香菇多糖和黄芪多糖对马立克氏病强毒感染雏鸡白细胞介素2活性和淋巴细胞增殖反应的影响

１日龄ＡＡ肉用雏鸡以马立克氏病强毒（ｖＭＤＶ）人工感染后,马立克氏病（ＭＤ）发病率３３．７５％,死亡率１１．２５％。同健康雏鸡相比,ＩＬ－２诱生活性和Ｔ淋巴细胞增殖反应降低（Ｐ＞０．０５）和显著降低（Ｐ＜０．０５）。ｖＭＤＶ感染雏鸡注射香菇多糖和黄芪多糖,ＭＤ发病率分别为２０％、１７．５％,死亡率分别为７．５％、５％。同感染组相比,感染／香菇组和感染／黄芪组的ＩＬ－２诱生活性和Ｔ淋巴细胞增殖反应均升高（Ｐ＞０．０５）和显著升高（Ｐ＜０．０５）。     

马立克氏病病毒感染雏鸡的SOD活性变化

１日龄肉用ＡＡ雏鸡被马立克氏病病毒（ＭＤＶ）强毒人工感染后，马立克氏病（ＭＤ）发病率６２％，死亡率３４％；脾脏、胸腺、法氏囊、心脏、肝脏、肾脏和性腺超氧化物歧化酶（ＳＯＤ）活性与健康雏鸡相比，Ｔ－ＳＯＤ和Ｍｎ－ＳＯＤ活性均有显著降低（Ｐ＜０．０５），而Ｃｕ，Ｚｎ－ＳＯＤ活性无显著变化（Ｐ＞０．０５）。     

雏鸡vMDV感染后硒谷胱甘胱过氧化物酶的活性变化

１日龄雏鸡马立克氏病强毒人工感染后，马立克氏病发病率６２％，ＭＤ死亡率３４％，脾脏、胸脾、法氏囊、心脏、肝脏、肾脏和性腺硒谷胱甘肽过氧化物酶活性比健康对照雏鸡显著降低（Ｐ〈０．０５）。     

vMDV感染雏鸡的Se-GSH-PX活性和LPO含量

以马立克氏病强毒（ｖＭＤＶ）人工感染１日龄ＡＡ肉用雏鸡,于感染后７,１４,２８,４２和５６日龄分别检测雏鸡中枢、外周淋巴器官及主要内脏器官的含硒谷胱甘肽过氧化物酶（Ｓｅ－ＧＳＨ－ＰＸ）活性和脂质过氧化物（ＬＰＯ）含量的变化。结果表明,ｖＭＤＶ感染雏鸡各器官Ｓｅ－ＧＳＨ－ＰＸ活性在检测各时期多显著低于健康对照雏鸡（Ｐ＜０．０５,Ｐ＜０．０１）,而各器官ＬＰＯ含量则多显著高于健康对照雏鸡（Ｐ＜０．０５,Ｐ＜０．０１）,提示马立克氏病（ＭＤ）及其肿瘤的发生和发展与Ｓｅ－ＧＳＨ－ＰＸ抗氧化活性降低和ＬＰＯ及其降解物对雏鸡的广泛病理损伤有关。     

雏鸡感染马立克氏病强毒后抗氧化酶活性和丙二醛水平的变化

对１０日龄雏鸡人工感染马立克氏病毒后，马立克氏病发病率为７８．０％，死亡率为７６．０％，在攻毒后２，４和６周，感染鸡血清中超氧化物歧化酶（ＳＯＤ），血液中过氧化氢酶（ＣＡＴ）和谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活性在总体上的均显著低健康对照组鸡（Ｐ〈０．０５），血清丙二醛水平极显著地高于健康对照组鸡（Ｐ〈０．０１）。结合对马立克氏病临床病例的研究结果认为，氧自由基介入了马立克氏病的发病过程。     

雏鸡马立克氏病强毒感染后淋巴细胞化学发光的变化

本研究采用化学发光（ＣＬ）法测定雏鸡马立克氏病强毒（ｖＭＤＶ）人工感染后免疫器官淋巴细胞活性氧自由基（ＡＯＲ）产生水平。结果为：脾脏淋巴细胞ＣＬ值于７、１４和５６日龄显著高于健康对照雏鸡（Ｐ＜０．０５，Ｐ＜０．０１）；胸腺淋巴细胞ＣＬ值４２和５６日龄显著高于健康对照雏鸡（Ｐ＜０．０５）；法氏囊淋巴细胞ＣＬ值１４、２８和４２日龄显著高于健康对照雏鸡（Ｐ＜０．０５）。     

雏鸡HVT疫苗免疫后Se—GSHPx的活性变化

火鸡疱疹病毒（ＨＶＴ）疫苗免疫雏鸡，地２８、４２和５６日龄脾脏、胸腺、法氏囊以及肝脏、肾脏和性腺含硒谷胱甘肽过氧化物酶（Ｓｅ－ＧＳＨＰｘ）活性比健康对照雏鸡显著和极显著增强（Ｐ〈０．０５，Ｐ〈０．０１），可有产防止马立工病强毒（ｖＭＤＶ）感当导致的脂质过经作用和细胞是性损作，避免马立克氏病（ＭＤ）肿瘤的发生     

鸡马立克氏病毒致鸡淋巴细胞糖皮质激素受体改变的特性

研究证明，鸡感染马立克氏病毒（ＭＤＶ）后，外周血淋巴细胞（ＰＢＬ）糖皮质激素受体（ＧＲ）含量减少，其减少程度随病情的发展而加重，不因攻毒后时间的延伸而改变，提示鸡马立克氏病（ＭＤ）的发生与发展，与病毒所致ＰＢＬ的抗应激能力降低有关；ＭＤ肿瘤组织的ＧＲ含量较正常鸡ＰＢＬ的减少４０％；而含瘤病鸡的ＰＢＬ ＧＲ含量与之基本相同（Ｐ＞０．０５），说明发生肿瘤的ＭＤ鸡，其ＰＢＬ与瘤组织细胞的变化程度相似；Ｍ     

马立克氏病乌黑鸡群血清学研究

对４月龄感染了马立克氏病的２月龄－６月龄乌黑鸡群血清蛋白及血清酶的研究结果表明;２月龄～３月龄健康乌黑鸡如血清蛋白升高极显著（Ｐ〈０．０１）,血清ＡＬＰ活性下降显著（Ｐ〈０．０５）,ＡＭＳ活性下降不明显（Ｐ〉０．０５）,ＣＨＥ活性升高不明显（Ｐ〉０．０５）,４月龄感染ＭＤ后,血清蛋白显著降低（Ｐ〈０．０５）,而后,白脓月回升,变化均不明显（Ｐ〉０．０５）,白蛋白在５月龄再次极显著降低（Ｐ〈０．０５     

雏鸡HVT疫苗免疫后SOD活性的变化

雏鸡ＨＶＴ疫苗免疫后ＳＯＤ活性的变化＊迟玉杰李庆章（东北农业大学动物医学系，哈尔滨１５００３０）于洪祥（哈尔滨原种鸡场）在马立克氏病（ＭＤ）及其疫苗免疫的国内外研究中，马立克氏病病毒（ＭＤＶ）的分子生物学及病原诊断、疫苗研制及应用、ＭＤ病理等方面已取...     

AUS in the prevention of Marek's disease

Aminoureidosulfone (AUS) was used as a feed additive to prevent mortality in Marek's disease (MD)-infected chickens in the laboratory. Chicks infected with MD virus (5000 plaque-forming units) at 1 day of age were given AUS in the feed from 1 day of age until the experiment was terminated. AUS, at all concentrations tested, reduced mortality due to Marek's disease. Chickens receiving AUS at the 0.002% level had a 4% mortality rate, those receiving 0.005% had 9% mortality, and those receiving 0.01% had 2% mortality; mortality rates in the respective controls were 44%, 49%, and 50%. However, lesion reduction in surviving chicks was minimal. When AUS was withdrawn from the feed, MD-induced mortality increased within two weeks; average body weight decreased also.     

Delayed replication of Marek's disease virus following in ovo inoculation during late stages of embryonal development

Several oncogenic and non-oncogenic isolates of Marek's disease virus (MDV) were inoculated into embryonated eggs on embryonation day (ED) 16 to 18, and embryos or chicks hatching from inoculated eggs were examined for infectious virus and viral internal antigen (VIA) in lymphoid organs. There was no evidence of extensive replication of MDV in any of the embryonic tissues examined. Levels of VIA peaked 4-5 days after chicks hatched. This indicated that MDV remained inactive during embryonation and did not initiate pathogenic events until chicks hatched. Because HVT replicated rapidly in the embryo but MDV did not, in ovo inoculation of HVT simultaneously with oncogenic MDV or several days after MDV resulted in significant protection (P less than 0.025) of hatched chicks against Marek's disease (MD). Little protection was obtained if HVT was given simultaneously with MDV or after MDV to chicks already hatched. The relative susceptibility of the embryo to extensive replication of the vaccine virus but not the challenge virus apparently accounted for protection against MD in chicks hatching from dually infected eggs.     

Effects of IgY antibody on the development of Marek's disease.

The effects of passive immunization with immunoglobulin Y (IgY) on the pathogenesis of Marek's disease (MD) were examined in an experimental line of White Leghorn chickens highly susceptible to MD. Purified IgY with anti-MDV antibody activity, when injected into chicks, delayed the development of MDV viremia and lesions until 9 days postinoculation (PI) with Marek's disease virus (MDV). The blastogenic response of spleen cells to concanavallin-A was depressed at 6 days PI in the birds without passive immunization, whereas it was not totally depressed until 17 days in birds passively immunized with IgY anti-MDV antibody.     

A comparison of the efficacy against Marek's disease of cell-free and cell-associated turkey herpesvirus vaccine.

One-day-old White Leghorn and broiler chicks with maternal antibody to turkey herpesvirus (HVT) were vaccinated with 300 or 1,000 plaque-forming units (PFU) of cell-free or cell-associated HVT vaccine and challenged with virulent Marek's disease virus (MDV) by contact exposure. Broiler chicks receiving 300 PFU of cell-associated HVT had a 3.3% incidence of MD lesions, whereas only 2.0% of those receiving 1,000 PFU had macroscopic lesions. Broiler chicks vaccinated with 300 PFU of cell-free vaccine had 6.8% gross lesions, and 0.67% of the birds receiving 1,000 PFU had MD lesions. Unvaccinated broiler chickens had a 28.3% incidence of MD lesions. Unvaccinated White Leghorn chickens had a 48.9% incidence of macroscopic lesions, whereas 5.4% of the birds receiving 300 PFU of cell-associated HVT had gross lesions, and 8.3% of the birds vaccinated with 1,000 PFU had lesions. In contrast, 6.7% of the chicks vaccinated with 300 PFU of cell-free HVT had MD lesions, and only 4.0% of those receiving 1,000 PFU of cell-free HVT had macroscopic lesions.     

Anti-idiotype antibodies to Marek''s disease-associated tumour surface antigen in protection against Marek''s disease

Marek's disease-associated tumour surface antigen (MATSA) removed by enzymatic (papain) digestion of Marek's disease tumour cells was fractionated by gel filtration chromatography. The first peak (F1) was used to raise antibody in rabbits. Monoclonal antibody (RPH-6) directed against MATSA and the anti-F1 IgG were used as idiotypic antibodies to raise polyclonal anti-idiotype serum in heterologous hosts; rabbit and goat, respectively. The anti-idiotypes (anti-Id) were purified by affinity chromatography and characterized by competitive binding assay using immunofluorescent (IF) tests.

Day-old white Leghorn chicks were immunized with anti-Id to MATSA (Group 1) or anti-Id to F1 (Group 3) and challenged with virulent Marek's disease virus (MDV) on the tenth day post immunization. In positive control groups, the day-old chicks were inoculated with anti-BALB/c mouse globulin (Group 2) and anti-rabbit globulin (Group 4) and challenged with virulent MDV on the tenth day post inoculation. As compared with positive control groups, the vaccinated groups (1 and 3) had considerably lower level of MATSA positive cells during the post challenge observation period. The protection level against MD in the immunized groups was 66.6% (Group 1) and 86.6% (Group 3).     

Evolution of Marek's disease -- a paradigm for incessant race between the pathogen and the host

Marek's disease (MD) is a highly contagious lymphoproliferative disease of poultry caused by the oncogenic herpesvirus designated Marek's disease virus (MDV). MD has a worldwide distribution and is thought to cause an annual loss over 1 bn US dollars to the poultry industry. Originally described as a paralytic disease, today MD is mostly manifested as an acute disease with tumours in multiple visceral organs. MD is controlled essentially by the widespread use of live vaccines administered either in ovo into 18-day-old embryos or into chicks immediately after they hatch. In spite of the success of the vaccines in reducing the losses from the disease in the last 30 years, MDV strains have shown continuous evolution in virulence acquiring the ability to overcome the immune responses induced by the vaccines. During this period, different generations of MD vaccines have been introduced to protect birds from the increasingly virulent MDV strains. However, the virus has countered each new vaccine with ever more virulent strains. This continuous race between the virus and the host is making the control of this poultry health problem a major challenge for the future.     

Influence of turkey herpesvirus vaccination on the B-haplotype effect on Marek's disease resistance in 15.B-congenic chickens.

Eight recently developed 15.B congenic lines of chickens were tested for Marek's disease (MD) resistance by intra-abdominal injection of cell-associated preparations of MD virus of a virulent strain (JM), a very virulent strain (Md5), or Md5 after vaccination with turkey herpesvirus (HVT) strain FC126. Chickens of the 15.N congenic line (B15B21 or B21B21) were very resistant to JM-induced MD, in contrast to chickens homozygous for the B-haplotypes 2, 5, 12, 13, 15, or 19. After Md5 infection, more than 88% of the chickens in all of the congenic lines developed MD. However, when chickens were vaccinated with HVT before being inoculated with Md5, the B5 and B12 homozygotes were more resistant to MD than were the B2, B13, or B19 homozygotes, and B15 and B21 homozygotes had intermediate resistance. B5B5 and B2B5 F2 chicks inoculated with HVT and Md5 had a lower prevalence of MD than B2B2 sibs. These results demonstrate that a protocol involving HVT vaccination of chicks followed by infection with very virulent MD virus will allow the detection of B-haplotypes determining MD resistance, some of which are not detectable in unvaccinated chicks challenged with virulent MD.     

Protecting chickens against Marek's disease under laboratory conditions by the administration of Marvak, a Czechoslovak produced vaccine and vaccine imported from East Germany

Laboratory trials were conducted to compare the efficiency of two vaccines against Marek's disease (MD) on the basis of the dynamics of post-vaccination viraemia and by means of a challenge test. Two groups of the HX-SL hybrid layers, each containing 40 birds, were vaccinated with the MARVAK cellular vaccine manufactured in Czechoslovakia (100 PFU per chick) or with the Insel Riems vaccine manufactured in the GDR (1000 PFU per chick). In weekly intervals, half the birds of each group were tested for post-vaccination viraemia and the other half, including 20 non-vaccinated birds, were infected by contact with the pathogenic virus of MD from the second day of age. The viraemia in the birds vaccinated with MARVAK culminated in the third week of age when it reached the average value of 25 PFU/10(7) leucocytes; later on, by the eighth week of age, it decreased to 0.62 PFU/10(7) leucocytes. The maximum number of viraemic chicks was found in the third and fourth week of age (80%); on an average it ranged from 60%. The average viraemia in the chickens treated with the vaccine from the GDR ranged from 1.6 to 3.6 PFU/10(7) leucocytes in the second to eighth week of age. A 100% positivity of the tested birds was found in the sixth week of age; it ranged around 70% on an average. In all the challenged groups of birds the precipitation antigen of Marek's disease was detected in feather follicles already 14 weeks from contact infection.(ABSTRACT TRUNCATED AT 250 WORDS)