Explore the vast range of titles available.

Newcastle disease (ND), caused by Newcastle disease virus (NDV), is a contagious disease that affects a variety of domestic and wild avian species. Though ND is vaccine-preventable, it is a persistent threat to poultry industry across the globe. The disease represents a leading cause of morbidity and mortality in chickens. To better understand the epidemiology of NDV among commercial and backyard chickens of Odisha, where chicken farming is being prioritized to assist with poverty alleviation, a cross-sectional study was conducted in two distinct seasons during 2018. Choanal swabs ( n = 1361) from live birds (commercial layers, broilers, and backyard chicken) and tracheal tissues from dead birds ( n = 10) were collected and tested by real-time reverse transcription polymerase chain reaction (RT-PCR) for the presence of matrix (M) and fusion (F) genes of NDV. Risk factors at the flock and individual bird levels (health status, ND vaccination status, geographical zone, management system, and housing) were assessed using multivariable logistic regression analyses. Of the 1371 samples tested, 160 were positive for M gene amplification indicating an overall apparent prevalence of 11.7% (95% CI 10.1–13.5%). Circulation of virulent NDV strains was also evident with apparent prevalence of 8.1% (13/160; 95% CI: 4.8–13.4%). In addition, commercial birds had significantly higher odds (75%) of being infected with NDV as compared to backyard poultry ( p = 0.01). This study helps fill a knowledge gap in the prevalence and distribution of NDV in apparently healthy birds in eastern India, and provides a framework for future longitudinal research of NDV risk and mitigation in targeted geographies—a step forward for effective control of ND in Odisha.

In recent years, fowl adenovirus (FAdV)-induced diseases became a global problem with considerable impact on chicken health and welfare. This has prompted numerous studies to focus on experimental immunization strategies using whole virus formulations (live or killed vaccines), some of them modified as recombinantly constructed vector vaccines. In addition, FAdV capsid proteins were frequently reported as immunizing antigens (subunit vaccines), with fiber proteins being amongst the most successful candidates. To date, there is no standardized protocol to assess vaccine efficacy in experimental FAdV protection studies, with the consequence that the experimental settings present several degrees of variations even when sharing similar premises. Differences in formulation preparations, route of inoculation, antigen dose, vaccination scheme, choice of challenge strain, or type and age of the birds are capable to greatly influence the magnitude of the immune response and the consequent protective efficacy, altogether addressing remaining challenges. Beyond the antigen composition of a vaccine, the epidemiology of FAdVs with the potential of vertical transmission of virus and/or antibodies from breeders to progenies has a substantial impact on protection strategies. The goal of this review is to outline a broad overview of the findings made thus far regarding immunization strategies against diseases associated to FAdV infections, considering the literature published since the appearance of hepatitis-hydropericardium syndrome (HHS) in the late Eighties, in order to emphasize the current knowledge on FAdV vaccines and highlight fields of future research and intervention.

Infectious bursal disease virus (IBDV) is an acute and highly infectious RNA virus known for its immunosuppressive capabilities, chiefly inflicting rapid damage to the bursa of Fabricius (BF) of chickens. Current clinical control of IBDV infection relies on vaccination. However, the emergence of novel variant IBDV (nVarIBDV) has posed a threat to the poultry industry across the globe, underscoring the great demand for innovative and effective vaccines. Our previous studies have highlighted the critical role of IBDV VP5 as an apoptosis-inducer in host cells. In this study, we engineered IBDV mutants via a reverse genetic system to introduce amino acid mutations in VP5. We found that the mutant IBDV-VP5/3m strain caused reduced host cell mortality, and that strategic mutations in VP5 reduced IBDV replication early after infection, thereby delaying cell death. Furthermore, inoculation of chickens with IBDV-VP5/3m effectively reduced damage to BF and induced neutralizing antibody production comparable to that of parental IBDV WT strain. Importantly, vaccination with IBDV-VP5/3m protected chickens against challenges with nVarIBDV, an emerging IBDV variant strain in China, reducing nVarIBDV loads in BF while alleviating bursal atrophy and splenomegaly, suggesting that IBDV-VP5/3m might serve as a novel vaccine candidate that could be further developed as an effective vaccine for clinical control of IBD. This study provides a new clue to the development of novel and effective vaccines.

Avian pathogenic Escherichia coli (APEC) strains cause severe respiratory and systemic disease, threatening food security and avian welfare worldwide. Intensification of poultry production and the quick expansion of free-range production systems will increase the incidence of colibacillosis through greater exposure of birds to pathogens and stress. Therapy is mainly based on antibiotherapy and current vaccines have poor efficacy. Serotyping remains the most frequently used diagnostic method, only allowing the identification of a limited number of APEC strains. Several studies have demonstrated that the most common virulence factors studied in APEC are rarely all present in the same isolate, showing that APEC strains constitute a heterogeneous group. Different isolates may harbor different associations of virulence factors, each one able to induce colibacillosis. Despite its economical relevance, pathogenesis of colibacillosis is poorly understood. Our knowledge on the host response to APEC is based in very descriptive studies, mostly restricted to bacteriological and histopathological analysis of infected organs, mostly lungs. Furthermore, only a small number of APEC isolates has been used in experimental studies. In the present review we discuss current knowledge on APEC diversity and virulence, including host-response to infection and the associated inflammatory response with a focus on pulmonary colibacillosis.

Marek’s disease (MD), caused by Marek’s disease virus (MDV), is a commercially important neoplastic disease of poultry which is only controlled by mass vaccination. Importantly, vaccines that can provide sterile immunity and inhibit virus transmission are lacking; such that vaccines are only capable of preventing neuropathy, oncogenic disease and immunosuppression, but are unable to prevent MDV transmission or infection, leading to emergence of increasingly virulent pathotypes. Hence, to address these issues, developing more efficacious vaccines that induce sterile immunity have become one of the important research goals for avian immunologists today. MDV shares very close genomic functional and structural characteristics to most mammalian herpes viruses such as herpes simplex virus (HSV). MD also provides an excellent T cell lymphoma model for gaining insights into other herpesvirus-induced oncogenesis in mammals and birds. For these reasons, we need to develop an in-depth knowledge and understanding of the host-viral interaction and host immunity against MD. Similarly, the underlying genetic variation within different chicken lines has a major impact on the outcome of infection. In this review article, we aim to investigate the pathogenesis of MDV infection, host immunity to MD and discuss areas of research that need to be further explored.

Infectious bursal disease (IBD), caused by the infectious bursal disease virus (IBDV), significantly threatens global poultry health by inducing immunosuppression and causing economic losses. To enhance vaccination efficacy, we engineered a transgenic strain of Eimeria acervulina (Ea-2C3d) expressing a fusion protein composed of IBDV VP2 and three tandem C3d segments (3C3d), utilizing C3d's adjuvant properties to boost immune responses. The transgene was generated by integrating codon-optimized VP2 and 3C3d sequences into the E. acervulina genome using restriction enzyme-mediated transfection. PCR, protein, and genome sequencing confirmed the successful integration and expression of VP2 fusion C3d, but only two copies of C3d were successfully expressed, due to a partial deletion of one C3d copy during the transfection process. In vivo studies demonstrated that Ea-2C3d elicited significantly higher anti-VP2 antibody titers than the parental Ea-VP2 strain (P < 0.05), especially following second immunization. Upon challenge with virulent IBDV, chickens immunized with Ea-2C3d displayed reduced bursal lesions (histopathological score ≤ 1) and maintained bursal integrity (bursal index >0.7), comparable to those receiving a commercial subunit vaccine. Despite reduced reproductive capacity in the transgenic parasites, Ea-2C3d maintained its immunogenicity and safety. These findings highlight that C3d adjuvant enhances VP2-mediated protection in a coccidial vector, presenting a novel dual-protection strategy against IBD and coccidiosis.

Newcastle disease is regarded as one of the most important avian diseases throughout the world and continues to be a threat and economic burden to the poultry industry. With no effective treatment, poultry producers rely primarily on stringent biosecurity and vaccination regimens to control the spread of this devastating disease. This concise review provides an historical perspective of Newcastle disease vaccination and how fundamental research has paved the way for the development of instrumental techniques which are still in use today. Although vaccination programmes have reduced the impact of clinical disease, they have historically been ineffective in controlling the spread of virulent viruses and therefore do not always offer an adequate solution to the world’s food security problems. However, the continued development of novel vaccine technology and improved biosecurity measures through education may offer a solution to help reduce the global threat of Newcastle disease on the poultry industry.

The inflammatory response is an essential component of innate immunity to defense against pathogens. Infectious bursal disease (IBD) is the most important immunosuppressive disease in chickens and is caused by the infectious bursal disease virus (IBDV). Acute inflammation is a typical pathogenic process for IBD, however, the underlying mechanism is not clear. Here, we report that IBDV induces obvious inflammatory response in vivo and in vitro . Furthermore, viral VP2 is identified as an important inflammatory stimulus. It is observed that IBDV VP2 can activate NF-κB signaling pathway and then increase IL-1β production. In detail, IBDV VP2 interacts with myeloid differentiation primary response gene 88 (MyD88), potentiates the oligomerization of MyD88 and assembly of MyD88 complex, which is one important element leading to NF-κB signaling pathway activation and IL-1β production increase. More meaningfully, residues 253/284 of viral VP2 are significantly involved in IBDV-induced inflammatory response through modulating the interaction strength between VP2 and MyD88 and the following MyD88-NF-κB-IL-1β signaling pathway. This study reveals one molecular mechanism that trigger inflammation during IBDV infection, which is of great significance for a deeper understanding of the pathogenic mechanisms of IBDV.

Marek's disease virus (MDV) is an alphaherpesvirus that infects chickens, causing immunosuppression, neurological symptoms, and fatal lymphoma. Vaccines are used to protect billions of chickens, but remain poorly understood. To investigate the role of B-cells in vaccine protection, we vaccinated B-cell knockout (JH−/−) chickens with the commercial HVT vaccine and challenged them with very virulent MDV. Vaccinated JH−/− chickens showed significantly increased disease incidence and neurological symptoms compared to wild-type siblings, indicating that B-cells contribute to protection against clinical disease. Tumor incidence remained low and comparable to wild-type, suggesting that B-cells are dispensable for preventing tumors. Aside from the absence of B-cells, no major changes in T-cell subsets were detected. Viral genome levels were comparable in the blood and spleen, but elevated in skin and dust in JH−/− birds early on. These findings reveal that B cells are critical for full HVT vaccine protection and limiting early virus shedding.

Live-attenuated vaccines are commonly used to control chronic respiratory disease (CRD) caused by Mycoplasma gallisepticum in poultry. A previous review found that measures of tracheal lesions are better indicators of the validity of a vaccine efficacy test than air sac lesions. Here we extend those observations by comparing the raw tracheal mucosal thickness (TMT) and gross air sac lesion score (ALS) data from published vaccine efficacy studies to provide insights into standardising methods for evaluation of M. gallisepticum vaccine efficacy by identifying the most discriminative and reproducible parameter to demonstrate the efficacy of vaccines and the validity of immunogenicity tests. Our analyses revealed that a higher proportion of trials detected a ≥ 80 % effectiveness of challenge based on TMT, with a significantly lower number of biological replicates, than ALS. Furthermore, a significantly higher proportion of vaccinated-and-challenged groups had a proportion protected of ≥80 %, a reduction in lesions of ≥30 % and a mitigated fraction of ≥0.80, with a significantly lower number of biological replicates, compared to the positive-control group when analyses were based on TMT rather than ALSs. These findings indicate that TMT is a more discriminative and reproducible parameter to assess the efficacy of a vaccine and the validity of an efficacy test, and hence that this should be the primary outcome variable used to evaluate M. gallisepticum vaccine efficacy studies. Furthermore, the ability of TMT to discriminate these groups with fewer biological replicates enhances animal welfare by reducing the number of animals needed for efficacy studies.