Maimone D, Annunziata P, Cioni C, Leonardi A, Guazzi G C
Institute of Neurological Sciences, University of Siena, Italy.
Acta Neurol Scand. 1994 Oct;90(4):285-92. doi: 10.1111/j.1600-0404.1994.tb02723.x.
Human immunodeficiency virus type 1 (HIV-1)-infected individuals frequently develop a broad spectrum of neurological syndromes, classified as HIV-1-associated cognitive/motor complex. Diffuse demyelination of hemispheric white matter is a commonly observed in HIV-1 infected brain, but the events leading to myelin destruction are still obscure. Since oligodendrocyte infection by HIV-1 is not proven as yet, myelin damage in HIV-1 infection may result from indirect mechanisms such as the excessive release of myelinotoxic substances or the triggering of autoimmune responses directed to myelin constituents. To verify the latter hypothesis, we searched for elevated anti-myelin basic protein (MBP) IgG levels in the cerebrospinal fluid (CSF) and serum of 25 patients with HIV-1 infection, 12 with multiple sclerosis (MS), and 9 with non-inflammatory neurological diseases (NIND). CSF, but not serum, anti-MBP IgG levels were more frequently elevated in HIV-1+ (16/25, 64%) than in MS (3/12, 25%) or NIND (0/9) patients. By using the anti-MBP IgG index, the anti-MBP IgG antibody specificity index (ASI), and the search for anti-MBP oligoclonal IgG, we ascertained that anti-MBP IgG were produced within the CNS in 13 of 25 (52%) HIV-1+, in 6 of 12 (50%) MS, and in none of NIND patients. The incidence of increased CSF anti-MBP IgG levels was higher among HIV-1+ patients at stage II-III (4/4, 100%) or at stage IV B (7/9, 78%) than among those at stage IV C-IV D (5/12, 42%). Although our data indicate that intrathecal anti-MBP IgG may occur early during HIV-1 infection and that they are more common in patients with HIV-1-associated cognitive/motor complex, the possible demyelinating role of these antibodies remains to be demonstrated.
1型人类免疫缺陷病毒（HIV-1）感染个体常出现一系列广泛的神经综合征，归类为HIV-1相关认知/运动复合体。半球白质的弥漫性脱髓鞘在HIV-1感染的大脑中很常见，但导致髓鞘破坏的事件仍不清楚。由于尚未证实HIV-1可感染少突胶质细胞，HIV-1感染中的髓鞘损伤可能是由间接机制引起的，如髓鞘毒性物质的过度释放或针对髓鞘成分的自身免疫反应的触发。为了验证后一种假设，我们检测了25例HIV-1感染患者、12例多发性硬化症（MS）患者和9例非炎性神经疾病（NIND）患者脑脊液（CSF）和血清中抗髓鞘碱性蛋白（MBP）IgG水平的升高情况。与MS患者（3/12，25%）或NIND患者（0/9）相比，HIV-1阳性患者（16/25，64%）的CSF而非血清中抗MBP IgG水平更常升高。通过使用抗MBP IgG指数、抗MBP IgG抗体特异性指数（ASI）以及检测抗MBP寡克隆IgG，我们确定25例HIV-1阳性患者中有13例（52%）、12例MS患者中有6例（50%）在中枢神经系统内产生了抗MBP IgG，而NIND患者中无一例产生。HIV-1阳性患者中处于II-III期（4/4，100%）或IV B期（7/9，78%）的患者脑脊液抗MBP IgG水平升高的发生率高于处于IV C-IV D期（5/12，42%）的患者。尽管我们的数据表明鞘内抗MBP IgG可能在HIV-1感染早期出现，并且在HIV-1相关认知/运动复合体患者中更常见，但这些抗体可能的脱髓鞘作用仍有待证实。
