scholarly journals Pathogenicity of field strain of fowl aviadenovirus serotype 11 isolated from chickens with inclusion body hepatitis in Morocco

PLoS ONE ◽  
2021 ◽  
Vol 16 (12) ◽  
pp. e0261284
Author(s):  
Samira Abghour ◽  
Mohamed Mouahid ◽  
Sami Darkaoui ◽  
Jaouad Berrada ◽  
Khalil Zro ◽  
...  
Keyword(s):  
Inclusion Body ◽  
Chicken Embryo Fibroblast ◽  
Fibroblast Cell ◽  
Hepatic Necrosis ◽  
Tissue Homogenate ◽  
Economic Losses ◽  
Chicken Embryo Fibroblast Cell ◽  
Control Group ◽  
Inclusion Body Hepatitis ◽  
Poultry Farms

Outbreaks of inclusion body hepatitis have emerged in Morocco since 2013 and has resulted in significant economic losses to poultry farms. Three isolates of the causative virus, Fowl adenonovirus (FAdV)were characterized from chickens with IBH, but their pathogenicity has never been investigated. In this work, the pathogenicity of an isolate FAdV 11 (MOR300315 strain) was evaluated by inoculating a group of 40 SPF chickens at 3 days of age by oral route. A group of 40 chicks injected with phosphate-buffered saline solution was used as a control group. The infected chickens showed decreased weight gain from 3dpi. Necropsy displayed pallor and enlargement in liver, swelling and slight hemorrhage in kidney and spleen at 6 dpi. Histopathological changes were mainly characterized by severe and extensive hepatic necrosis associated with the presence of basophilic intra-nuclear inclusion bodies within hepatocytes. The FAdV was reisolated in chicken embryo fibroblast cell culture from liver tissue homogenate of infected chicken from 3 to 6 dpi. Viral DNA was detected by PCR in liver, kidney, spleen and cloacal swabs from 3 to 13 dpi. Antibody response against inoculated FAdV was appeared from 9 dpi. These results confirmed that the FAdV 11 strain is pathogenic in chicken. This study is the first experimental infection of FAdV 11 in chicken in Morocco, which increase our understanding of its pathogenicity in chickens and indicate that preventive measures against FAdV infection in poultry farms should be implemented in Morocco.

scholarly journals Cholesterol-25-hydroxylase Is a Chicken ISG That Restricts ALV-J Infection by Producing 25-hydroxycholesterol

Viruses ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 498 ◽  
Author(s):  
Tingting Xie ◽  
Min Feng ◽  
Manman Dai ◽  
Guodong Mo ◽  
Zhuohao Ruan ◽  
...  
Keyword(s):  
Core Promoter ◽  
Chicken Embryo Fibroblast ◽  
Antiviral Agent ◽  
Distinct Group ◽  
Fibroblast Cell ◽  
Economic Losses ◽  
Chicken Embryo Fibroblast Cell ◽  
Interferon Α ◽  
Type I ◽  
Peripheral Blood Mononuclear

The avian leukosis virus subgroup J (ALV-J) belongs to the chicken retrovirus that causes enormous economic losses in the poultry industry. Interferon-stimulated genes (ISGs) are critical for controlling virus infections. Here, we identified 897 type I ISGs induced by interferon-α (IFN-α) in chicken peripheral blood mononuclear cell (PBMC) by RNA-Seq. In addition, we further identified 152 potential anti-ALV-J chicken type I ISGs. Among these potential anti-ALV-J ISGs, chicken cholesterol 25-hydroxylase (chCH25H) was selected for further antiviral mechanism studies in chicken embryo fibroblast cell lines (DF1). The gene chCH25H is located on chromosome 6 and clustered in a distinct group with mammals CH25H in the phylogenetic tree. The core promoter region of chCH25H was located within −75/−1 sequence. We found that chCH25H was induced by chicken IFN-α and ALV-J in DF1 cells. The overexpression of chCH25H significantly inhibited ALV-J replication in DF1 cells at 48 h post infection (hpi). In addition, ALV-J replication was significantly enhanced in the chCH25H- knockout DF1 cells. Furthermore, we demonstrated that chCH25H restricted ALV-J infection through the production of 25-hydroxycholesterol (25HC), rather than type I and II interferon. Our results identified 152 potential anti-ALV-J chicken type I ISGs and revealed that 25HC, the product of chCH25H, could be used as a natural antiviral agent to control ALV-J infection.

scholarly journals Role of Interferon Antagonist Activity of Rabies Virus Phosphoprotein in Viral Pathogenicity

2010 ◽  
Vol 84 (13) ◽  
pp. 6699-6710 ◽  
Author(s):  
Naoto Ito ◽  
Gregory W. Moseley ◽  
Danielle Blondel ◽  
Kenta Shimizu ◽  
Caitlin L. Rowe ◽  
...  
Keyword(s):  
Rabies Virus ◽  
Nuclear Export ◽  
Nuclear Translocation ◽  
Chicken Embryo Fibroblast ◽  
Fibroblast Cell ◽  
Chicken Embryo Fibroblast Cell ◽  
Adult Mice ◽  
P Gene ◽  
P Protein ◽  
P Proteins

ABSTRACT The fixed rabies virus (RV) strain Nishigahara kills adult mice after intracerebral inoculation, whereas the chicken embryo fibroblast cell-adapted strain Ni-CE causes nonlethal infection in adult mice. We previously reported that the chimeric CE(NiP) strain, which has the phosphoprotein (P protein) gene from the Nishigahara strain in the genetic background of the Ni-CE strain, causes lethal infection in adult mice, indicating that the P gene is responsible for the different pathogenicities of the Nishigahara and Ni-CE strains. Previous studies demonstrated that RV P protein binds to the interferon (IFN)-activated transcription factor STAT1 and blocks IFN signaling by preventing its translocation to the nucleus. In this study, we examine the molecular mechanism by which RV P protein determines viral pathogenicity by comparing the IFN antagonist activities of the Nishigahara and Ni-CE P proteins. The results, obtained from both RV-infected cells and cells transfected to express P protein only, show that Ni-CE P protein is significantly impaired for its capacity to block IFN-activated STAT1 nuclear translocation and, consequently, inhibits IFN signaling less efficiently than Nishigahara P protein. Further, it was demonstrated that a defect in the nuclear export of Ni-CE P protein correlates with a defect in its ability to cause the mislocalization of STAT1. These data provide the first evidence that the capacity of the RV P protein to inhibit STAT1 nuclear translocation and IFN signaling correlates with the viral pathogenicity.

scholarly journals Inclusion body hepatitis associated with an outbreak of fowl adenovirus type 2 and type 8b in broiler flocks in South Africa

2014 ◽  
Vol 85 (1) ◽  
Author(s):  
Louis H. Maartens ◽  
Hilda W. Joubert ◽  
Henry Aitchison ◽  
Estelle H. Venter
Keyword(s):  
Sequence Analysis ◽  
Nucleotide Sequence ◽  
Inclusion Body ◽  
Virus Isolation ◽  
Adenovirus Type ◽  
Hepatic Necrosis ◽  
Splenic Tissue ◽  
Nucleotide Sequence Analysis ◽  
Fowl Adenovirus ◽  
Inclusion Body Hepatitis

Inclusion body hepatitis is an acute disease of chickens ascribed to viruses of the genus Aviadenovirus and referred to as fowl adenovirus (FAdV). There are 12 FAdV types (FAdV1to FAdV8a and FAdV8b to FAdV11), classified into five species based on their genotype (designated FAdVA to FAdVE). A total of 218 000 chickens, 2–29 days of age, were affected over a 1-year period, all testing positive by microscopy, virus isolation and confirmation with polymerase chain reaction (PCR). Affected birds were depressed, lost body weight,were weak and had watery droppings. Pathological changes observed during necropsy indicated consistent changes in the liver, characterised by hepatomegaly, cholestasis and hepatitis. Lesions were also discernible in the spleen, kidney and gizzard wall and were characterised by splenomegaly, pinpoint haemorrhages, nephritis with haemorrhage,visceral gout and serosal ecchymosis of the gizzard wall. Histopathological lesions were most consistently observed in the liver but could also be seen in renal and splenic tissue. Virus isolation was achieved in embryonated eggs and most embryos revealed multifocalto diffuse hepatic necrosis, with a mixed cellular infiltrate of macrophages and heterophils(necro-granulomas), even in the absence of macroscopic pathology. Virus isolation results were verified by histopathology and PCR on embryonic material and further characterised by nucleotide sequence analysis. Two infectious bursal disease virus isolates were also made from the Klerksdorp flock. Nucleotide sequence analysis of the L1 hexon loop of all the FAdV isolates indicated homology (99%) with prototype strains P7-A for FAdV-2, as well as for FAdV-8b.

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