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通过与B亚群共同接种抑制猫白血病病毒A亚群感染

Inhibition of feline leukemia virus subgroup A infection by coinoculation with subgroup B.

作者信息

Phipps A J, Hayes K A, Al-dubaib M, Roy-Burman P, Mathes L E

机构信息

Department of Veterinary Biosciences, The Center for Retrovirus Research, Comprehensive Cancer Center, The Ohio State University, 1925 Coffey Road, Columbus, Ohio, 43210, USA.

出版信息

Virology. 2000 Nov 10;277(1):40-7. doi: 10.1006/viro.2000.0606.

Abstract

Feline leukemia virus (FeLV) subgroup B arises de novo through recombination between the env genes of exogenous FeLV subgroup A and endogenous FeLV-like sequences. FeLV-B, which by itself is poorly infectious, will increase to high titer in the presence of FeLV-A, and is associated with FeLV-related neoplastic disease. Although the participation of FeLV-B in disease progression has not been definitively proven, circumstantial evidence supports the hypothesis that the generation of FeLV-B is linked to disease progression. The present study was designed to evaluate whether increasing the levels of FeLV-B early in FeLV-A infection could result in reduction of the incubation period for development of neoplastic disease. For this study, an isolate of FeLV-B, designated FeLV-1B3, was biologically cloned, partially sequenced, and subgroup typed. In in vivo studies, none of the neonatal cats inoculated with FeLV-1B3 alone converted to viremia positive, and all remained healthy throughout the observation period. All of the kittens inoculated with FeLV-A alone became chronically viremic, and those held for long-term observation all developed either neoplastic disease or anemia. However, kittens inoculated with the combination of FeLV-1B3 and FeLV-A showed attenuated infections whereby the majority of cats failed to develop chronic viremia. The apparent interference of FeLV-A infection by FeLV-B was time and titer dependent. This unexpected result suggests that FeLV-B may act as an attenuated virus, causing inhibition of FeLV-A possibly through an immune-mediated mechanism. Partial support for this view was provided by postmortem examination of cats inoculated with FeLV-1B3 alone. Even though none of these cats became viremic, FeLV antigen was detected as focal infections in select tissues, especially salivary gland epithelium, where enough antigen may be expressed to provide an immunizing dose against gag and pol cross-reacting antigens. This work may also provide another approach to vaccine development based on endogenous retrovirus vector systems.

摘要

猫白血病病毒(FeLV)B亚群通过外源性FeLV A亚群的env基因与内源性FeLV样序列之间的重组而从头产生。FeLV-B本身传染性很差,但在FeLV-A存在的情况下会增加到高滴度,并且与FeLV相关的肿瘤性疾病有关。尽管FeLV-B参与疾病进展尚未得到明确证实,但间接证据支持FeLV-B的产生与疾病进展相关的假说。本研究旨在评估在FeLV-A感染早期增加FeLV-B水平是否会导致肿瘤性疾病潜伏期缩短。在本研究中,对一株名为FeLV-1B3的FeLV-B分离株进行了生物学克隆、部分测序和亚群分型。在体内研究中,单独接种FeLV-1B3的新生猫均未转为病毒血症阳性,并且在整个观察期内均保持健康。单独接种FeLV-A的所有小猫都变成了慢性病毒血症,长期观察的小猫都发生了肿瘤性疾病或贫血。然而,接种FeLV-1B3和FeLV-A组合的小猫感染减弱,大多数猫未能发展为慢性病毒血症。FeLV-B对FeLV-A感染的明显干扰是时间和滴度依赖性的。这一意外结果表明,FeLV-B可能作为一种减毒病毒,可能通过免疫介导机制抑制FeLV-A。对单独接种FeLV-1B3的猫进行尸检为这一观点提供了部分支持。尽管这些猫都没有出现病毒血症,但在选定组织中检测到FeLV抗原为局灶性感染,尤其是唾液腺上皮,在那里可能表达足够的抗原以提供针对gag和pol交叉反应抗原的免疫剂量。这项工作也可能为基于内源性逆转录病毒载体系统的疫苗开发提供另一种方法。

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