Avian Immunosuppressive Diseases and Immune Evasion

Schat, Karel A.; Skinner, Michael A.

doi:10.1016/b978-012370634-8.50019-6

Cited by 26 publications

(23 citation statements)

References 157 publications

(167 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Embryo-adaptation of the AE vaccine virus is considered to be the most likely cause of the disease. It is known that environmental stressors cause stress-induced immunosuppression by enhancing the production of corticosteroids (8). Therefore, overcrowding during growout may have contributed to the more severe clinical presentation of the vaccine-induced AE in Company A, in which lymphoid depletion was found in the bursa of Fabricius, suggesting immunosuppression.…”

Section: Discussionmentioning

confidence: 99%

Avian Encephalomyelitis in Layer Pullets Associated with Vaccination

Sentíes–Cué¹,

Gallardo²,

Reimers³

et al. 2016

Avian Diseases

View full text Add to dashboard Cite

Avian encephalomyelitis (AE) was diagnosed in three flocks of leghorn layer pullets following AE vaccination. Ages of the birds were 11, 12, and 14 wk. The submissions came from three different companies located in two geographic areas of the Central Valley of California. The clinical signs included birds down on their legs, unilateral recumbency or sitting on their hocks, lethargy, reluctance to move, dehydration, unevenness in size, low weight, tremors of the head in a few birds, and mildly to moderately elevated mortality. The flocks had been vaccinated against fowl pox and AE with a combined product in the wing-web 2 wk prior to the onset of AE clinical signs. Histopathologic examination revealed lesions consistent with AE, including lymphocytic perivascular infiltration and neuronal central chromatolysis in the brain and spinal cord, as well as gliosis in the cerebellar molecular layer. The AE virus was detected by reverse-transcriptase PCR in the brain homogenate from three cases and peripheral nerves in one case. Additionally, the AE virus was isolated in specific-pathogen-free (SPF) embryonated eggs from brain tissue pool samples. Other avian viral infections capable of causing encephalitis, including avian paramyxoviruses, avian influenza virus (AIV), West Nile virus (WNV), eastern equine encephalitis virus (EEEV), and western equine encephalitis virus (WEEV), were ruled out by attempting virus isolation and molecular procedures.

show abstract

Section: Discussionmentioning

confidence: 99%

Avian Encephalomyelitis in Layer Pullets Associated with Vaccination

Sentíes–Cué¹,

Gallardo²,

Reimers³

et al. 2016

Avian Diseases

View full text Add to dashboard Cite

show abstract

“…Moreover, IBDV continues to be a serious threat to commercial chickens, with both antigenic variation and increase in virulence reported (reviewed in Ingrao et al 2013; Mahgoub et al 2012; Müller et al 2003, 2012; Schat and Skinner 2008; van den Berg 2000). While the poultry industry generally controls IBDV through inactivated vaccines that work through class II molecules (which also show the phenomenon of MHC-determined differences in response), some attenuated viral vaccines are used, particularly in ovo (reviewed in Müller et al 2012).…”

Section: Discussionmentioning

confidence: 99%

“…Gumburo disease is caused by an immunosuppressive birnavirus called infectious bursal disease virus (IBDV) that infects and kills cells of the B lineage in chickens (reviewed in Ingrao et al 2013; Mahgoub et al 2012; Müller et al 2003, 2012; Schat and Skinner 2008; van den Berg 2000). There is biphasic age-related resistance.…”

Section: Introductionmentioning

confidence: 99%

The peptide motif of the single dominantly expressed class I molecule of the chicken MHC can explain the response to a molecular defined vaccine of infectious bursal disease virus (IBDV)

et al. 2013

View full text Add to dashboard Cite

In contrast to typical mammals, the chicken MHC (the BF-BL region of the B locus) has strong genetic associations with resistance and susceptibility to infectious pathogens as well as responses to vaccines. We have shown that the chicken MHC encodes a single dominantly expressed class I molecule whose peptide-binding motifs can determine resistance to viral pathogens, such as Rous sarcoma virus and Marek’s disease virus. In this report, we examine the response to a molecular defined vaccine, fp-IBD1, which consists of a fowlpox virus vector carrying the VP2 gene of infectious bursal disease virus (IBDV) fused with β-galactosidase. We vaccinated parental lines and two backcross families with fp-IBD1, challenged with the virulent IBDV strain F52/70, and measured damage to the bursa. We found that the MHC haplotype B15 from line 15I confers no protection, whereas B2 from line 61 and B12 from line C determine protection, although another locus from line 61 was also important. Using our peptide motifs, we found that many more peptides from VP2 were predicted to bind to the dominantly expressed class I molecule BF2*1201 than BF2*1501. Moreover, most of the peptides predicted to bind BF2*1201 did in fact bind, while none bound BF2*1501. Using peptide vaccination, we identified one B12 peptide that conferred protection to challenge, as assessed by bursal damage and viremia. Thus, we show the strong genetic association of the chicken MHC to a T cell vaccine can be explained by peptide presentation by the single dominantly expressed class I molecule.

show abstract

“…The damaged immune system inflicts severe immune-suppression on the infected chickens, accompanied with increased susceptibility to other infectious diseases (Schat and Skinner, 2013). IBDV infection can cause a high mortality in young chickens of 3–6 weeks when they are at the maximal stage of BF development (Mahgoub, 2012).…”

Section: Introductionmentioning

confidence: 99%

VP2 of Infectious Bursal Disease Virus Induces Apoptosis via Triggering Oral Cancer Overexpressed 1 (ORAOV1) Protein Degradation

Qin

Wang

et al. 2017

Front. Microbiol.

View full text Add to dashboard Cite

Infectious bursal disease (IBD) is an acute, highly contagious and immunosuppressive avian disease caused by IBD virus (IBDV). Cell apoptosis triggered by IBDV contributes to the dysfunction of immune system in host. VP2 of IBDV is known to induce cell death but the underlying mechanism remains unclear. Here we demonstrate that VP2 interacts with the oral cancer overexpressed 1 (ORAOV1), a potential oncoprotein. Infection by IBDV or ectopic expression of VP2 causes a reduction of cellular ORAOV1 and induction of apoptosis, so does knockdown of ORAOV1. In contrast, over-expression of ORAOV1 leads to the inhibition of VP2- or IBDV-induced apoptosis, accompanied with the decreased viral release (p < 0.05). Thus, VP2-induced apoptosis during IBDV infection is mediated by interacting with and reducing ORAOV1, a protein that appears to act as an antiapoptotic molecule and restricts viral release early during IBDV infection.

show abstract

Avian Immunosuppressive Diseases and Immune Evasion

Cited by 26 publications

References 157 publications

Avian Encephalomyelitis in Layer Pullets Associated with Vaccination

Avian Encephalomyelitis in Layer Pullets Associated with Vaccination

The peptide motif of the single dominantly expressed class I molecule of the chicken MHC can explain the response to a molecular defined vaccine of infectious bursal disease virus (IBDV)

VP2 of Infectious Bursal Disease Virus Induces Apoptosis via Triggering Oral Cancer Overexpressed 1 (ORAOV1) Protein Degradation

Contact Info

Product

Resources

About