolate contained open reading frame (ORF) 19, ORF27, and ORF48 genomic deletions. The phylogenetic analysis revealed that FAdV-4 could be divided into two major clades, of which Chinese FAdV-4 were located at a distinct clade.
Hydropericardium syndrome (HPS) is one of the important emerging diseases causing huge losses to the poultry industry. It affects mainly 3- to 6-week-old broiler chickens and rarely occurs in breeding and laying flocks. Recently, an HPS case was recorded with a sudden heavy mortality in a 100-day-old laying flock. A fowl adenovirus serotype 4 (FAdV-4), named as GDMZ strain, was isolated and identified using polymerase chain reaction coupled with electron microscopy. The animal experiment showed that a mortality of 100% was recorded with hydropericardium as a conspicuous lesion throughout the course of infection. Microscopically, vacuolar changes and intranuclear inclusion bodies were observed in the liver and vacuolar changes were observed in the heart. The complete genome sequence of GDMZ strain was determined to investigate the molecular properties of GDMZ strain. The comparative analysis revealed that the novel Chinese FAdV-4 isolate contained open reading frame (ORF) 19, ORF27, and ORF48 genomic deletions. The phylogenetic analysis revealed that FAdV-4 could be divided into two major clades, of which Chinese FAdV-4 were located at a distinct clade.
Avian reovirus (ARV) is a cause of infections of broiler and turkey flocks, as well as waterfowl birds. This case report describes a reovirus detection in a fattening goose flock. GRV-infected geese suffer from severe arthritis, tenosynovitis, pericarditis, depressed growth, or runting-stunting syndrome (RSS), malabsorption syndrome, and respiratory and enteric diseases. GRV (goose reovirus) caused pathological lesions in various organs and joints, especially in the liver and spleen. GRV infection causes splenic necrosis, which induces immunosuppression, predisposing geese to infection with other pathogens, which could worsen the disease and lead to death. Our results showed that GRV was detected via RT-PCR and isolated in SPF (Specific Pathogen Free) embryos. This is the first report of the involvement of reovirus in arthritis, and the generalized infection of young geese in Poland, resulting in pathological changes in internal organs and sudden death. This study also provides new information about the GRV, a disease that is little known and underestimated.
Major histocompatibility complex class I (MHC-I) molecules play a critical role in the host’s antiviral response by presenting virus-derived antigenic peptides to cytotoxic T lymphocytes (CTLs), enabling the clearance of virus-infected cells. Human adenoviruses evade CTL-mediated cell lysis, in part, by interfering directly with the MHC-I antigen presentation pathway through the expression of E3-19K, which binds both MHC-I and the transporter associated with antigen processing protein and sequestering MHC-I within the endoplasmic reticulum. Fowl adenoviruses have no homologues of E3-19K. Here, we show that representative virus isolates of the species Fowl aviadenovirus C, Fowl aviadenovirus D, and Fowl aviadenovirus E downregulate the cell surface expression of MHC-I in chicken hepatoma cells, resulting in 71%, 11%, and 14% of the baseline expression level, respectively, at 12 h post-infection. Furthermore, this work reports that FAdV-9 downregulates cell surface MHC-I through a minimum of two separate mechanisms—a lysosomal-independent mechanism that requires the presence of the fowl adenovirus early 1 (FE1) transcription unit located within the left terminal genomic region between nts 1 and 6131 and a lysosomal-dependent mechanism that does not require the presence of FE1. These results establish a new functional role for the FE1 transcription unit in immune evasion. These studies provide important new information about the immune evasion of FAdVs and will enhance our understanding of the pathogenesis of inclusion body hepatitis and advance the progress made in next-generation FAdV-based vectors.
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