Tahiri-Alaoui Abdessamad, Smith Lorraine P, Kgosana Lydia, Petherbridge Lawrence J, Nair Venugopal
The Pirbright Institute, Compton Laboratory, Compton, Berkshire RG20 7NN, U.K.
Avian Dis. 2013 Jun;57(2 Suppl):387-94. doi: 10.1637/10322-080912-Reg.1.
In addition to tumors, Marek's disease (MD) virus (MDV) can induce a variety of syndromes linked to the central nervous system. In fact, early descriptions of MD suggested that it was a condition affecting mainly the nervous system. Cytokines and other immune-related genes have been suggested to play a crucial role in MDV-mediated neuropathology, but the mechanisms behind the viral-induced neurologic dysfunction are still poorly understood. In the present study we have used reverse genetic strategies to show that pp14 is not involved in the oncogenic phenotype of MDV1 and is not required for viral replication; however, we provide evidence indicating that the absence of pp14 expression is correlated with increased survival of MDV1-infected chickens, and that its expression is associated with enhanced viral neurovirulence. Our data identify for the first time pp14 as a neurovirulence factor from MDV1 and open the possibility to investigate the molecular mechanisms by which pp14 mediates the damage to the avian nervous system.
除肿瘤外，马立克氏病（MD）病毒（MDV）还可诱发多种与中枢神经系统相关的综合征。事实上，MD的早期描述表明它是一种主要影响神经系统的疾病。细胞因子和其他免疫相关基因被认为在MDV介导的神经病理学中起关键作用，但病毒诱导神经功能障碍背后的机制仍知之甚少。在本研究中，我们使用反向遗传策略表明pp14不参与MDV1的致癌表型，且病毒复制不需要它；然而，我们提供的证据表明，pp14表达缺失与MDV1感染鸡的存活率增加相关，而其表达与病毒神经毒力增强有关。我们的数据首次确定pp14是MDV1的神经毒力因子，并为研究pp14介导禽类神经系统损伤的分子机制开辟了可能性。
