Lee Lucy F, Kreager Kenton, Heidari Mohammad, Zhang Huanmin, Lupiani Blanca, Reddy Sanjay M, Fadly Aly
United States Department of Agriculture-Agricultural Research Service, Avian Disease and Oncology Laboratory, East Lansing, MI 48823, USA.
Avian Dis. 2013 Jun;57(2 Suppl):491-7. doi: 10.1637/10388-092612-Reg.1.
We have previously shown that deletion of the meq gene from the genome of Cosmid-cloned rMd5 strain of Marek's disease virus (MDV-1) resulted in loss of transformation and oncogenic capacity of the virus. The rMd5deltaMeq (Meq null) virus has been shown to be an excellent vaccine in maternal antibody positive (MAb+) chickens challenged with a very virulent plus (vv+) strain of MDV, 648A. The only drawback was that it retained its ability to induce bursa and thymus atrophy (BTA) like that of the parental rMd5 in maternal antibody negative (MAb-) chickens. We recently reported that the attenuated Meq null virus did not induce BTA at the 40th cell culture passage onward. Its protective ability against challenge with vv+ MDV, strain 686 was similar to the original virus at the 19th passage in MAb- chickens. In this study, we compared the same series of attenuated meq null viruses in commercial chickens. In commercial chickens with MAb, the attenuated viruses quickly lost protection with increasing cell culture attenuation. These data suggest that although attenuation of these meq null viruses eliminated BTA, it had no influence on their protective efficacy in MAb- chickens. However, in commercial chickens (MAb+), the best protection was provided by the original 19th passage; the attenuated 40th passage was as good as one of the currently commercial CVI988/Rispens vaccine, and it did not induce BTA. Therefore, protection against virulent MDV challenge and induction of lymphoid organ atrophy are simultaneously attenuated by serial passage in vitro.
我们之前已经表明,从马立克氏病病毒(MDV-1)的粘粒克隆rMd5株基因组中删除meq基因会导致该病毒丧失转化和致癌能力。rMd5deltaMeq(Meq缺失)病毒已被证明是一种出色的疫苗,可用于对感染超强毒力加(vv+)株MDV 648A的母源抗体阳性(MAb+)鸡进行免疫。唯一的缺点是,在母源抗体阴性(MAb-)鸡中,它仍保留像亲本rMd5那样诱导法氏囊和胸腺萎缩(BTA)的能力。我们最近报道,减毒后的Meq缺失病毒从第40代细胞培养传代起不再诱导BTA。在MAb-鸡中,其对vv+ MDV 686株攻击的保护能力在第19代时与原始病毒相似。在本研究中,我们在商品鸡中比较了同一系列的减毒Meq缺失病毒。在有母源抗体的商品鸡中,随着细胞培养传代次数增加,减毒病毒迅速失去保护作用。这些数据表明,尽管这些Meq缺失病毒的减毒消除了BTA,但对它们在MAb-鸡中的保护效力没有影响。然而在商品鸡(MAb+)中,第19代原始病毒提供了最佳保护;减毒后的第40代与目前市售的CVI988/Rispens疫苗效果相当,且不会诱导BTA。因此,通过体外连续传代可同时减弱对强毒MDV攻击的保护作用和诱导淋巴器官萎缩的能力。