Fletcher Nicola F, Brayden David J, Brankin Brenda, Callanan John J
School of Agriculture, Food Science and Veterinary Medicine, University College Dublin, Belfield, Dublin 4, Ireland.
Vet Immunol Immunopathol. 2008 May 15;123(1-2):134-7. doi: 10.1016/j.vetimm.2008.01.028. Epub 2008 Jan 19.
Feline immunodeficiency virus (FIV), like human immunodeficiency virus (HIV)-1, is a neurotropic lentivirus and is associated with neuropathology in natural and experimental infections. FIV enters the brain early following experimental infection, and virus has been proposed to enter the brain via the blood-brain barrier and blood-CSF barrier, within infected lymphocytes and monocytes/macrophages. However the entry of cell-free virus or the direct infection of brain endothelial cells and astrocytes of the blood-brain barrier may also contribute to CNS infection. This review explores the role played by the FIV model in the elucidation of mechanism of lentiviral entry to the brain and viral interactions with the CNS, particularly in relation to lymphotropic lentiviruses.
猫免疫缺陷病毒（FIV）与人类免疫缺陷病毒1型（HIV-1）一样，是一种嗜神经性慢病毒，在自然感染和实验感染中均与神经病理学有关。在实验感染后，FIV会早期进入大脑，有人提出病毒是通过血脑屏障和血脑脊液屏障，在受感染的淋巴细胞和单核细胞/巨噬细胞内进入大脑的。然而，无细胞病毒的进入或血脑屏障的脑内皮细胞和星形胶质细胞的直接感染也可能导致中枢神经系统感染。这篇综述探讨了FIV模型在阐明慢病毒进入大脑的机制以及病毒与中枢神经系统相互作用方面所起的作用，特别是与嗜淋巴性慢病毒相关的作用。
