Albright A V, Strizki J, Harouse J M, Lavi E, O'Connor M, González-Scarano F
Graduate Group in Molecular Biology, Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia 19104-6146, USA.
Virology. 1996 Mar 1;217(1):211-9. doi: 10.1006/viro.1996.0108.
The mechanism through which HIV-1 causes HIV dementia (HIVD) is not well understood. Myelin pallor is a common pathological finding in HIVD and could be explained by a direct infection of oligodendrocytes or interaction with HIV-1 gp 120. To determine if oligodendrocytes could be infected by HIV-1, we purified oligodendrocytes from adult human brain tissues obtained from temporal lobe resections. These cells were exposed to HIV-1 and infectivity was assayed by detection of p24gag antigen, PCR amplification, and cocultivation with CD4+ cells. These results indicate that HIV-1(IIIB and BaL) and one of four primary isolates tested can infect oligodendrocytes, resulting in the production of infectious virus. Furthermore, in an experiment that mimics a potential in vivo scenario, infected microglia were able to transmit virus to oligodendrocytes in a trans-well culture system. These experiments indicate that oligodendrocyte infection should be considered in studying the pathophysiology of HIVD.
人类免疫缺陷病毒1型(HIV-1)引发HIV痴呆(HIVD)的机制尚未完全明确。髓鞘苍白是HIVD常见的病理表现,其原因可能是少突胶质细胞受到直接感染,或者与HIV-1糖蛋白120发生相互作用。为确定HIV-1能否感染少突胶质细胞,我们从颞叶切除获取的成人脑组织中纯化出少突胶质细胞。将这些细胞暴露于HIV-1,并通过检测p24gag抗原、PCR扩增以及与CD4+细胞共培养来测定感染性。结果表明,HIV-1(IIIB和BaL)以及所测试的四种原发性分离株中的一种能够感染少突胶质细胞,从而产生有感染性的病毒。此外,在一项模拟潜在体内情况的实验中,受感染的小胶质细胞能够在跨孔培养系统中将病毒传播给少突胶质细胞。这些实验表明,在研究HIVD的病理生理学过程中应考虑少突胶质细胞感染。