Cross-immunity in chickens using seven isolates of avian infectious bronchitis virus

Groups of 75 chickens were each infected with one of 7 isolates of infectious bronchitis virus (Mass 41, Holland 52, SE 17, Ark 99, Clark 333, JMK, and Florida). Following recovery, they were challenged along with susceptible controls to the homologous and 6 heterologous isolates. Cross-immunity was determined by virus recovery 4 or 5 days post-challenge. Challenge with the homologous isolate resulted in 90-100% protection. Challenge with heterologous isolates gave variable results and an overall average resistance of 38%. The SE-17-recovered chickens had a 50% protection, whereas the Holland-52-recovered chickens ahd a 13.3% protection.     

Isolation of avian infectious bronchitis virus from experimentally infected chickens.

Virus was recovered from the faeces of chickens infected at three or four weeks of age for more than 20 weeks after infection with commercial vaccines or with the T strain of avian infectious bronchitis virus (IBV). Virus was not recovered from the trachea, liver, spleen, bursa or kidneys of T strain infected birds longer than 29 days after infection at which point IBV was recovered from the bursa of a single infected bird. In a subsequent experiment IBV was recovered from the caecal lymph nodes and faeces of one of five birds 14 weeks after infection with a commercial vaccine but no virus was isolated from the trachea, kidneys, duodenum, bursa, ovaries or testes of any of the five birds at this time.     

Coronavirus avian infectious bronchitis virus

Infectious bronchitis virus (IBV), the coronavirus of the chicken (Gallus gallus), is one of the foremost causes of economic loss within the poultry industry, affecting the performance of both meat-type and egg-laying birds. The virus replicates not only in the epithelium of upper and lower respiratory tract tissues, but also in many tissues along the alimentary tract and elsewhere e.g. kidney, oviduct and testes. It can be detected in both respiratory and faecal material. There is increasing evidence that IBV can infect species of bird other than the chicken. Interestingly breeds of chicken vary with respect to the severity of infection with IBV, which may be related to the immune response. Probably the major reason for the high profile of IBV is the existence of a very large number of serotypes. Both live and inactivated IB vaccines are used extensively, the latter requiring priming by the former. Their effectiveness is diminished by poor cross-protection. The nature of the protective immune response to IBV is poorly understood. What is known is that the surface spike protein, indeed the amino-terminal S1 half, is sufficient to induce good protective immunity. There is increasing evidence that only a few amino acid differences amongst S proteins are sufficient to have a detrimental impact on cross-protection. Experimental vector IB vaccines and genetically manipulated IBVs--with heterologous spike protein genes--have produced promising results, including in the context of in ovo vaccination.     

Characterization of an avian infectious bronchitis virus isolated in China from chickens with nephritis

One IBV isolate, SC021202, was isolated from the kidneys of the infected young chickens by inoculating embryonated eggs, and its morphology, physiochemical and haemagglutonating properties were detected. Virulence of the isolate SC021202 was determined with specific pathogen-free (SPF) chicken inoculation. Nucleotide acid sequence of S1 gene of the isolate SC021202 was further sequenced and analysed. The physiochemical and morphological properties of the isolate SC021202 were in accordance to that of typical infectious bronchitis virus (IBV). In a pathogenicity experiment, the clinical signs and related gross lesions resembling those of field outbreak were reproduced and the virus isolate SC021202 was re-isolated from the kidneys of the infected chicken. Sequence data demonstrated that the full length of the amplified S1 gene of the isolate SC021202 was composed of 1931 nucleotides, coding a polypeptide of 543 amino acid residues. Compared with IBV strains from GenBank, the nucleotide and deduced amino acid sequence of S1 gene of the isolate SC021202 shared 60.0-91.4% and 49.1-88.9% identities, respectively. A nucleotide fragment of 'CTTTTTAATTATACTAACGGA' was inserted at nucleotide site 208 in the S1 gene of the isolate. These results indicated that IBV isolate SC021202 was a new variant IBV isolate and responsible for field outbreak of nephritis.     

Effects of avian infectious bronchitis virus (Arkansas strain) on vaccinated laying chickens

Twenty-four-week-old white leghorn layers were inoculated subcutaneously with a killed Newcastle-infectious bronchitis (Massachusetts type) virus (MIBV) vaccine. The birds were challenged 194 days later intraocularly with Arkansas strain of infectious bronchitis virus (AIBV). The challenged hens laid significantly (P less than 0.005) fewer eggs than the unchallenged layers, and the eggs laid by the challenged groups weighed significantly less (P less than 0.001) than those laid by the unchallenged groups. Further, the internal quality (Haugh units) and shell quality of eggs laid by the challenged hens were significantly (P less than 0.005) inferior to the quality of eggs from unchallenged hens, and the challenged hens laid more soft-shelled, misshapen, and small-sized eggs than the unchallenged hens. The Arkansas serum hemagglutination-inhibition (AIBV-HI) titers of challenged birds increased continuously through 29 days post-challenge. The MIBV hemagglutination-inhibition (MIBV-HI) titers of killed-MIBV-vaccinated birds decreased during the same period. The study indicates that killed MIBV vaccine offered no protection to birds exposed to AIBV. The same vaccine was quite effective against a homologous (MIBV) virus challenge.     

The infection of primary avian tracheal epithelial cells with infectious bronchitis virus

Here we introduce a culture system for the isolation, passaging and amplification of avian tracheal epithelial (ATE) cells. The ATE medium, which contains chicken embryo extract and fetal bovine serum, supports the growth of ciliated cells, goblet cells and basal cells from chicken tracheas on fibronectin- or matrigel-coated dishes. Non-epithelial cells make up less than 10% of the total population. We further show that ATE cells support the replication and spread of infectious bronchitis virus (IBV). Interestingly, immunocytostaining revealed that basal cells are resistant to IBV infection. We also demonstrate that glycosaminoglycan had no effect on infection of the cells by IBV. Taken together, these findings suggest that primary ATE cells provide a novel cell culture system for the amplification of IBV and the in vitro characterization of viral cytopathogenesis.     

IBV感染雏鸡血清中SOD,GSH-Px活性与MDA含量的研究

将80只15日龄雏鸡随机分为对照组和试验组。试验组雏鸡用传染性支气管炎病毒尿囊液滴鼻染毒,攻毒后1,3,6,9,12d分别测定各组血清中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性与丙二醛(MDA)含量,研究血清中氧自由基在鸡传染性支气管炎发病过程中的动态变化。结果表明:试验组血清SOD,GSH-Px活性自攻毒后明显降低(P<0.05或P<0.01);MDA含量在攻毒后开始上升,且在感染后第6、第9天差异极显著(P<0.01)。提示氧化损伤可能参与调节了传染性支气管炎的发生发展过程。     

Chicken embryonal vaccination with avian infectious bronchitis virus

A commercial infectious bronchitis virus (IBV) vaccine of the Massachusetts 41 strain was injected in embryonating chicken eggs on embryonation day (ED) 18. The IBV vaccine was pathogenic for embryos, and it was passaged in chicken kidney tissue culture to reduce the pathogenicity. At the 40th tissue culture passage (P40-IBV), the virus became apathogenic for the embryos. Maternal antibody-positive or -negative chicks hatching from eggs injected with P40-IBV developed antibody to IBV and were protected against challenge exposure at 4 weeks of age with virulent Massachusetts 41 IBV. Although P40-IBV protected chicks when administered on ED 18, this virus did not protect chicks well if given at hatch. When combined with the turkey herpesvirus (HVT), P40-IBV given on ED 18 did not interfere with the protection against challenge exposure with virulent Marek's disease virus, nor did the presence of HVT interfere with protection by P40-IBV. Thus, under laboratory conditions, IBV vaccine could be combined with HVT to form a bivalent embryonal vaccine.     

Pathogenicity of infectious bronchitis virus isolates from Ontario chickens

Infectious bronchitis (IB) is one of the important viral diseases of chickens, and in spite of regular vaccination, IB is a continuous problem in Canadian poultry operations. In an earlier study using sentinel chickens we determined the incidence of infectious bronchitis virus (IBV) in Ontario commercial layer flocks. The objective of this study was to determine the pathogenicity of 5 nonvaccine-related IBV isolates recovered from the sentinel birds. The clinical signs, gross, and histological lesions in specific pathogen-free chickens indicated that all 5 isolates caused mild lesions in the respiratory tract. An important finding of this study was the significantly lower average daily weight gain among virus-inoculated groups of chickens during the acute phase of infection. Based on sequences of part of the S1 gene IBV-ON2, IBV-ON3, and IBV-ON5 formed a cluster and they were closely related to strain CU-82792. IBV-ON4 had 98.7% identity with the strain PA/1220/9, a nephropathogenic variant.     

雏鸡感染IBV后气管、肺及肾组织中血管活性肠肽(VIP)动态变化

80只14日龄SPF鸡随机均分为试验组和对照组,试验组用鸡传染性支气管炎病毒M41株人工感染,于感染后1,3,5,7,11,15 d分别测定试验组及对照组气管、肺和肾组织中血管活性肠肽(VIP)含量,探讨脑肠肽类物质VIP在鸡传染性支气管炎发病过程中的作用.结果表明:试验组气管组织中VIP含量自感染后一直高于对照组,并且于7,11d VIP含量显著高于对照组(P＜0.05);肺组织中VIP含量未出现明显变化;肾组织中VIP含量自感染后7 d开始上升,并且于7,11d显著高于对照组(P＜0.05).提示脑肠肽类物质VIP可能参与调节了呼吸系统疾病鸡传染性支气管炎的发生发展过程.     

Prevalence of Arkansas-type infectious bronchitis virus in Delmarva peninsula chickens

The prevalence of Arkansas (Ark)-type infectious bronchitis virus (IBV) in Delmarva peninsula broiler-type chickens was determined. The immunity of 5-to-11-week-old commercial broilers was evaluated by intraocular inoculation with Ark-type DPI strain (Ark DPI) challenge virus and collection of tracheal swabbings 5 days later. Serum Ark-type antibody titers were obtained using the virus-neutralization test. Eighty-five flocks were tested from January to August 1981. Nearly 60% of the flocks had substantial (greater than or equal to 70%) local immunity of the upper respiratory tract. Twenty-two percent had intermediate (50-69%) and 19% of the flocks had low (less than or equal to 40%) levels of local immunity. Serum antibody titers generally agreed with challenge results. In addition, high Ark-type IBV neutralizing-antibody titers were found in 16 Delmarva broiler breeder flocks. Seven current IBV field isolates were characterized for antigenic similarity to Ark DPI. Four isolates contained Ark antigen(s) based on significant neutralization in virus-neutralization tests and on substantial immunity to challenge afforded by Ark DPI virus immunization. Three isolates did not appear to contain Ark antigen(s). Immunization of chickens with Ark DPI virus afforded substantial protection against Connecticut- and homologous-type virus challenge, partial immunity (63%) against JMK, and no protection against the Massachusetts 41 strain of IBV.     

Comparative nephropathogenicity of infectious bronchitis virus in bursectomized and nonbursectomized chickens

A study was conducted to compare the responses of bursectomized (Bx) and nonbursectomized (non-Bx) specific-pathogen-free male chickens to Australian T strain of infectious bronchitis virus. Four chickens from each group were killed at 3, 5, 7, 14, 21, and 28 days after conjunctival inoculation of the virus. Clinical signs and gross and microscopic lesions were more severe in Bx than in non-Bx chickens. The non-Bx chickens had linear IgG deposits along the renal tubules. Virus-neutralizing titers were log10 2.74 to 4.33 for non-Bx chickens and less than log10 1.25 for the inoculated Bx and for broth-inoculated Bx and non-Bx chickens (controls). Early in the disease, renal lesions were of the same type in all infected chickens, but were more severe in Bx chickens. Later, nephritis was chronic and active in Bx chickens and was chronic in non-Bx chickens.     

Attenuation of avian infectious bronchitis virus by cold-adaptation.

Avian infectious bronchitis virus (IBV) Arkansas-type DPI strain was passaged 10 times in specific-pathogen-free (SPF) chicken embryos incubated at 28 C and 37 C. Virus grown at 28 C acquired cold-adapted (CA) and temperature-sensitive (TS) characteristics based on more-rapid growth at 28 C and a reduced ability to grown at 41 C, respectively, compared with non-cold-adapted (non-CA) virus grown at 37 C. The pathogenicity and immunogenicity were determined for CA and non-CA IBV in 1-day-old SPF chickens following intratracheal inoculation. The percentage of CA IBV-vaccinated chicks exhibiting respiratory disease exceeded 30% on only 1 day postinoculation (PI) (day 5 PI), compared with 8 days (days 2-9 PI) for birds given non-CA IBV. Mortality was 0% for CA IBV-vaccinated chickens and 6% for non-CA virus-vaccinated chickens. Microscopically, both CA and non-CA IBV caused diffuse tracheal deciliation, although mucosal hyperplasia, necrosis, and heterophil infiltration were more severe with non-CA IBV. Virus was reisolated from kidneys of chickens given CA IBV, suggesting the loss of the TS property. The instability of the TS property was confirmed by growth of the reisolated virus at 41 C. Both CA and non-CA viruses induced complete protection against homologous challenge virus infection of the upper respiratory tract.