Helbert M R, Walter J, L'Age J, Beverley P C
Imperial Cancer Research Fund Tumour Immunology Unit, University College Medical School, London, UK.
Clin Exp Immunol. 1997 Feb;107(2):300-5. doi: 10.1111/j.1365-2249.1997.280-ce1170.x.
HIV preferentially infects the RO+ memory subset of CD4+ lymphocytes, and these cells are lost earlier in HIV infection than their RA+ counterparts. Although both populations express similar amounts of CD4 and bind the HIV envelope glycoprotein (gp120) equally well, calcium signals and CD4 down-regulation subsequent to gp120 binding are not the same in both populations. Data suggest these disparities are mediated by differential tyrosine kinase (TK) regulation. Syncytium formation is enhanced in RO+ cells, partly a consequence of increased leucocyte function antigen-1 (LFA-1) expression and, again, partly due to altered TK regulation. After in vitro HIV infection, reverse transcription is not detected in RA+ cells, is minimal in the RO+ class II- population, but progresses well in RO+ class II+. Infection followed by mitogen stimulation permits reverse transcription in all cells. HIV infection of RO+ cells is enhanced moderately at multiple points in the virus life cycle.
HIV优先感染CD4+淋巴细胞的RO+记忆亚群,并且在HIV感染中,这些细胞比其RA+对应细胞更早丢失。尽管这两个群体表达相似数量的CD4且与HIV包膜糖蛋白(gp120)结合的能力相同,但gp120结合后两个群体中的钙信号和CD4下调情况并不相同。数据表明这些差异是由酪氨酸激酶(TK)调节差异介导的。RO+细胞中的合胞体形成增强,部分原因是白细胞功能抗原-1(LFA-1)表达增加,部分原因同样是TK调节改变。体外HIV感染后,RA+细胞中未检测到逆转录,RO+ II类阴性群体中逆转录极少,但在RO+ II类阳性群体中逆转录进展良好。有丝分裂原刺激后的感染可使所有细胞发生逆转录。在病毒生命周期的多个点上,RO+细胞的HIV感染适度增强。