Novel duck reovirus exhibits pathogenicity to specific pathogen-free chickens by the subcutaneous route.
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ABSTRACT:
SUBMITTER: Yu K
PROVIDER: S-EPMC8175558 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Avian reoviruses (ARVs) are ubiquitous in domestic poultry with 80% of them being non-pathogenic and they are frequently found in clinically healthy birds. ARVs have also been known to be the etiological agents of viral arthritis (VA), tenosynovitis, myocarditis, runting-stunting syndrome (RSS), and respiratory and enteric disease in chickens. Significant economic losses during the process of poultry husbandry are due, in part, to unmitigated ARV infections throughout the poultry industry. Recently, many isolates shared genetic similarities between those recovered from wild birds and those recovered from poultry. One explanation may be that there is a degree of spillover and spillback of ARVs between the two groups. However, studies on the role of wild birds in the epidemiology and pathogenicity of ARVs are insufficient. Here, we describe the pathogenicity in specific pathogen-free (SPF) chickens of ARV originating from wild birds. The challenge experiment was conducted in six groups including a negative control group, a positive control group (reference strain of S1133), and four groups (A15-157, A18-13, A18-205, A19-106) infected with ARVs from wild birds. The 7-day-old SPF chickens were inoculated with 106TCID50 ARV to evaluate the clinical signs, changes in weight gain, gross lesions, histological changes, virus replication, and serum antibody levels. The peak of clinical signs was from 3 to 5 days post infection (dpi). In addition, the death of one chicken was found in the group infected with the A18-13 isolate. Reduced body weight was also found in chickens infected with ARVs from wild birds compared to the negative control group. All the ARVs infection groups showed noticeable swelling of the footpad. In addition, ARVs were detected in the bursa, tendon, and hock joint by reverse transcription-polymerase chain reaction (RT-PCR) in all infected groups at 5 and 15 dpi. Histopathological observations revealed acute inflammatory responses on the synovium covering the joint surfaces (arthritis) and tendon sheaths (tenosynovitis), as well as bursa atrophy and lymphocyte depletion. The analysis of the humoral response was performed by ELISA assay, and chickens infected with ARVs showed seroconverted. In conclusion, this study described the typical severe disease of acute VA and tenosynovitis in SPF chickens infected with ARVs derived from wild birds. This study confirmed the pathogenicity of ARVs infection in SPF chickens for the first time, and these results enrich our understanding of the pathogenicity of ARVs derived from wild birds.
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Project description:Hypervirulent fowl adenovirus serotype 4 (hvFAdV-4) has emerged as a major pathogen of hepatitis-hydropericardium syndrome (HHS) with increased mortality in chickens, resulting in economic losses to the Chinese poultry industry since June 2015. Here, we isolated a hypervirulent FAdV-4 (hvFAdV-4) strain (designated GD616) from 25-day-old meat-type chickens with severe HHS in Guangdong Province China in June 2017. The whole genome of the strain GD616 shares high homology with those in the recently-reported hvFAdV-4 isolates in China, with natural deletions of ORF19 and ORF27. A comparative analysis of Hexon and Fiber-2 proteins revealed that 2 unique amino acid residues at positions 378 and 453 of the Fiber-2 protein might be associated with virulence due to their occurrences in all the hvFAdV-4 isolates only. To systemically evaluate the effect of age on the susceptibility of chickens to hvFAdV-4, we used this hvFAdV-4 strain to intramuscularly inoculate 7- to 180-day-old specific-pathogen-free chickens for the evaluation of pathogenicity. These results showed that the pathogenicity of the hvFAdV-4 strain GD616 to chickens exhibited age-relatedness, with younger than 59-day-old chickens showing 100% morbidity and mortality, while 180-day-old chickens still exhibited a hydropericardium syndrome-like clinicopathology with 60% morbidity and 20% mortality. These findings enrich the current available knowledge regarding the pathogenicity of the hypervirulent FAdV-4 virus in chickens with a wide range of ages, which assists with the selection of suitable-aged chickens for the evaluation of hvFAdV-4 vaccines.
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Project description:The novel duck reovirus (NDRV) emerged in southeast China in 2005. The virus causes severe liver and spleen hemorrhage and necrosis in various duck species, bringing serious harm to waterfowl farming. In this study, three strains of NDRV designated as NDRV-ZSS-FJ20, NDRV-LRS-GD20, and NDRV-FJ19 were isolated from diseased Muscovy ducks in Guangdong and Fujian provinces. Pairwise sequence comparisons revealed that the three strains were closely related to NDRV, with nucleotide sequence identities for 10 genomic fragments ranging between 84.8 and 99.8%. In contrast, the nucleotide sequences of the three strains were only 38.9-80.9% similar to the chicken-origin reovirus and only 37.6-98.9% similar to the classical waterfowl-origin reovirus. Similarly, phylogenetic analysis revealed that the three strains clustered together with NDRV and were significantly different from classical waterfowl-origin reovirus and chicken-origin reovirus. In addition, the analyses showed that the L1 segment of the NDRV-FJ19 strain was a recombinant of 03G and J18 strains. Experimental reproduction of the disease showed that the NDRV-FJ19 strain was pathogenic to both ducks and chickens and could lead to symptoms of hemorrhage and necrosis in the liver and spleen. This was somewhat different from previous reports that NDRV is less pathogenic to chickens. In conclusion, we speculated that the NDRV-FJ19 causing duck liver and spleen necrosis is a new variant of a duck orthoreovirus that is significantly different in pathogenicity from any previously reported waterfowl-origin orthoreovirus.
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Project description:In this study, Kunming mice were used as the animal models to study the pathogenicity of TMUV. Three groups of 3-week-old female Kunming mice (n = 15 mice per group) were infected with the SDSG strain of TMUV in 50 ?L allantoic fluid (10(4.8) ELD50/0.2 ml) respectively by the intracerebral (i.c.), subcutaneous (s.c.) and intranasal (i.n.) routes. The control group (n = 15 mice) was inoculated with 50 ?L sterile phosphate-buffered saline. Clinical signs, gross, and microscopic lesions, viral loads in different tissues, and serum antibody titers were examined and recorded. Kunming mice infected intracerebrally showed typical clinical symptoms, including severe hindlimb paralysis, weight loss and death. Only dead mice presented severe intestinal mucosal edema. No gross lesions were observed in mice sequentially euthanized. However, microscopic lesions in the brain, spleen, liver, kidney, and lung were very typical including varying degrees of viral encephalitis, lymphocytes depletion, liver cell necrosis and nephritis, etc. Viral loads in different tissues were detected by the SYBR Green I real-time PCR assay. Viral loads in the brain, liver, and spleen were first detected and maintained a longer time, which indicated that these organs may be the target organs of TMUV. The level of viral loads was consistent with the severity of clinical signs and microscopic lesions in different tissues. The neutralizing antibody began to seroconvert at 8 dpi. Clinical signs, microscopic lesions, viral loads and serum neutralizing antibodies weren't observed in other groups. In summary, TMUV can cause systemic infections and death in Kunming mice by i.c., which provides some experimental basis for further study of the significance of TMUV in public health.
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Project description:In March 2017, H7N9 highly pathogenic avian influenza (HPAI) virus was detected in 2 broiler breeder farms in the state of Tennessee, USA. Subsequent surveillance detected the low pathogenicity avian influenza (LPAI) virus precursor in multiple broiler breeder farms and backyard poultry in Tennessee and neighboring states. The pathogenesis of the H7N9 LPAI virus was investigated in commercial broiler breeders, the bird type mostly affected in this outbreak. Infectivity, transmissibility, and pathogenesis of the H7N9 HPAI and LPAI viruses were also studied in 4-week-old specific pathogen free (SPF) leghorn chickens. The mean bird infectious doses (BID50) for the LPAI isolate was 5.6 log10 mean egg infectious dose (EID50) for broiler breeders and 4.3 log10 EID50 for SPF layer chickens, and no transmission to contact-exposed birds was observed. In both bird types, virus shedding was almost exclusively from the oropharyngeal route. These findings suggest sub-optimal adaptation for sustained transmission with the H7N9 LPAI isolate, indicating that factors other than the birds genetic background may explain the epidemiology of the outbreak. The BID50 for the HPAI isolate in SPF layer chickens was more than 2 logs lower (<2 log10 EID50) than the LPAI isolate. Also, the HPAI virus was shed by both the oropharyngeal and cloacal routes and transmitted to contacts. Greater susceptibility and easier transmission of the H7N9 HPAI virus are features of the HP phenotype that could favor the spread of HPAI over LPAI viruses during outbreaks.
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Project description:Novel Duck Reovirus (NDRV) that has been found throughout the world in waterfowl, and it has been extensively described. Here, we report the complete genome sequence of a NDRV strain isolated in China called NDRV YF10. This strain was collected from 87 samples with infected ducks in South Coastal Area. The NDRV genome consists of 23,419 bp. With the assistance of computer analysis, the promoter and terminator of each gene segment and 10 viral genes segments were identified, which encode polypeptides ranging from 98 to 1,294 amino acids. All gene fragments of this virus strain were determined and compared to previously reported strains, revealing genetic variation with similarity rates ranging from 96 to 99% for each gene segment. Each gene segment formed 2 host-associated groups, the waterfowl-derived reovirus and the avian-derived reovirus, except for the S1 gene segment, which was closely related to ARV evolution and formed a host-independent subcluster. This difference may be due to Avian Reovirus (ARV) evolving in a host-dependent manner. In order to evaluate the pathogenicity of YF10, a novel isolated strain of NDRV was tested in 2 types of ducks. It was observed that the YF10 isolated strain exhibits varying degrees of virulence, highlighting the potential risk posed to different types of ducks. In conclusion, our findings emphasize the importance of epidemiology studies, molecular characterization, and prevention of NDRV in waterfowl.
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Project description:Since September 2020, the clinical symptoms of Muscovy duck spleen spots have appeared in Guangdong, Guangxi, Jiangxi, Hunan, Hubei, and other provinces, resulting in a large number of Muscovy duck deaths and great economic losses. The absence of the typical clinical symptoms caused by pathogenic microorganisms makes the cause of the spotted spleen a mystery. High-throughput sequencing results suggested that Riemerella anatipestifer (R. anatipestifer) may be the pathogen. Then, R. anatipestifer was regarded as the research target for isolation, identification, and pathogenicity assessment. After biochemical test, PCR amplification, and serotype determination, it was confirmed that the isolated strain CZG-1 was serotype 15 R. anatipestifer. Typical spotted spleen symptoms were observed after CZG-1 infection. Furthermore, drug sensitivity assays showed the similar drug-resistant spectrum of R. anatipestifer serotype 15 to other serotypes; for example, all test strains were resistant to polymyxin, gentamicin, and neomycin. The CZG-1 strain has high pathogenicity, and its lethal dose of 50% (LD50) is 35.122 CFU/ml. Virulence gene determination showed that the CZG-1 strain had at least five virulence genes, bioF, TSS9-1, TSS9-2, PncA, and 0373Right. Above all, this study identified and proved that the pathogen of spotted spleen in ducks was R. anatipestifer serotype 15, which caused death of ducks without the typical symptoms of bacterial infection. The results of this study enriched the knowledge of symptom after R. anatipestifer infection, provided a reference to the identification of the pathogen of spotted spleen, and provided theoretical basis for prevention and control of spotted spleen.
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Project description:This study aimed to investigate the effects of selenide chitosan sulfate (Se-CTS-S) on glutathione (GSH) system in hepatocytes and chickens. Chitosan, sodium selenite (Na2SeO3), selenide chitosan, chitosan sulfate (CTS-S), and Se-CTS-S were added to the culture medium and the basal diets; glutathione peroxidase (GSH-Px) activity, GSH content, total antioxidant capacity (T-AOC), and mRNA levels of cellular GPx (GPx-1) and phospholipid hydroperoxide GPx (GPx-4) in vivo and in vitro were determined. The results showed that Se-CTS-S increased (P < 0.05) GPx-1 and GPx-4 mRNA levels in hepatocytes and livers, and GSH-Px activity, GSH content, and T-AOC in the medium, hepatocytes, plasma, and livers compared with the control and chitosan treatments. Compared with CTS-S, Se-CTS-S treatments increased (P < 0.05) GPx-1 and GPx-4 mRNA levels in hepatocytes and livers, and GSH-Px activity, GSH content, and T-AOC capacity in the medium, hepatocytes, and livers. Compared with Na2SeO3 and CTS-Se, Se-CTS-S increased (P < 0.05) GPx-1 mRNA levels in hepatocytes and livers, GPx-4 mRNA levels in hepatocytes and livers, GSH-Px activity in the medium, hepatocytes, and livers, GSH contents in plasma and livers, and T-AOC in the medium, plasma, and livers. Thus, Se-CTS-S showed better biological activity that mainly benefited from the synergistic effects of Se and sulfate on GSH system.
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Project description:Chicken parvovirus (ChPV) is an agent frequently associated with runting stunting syndrome (RSS). This syndrome has been reported in association with ChPV in many countries, including Brazil; however, studies characterizing the virus on a molecular level are scarce, and ChPV pathogenicity in day-old chicks remains unclear. The aim of the present work was to establish the molecular characteristics of ChPV, determine the pathogenicity of ChPV in SPF chicks and detect and quantify ChPV by qPCR in several tissues and chicks of different ages. The experimental challenge was performed at one day of age, and daily and weekly observations were performed and five birds from each experimental group (mock and infected birds) were euthanized to perform the different analysis. ChPV genome copies were detected and quantified by qPCR in gut, spleen, thymus, kidney, pancreas, proventriculus and bursa. Clinically, the infected group presented with diarrhea 24 h post-infection, which persisted until 42 days of age. The small intestine was distended, and its contents were aqueous and foamy. Enteritis and dilated crypts with cyst shapes were observed in intestinal segments. Acute pancreatitis associated with lymphocytic nodules, infiltrating lymphocytes and plasma cells between the pancreatic acinus was observed. Koch's postulate was demonstrated and the genetic characterization of the VP1 gene showed that the Brazilian ChPV isolate belongs to the ChPV II group.
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Project description: Not available
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