ALV-J-contaminated commercial live vaccines induced pathogenicity in Three-Yellow chickens: one of the transmission routes of ALV-J to commercial chickens.
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ABSTRACT:
SUBMITTER: Wang P
PROVIDER: S-EPMC8258576 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:One avian leukosis virus of subgroup J (ALV-J) strain GX14YYA1 was isolated from a commercial bivalent Newcastle disease (ND)-infectious bronchitis (IB) vaccine in our previous study. To evaluate the pathogenicity of the ALV-J-contaminated vaccine on commercial chickens, day-old Three-Yellow chicks in group I were vaccinated with ALV-J-contaminated bivalent ND-IB live vaccine by intranasal and eye drop at 1-day-old for the primary vaccination and at 7-day-old for the secondary vaccination. Groups II and III were kept as the normal vaccination group with the noncontaminated ND-IB vaccine and blank control groups, respectively. The birds of different groups were maintained separately in isolators for 175 d. The first viremia was detected at 4 wk of age and 20% (2/10) of the birds maintained viremia during 11 to 25 wk of age. At the same time, the birds in group I experienced a significant suppression of body weight gain when compared with those of groups II and III (P < 0.05). In addition, the birds in group I showed obvious ALV-J hemangioma-type anatomical lesions in the liver and tumors were observed in the abdominal cavity. The results demonstrated that the ALV-J contaminated commercial live vaccines can induce pathogenicity in commercial Three-Yellow chickens and indicate that ALV-J-contaminated commercial live vaccines could be one of the transmission routes of ALV-J to commercial chickens.
| S-EPMC7921873 | biostudies-literature
Project description:One natural recombinant avian leukosis virus (ALV) strain GX14DJ3-18 was isolated from a native gamecock by DF-1 cell culture and identified with Polymerase Chain Reaction (PCR), immunofluorescence assay and the viral genome's nucleotide sequencing. This strain was revealed as a novel recombinant virus with nucleotide sequence similarities of 95.4% Long Terminal Repeated (LTR), 95.8% 5', UTR, 97.9% gag, and 92.9% 3'untranslated regions (UTR) in ALV-J. Also we found sequence similarities of 99.3% pol and 99.0% gp37 in ALV-E, and 89.9% gp85 in ALV-A. The simulated congenital infection with GX14DJ3-18 in Three-Yellow chickens exhibited a significant negative effect on the development of immune organs (P < 0.05). Also, lower antibody responses were found to vaccinations with the commercial vaccines of Newcastle disease virus and with subtypes H5 and H9 of avian influenza virus (P < 0.05). The incidence of tumor or tumor-like lesions in the challenged birds was 14.28% (5/35), while none were observed in the un-challenged control group (0/35). These results suggested that GX14DJ3-18 is a novel recombinant ALV that can induce pathogenicity in the commercial Three-Yellow chickens. We speculated that cross-provincial sales of gamecocks in which ALVs have not been eradicated thoroughly might be a potential route for the transmission of ALVs to commercial chickens.
| S-EPMC6870561 | biostudies-literature
Project description:Yellow fever is a vector-borne disease endemic in tropical regions of Africa, where 90% of the global burden occurs, and Latin America. It is notoriously under-reported with uncertainty arising from a complex transmission cycle including a sylvatic reservoir and non-specific symptom set. Resulting estimates of burden, particularly in Africa, are highly uncertain. We examine two established models of yellow fever transmission within a Bayesian model averaging framework in order to assess the relative evidence for each model's assumptions and to highlight possible data gaps. Our models assume contrasting scenarios of the yellow fever transmission cycle in Africa. The first takes the force of infection in each province to be static across the observation period; this is synonymous with a constant infection pressure from the sylvatic reservoir. The second model assumes the majority of transmission results from the urban cycle; in this case, the force of infection is dynamic and defined through a fixed value of R0 in each province. Both models are coupled to a generalised linear model of yellow fever occurrence which uses environmental covariates to allow us to estimate transmission intensity in areas where data is sparse. We compare these contrasting descriptions of transmission through a Bayesian framework and trans-dimensional Markov chain Monte Carlo sampling in order to assess each model's evidence given the range of uncertainty in parameter values. The resulting estimates allow us to produce Bayesian model averaged predictions of yellow fever burden across the African endemic region. We find strong support for the static force of infection model which suggests a higher proportion of yellow fever transmission occurs as a result of infection from an external source such as the sylvatic reservoir. However, the model comparison highlights key data gaps in serological surveys across the African endemic region. As such, conclusions concerning the most prevalent transmission routes for yellow fever will be limited by the sparsity of data which is particularly evident in the areas with highest predicted transmission intensity. Our model and estimation approach provides a robust framework for model comparison and predicting yellow fever burden in Africa. However, key data gaps increase uncertainty surrounding estimates of model parameters and evidence. As more mathematical models are developed to address new research questions, it is increasingly important to compare them with established modelling approaches to highlight uncertainty in structures and data.
| S-EPMC6779277 | biostudies-literature
Project description:The coinfection of ALVs (ALV-J plus ALV-A or/and ALV-B) has played an important role in the incidence of tumors recently found in China in local breeds of yellow chickens. The study aims to obtain a better knowledge of the function and relevance of ALV coinfection in the clinical disease of avian leukosis, as well as its unique effect on the pathogenicity in Three-yellow chickens. One-day-old Three-yellow chicks (one day old) were infected with ALV-A, ALV-B, and ALV-J mono-infections, as well as ALV-A + J, ALV-B + J, and ALV-A + B + J coinfections, via intraperitoneal injection, and the chicks were then grown in isolators until they were 15 weeks old. The parameters, including the suppression of body weight gain, immune organ weight, viremia, histopathological changes and tumor incidence, were observed and compared with those of the uninfected control birds. The results demonstrated that coinfection with ALVs could induce more serious suppression of body weight gain (P < 0.05), damage to immune organs (P < 0.05) and higher tumor incidences than monoinfection, with triple infection producing the highest pathogenicity. The emergence of visible tumors and viremia occurred faster in the coinfected birds than in the monoinfected birds. These findings demonstrated that ALV coinfection resulted in considerably severe pathogenic and immunosuppressive consequences.
| S-EPMC10832069 | biostudies-literature
Project description:The existence of vertical transmission in chickens under commercial settings, where chicks are raised separately from adults, is unclear. To answer this question, the fecal microbiota of chicks hatched and grown separately was compared with their mothers' microbiota. Most amplicon sequence variants (ASVs) identified in hens were not detected at all in chicks up to two weeks of age by 16S rDNA sequencing, and those that were detected had a low incidence among the chicks. Nevertheless, a few ASVs that were common with the hens were highly prevalent among the chicks, implying that they were efficiently transmitted to chicks. These ASVs were culturable from the reproductive tract of hens and eggshells. Furthermore, interventions attempting to disrupt transmission resulted in a reduction in the prevalence of specific phylogenetic groups in chicks. To conclude, vertical transmission in commercial poultry grown separately from adults likely exists but is not efficient, possibly resulting in impairment of microbiota function. This implies that artificial exposure to adult bacterial strains might improve microbiota functioning.
| S-EPMC10566040 | biostudies-literature
Project description:Infectious bursal disease (IBD) causes increased mortality and severe immunosuppression in commercial chickens. Currently, vaccination mainly used to control IBD. In this study, Group A (n = 30) received the HVT-IBD vector vaccine (Vaxxitek®) s/c and Group B (n = 30) received the immune complex vaccine (Bursa-Plex®) s/c at 1 day of age. Group C (n = 30) received a single dose of intermediate plus vaccine (228E) through the eye-drop route at 14 days of age. Group D (n = 30) was vaccinated twice with the intermediate vaccine (D78) at 12 and 22 days of age by eye-drop. Group E (n = 30) had the same treatment as group D along with the IBD killed vaccine (Nobilis G®) at 5 days of age. The PC (n = 20) and NC (n = 20) groups were non IBD vaccinated birds either challenged or not with vvIBDV, respectively; 20 chicks from each group were challenged with vvIBDV at 4 weeks of age. Based on clinical signs, postmortem gross lesions, histopathological changes, mortality rate, feed conversion rate, serology, bursal and spleen indices, the HVT-IBD vector vaccine administered was found to be safer and provided better protection against the vvIBDV challenge. The use of a killed IBD vaccine at an earlier age in broilers strengthened the protection induced by double doses of intermediate vaccines in broilers with high maternally derived antibodies against the vvIBDV challenge.
| S-EPMC6466201 | biostudies-literature
Project description:We bed ALV-J-susceptible and ALV-J-resistant chickens. In this work, we find the difference DNA methylation states between ALV-J-susceptible and ALV-J-resistant chickens
2020-01-10 | GSE143336 | GEO
Project description:We bed ALV-J-susceptible and ALV-J-resistant chickens. In this work, we find the different gene expression between ALV-J-susceptible and ALV-J-resistant chickens
2020-12-15 | GSE163135 | GEO
Project description:The live-attenuated yellow fever 17D virus is one of the most outstanding human vaccines ever developed. It induces efficacious immune responses at a low production cost with a well-established manufacture process. These advantages make the YF17D virus attractive as a vector for the development of new vaccines. At the beginning of vector development studies, YF17D was genetically manipulated to express other flavivirus prM and E proteins, components of the viral envelope. While these 17D recombinants are based on the substitution of equivalent YF17D genes, other antigens from unrelated pathogens have also been successfully expressed and delivered by recombinant YF17D viruses employing alternative strategies for genetic manipulation of the YF17D genome. Herein, we discuss these strategies in terms of possibilities of single epitope or larger sequence expression and the main properties of these replication-competent viral platforms.
| S-EPMC4896586 | biostudies-other
Project description:Background: Avian leukosis virus subgroup J (ALV-J) is an oncogenic virus that causes serious economic losses in the poultry industry; unfortunately, there is no effective vaccine against ALV-J. DNA methylation plays a crucial role in several biological processes, and an increasing number of diseases have been proven to be related to alterations in DNA methylation. In this study, we screened ALV-J-positive and -negative chickens. Subsequently, we generated and provided the genome-wide gene expression and DNA methylation profiles by MeDIP-seq and RNA-seq of ALV-J-positive and -negative chicken samples; 8,304 differentially methylated regions (DMRs) were identified by MeDIP-seq analysis (p ≤ 0.005) and 515 differentially expressed genes were identified by RNA-seq analysis (p ≤ 0.05). As a result of an integration analysis, we screened six candidate genes to identify ALV-J-negative chickens that possessed differential methylation in the promoter region. Furthermore, TGFB2 played an important role in tumorigenesis and cancer progression, which suggested TGFB2 may be an indicator for identifying ALV-J infections.
| S-EPMC8203102 | biostudies-literature