Polacino P S, Liang H A, Clark E A
Washington Regional Primate Research Center, University of Washington, Seattle 98195, USA.
J Exp Med. 1995 Aug 1;182(2):617-21. doi: 10.1084/jem.182.2.617.
Although immunodeficiency viruses can enter resting CD4+ T lymphocytes, activation of T cells is required for complete viral cDNA synthesis and transport of double-stranded viral DNA to the nucleus. Cross-linking T cell receptors (TCRs) on resting CD4+ T cells induces reverse transcription of full-length simian immunodeficiency virus (SIV) genomes, but TCR engagement alone is insufficient to stimulate SIV DNA to move to the nucleus and form long terminal repeat (LTR) circles. Neither ligation of TCR or CD28 receptors nor interleukin 2 (IL-2) alone induces formation of LTR circles; however, the combination of TCR ligation with either CD28 ligation or IL-2 doses. Anti-IL-2 serum inhibits the formation of LTR circles induced by cross-linking CD3 and CD28, but has no effect on the induction of increased viral reverse transcription. Thus, two signals appear to be required for immunodeficiency viruses to move to the T cell nucleus, one from the TCR to promote reverse transcription of the viral genome, the other through an IL-2-dependent process leading to formation of LTR circles.
尽管免疫缺陷病毒能够进入静息的CD4+ T淋巴细胞,但病毒双链cDNA的完全合成以及双链病毒DNA转运至细胞核需要T细胞的激活。交联静息CD4+ T细胞上的T细胞受体(TCR)可诱导全长猴免疫缺陷病毒(SIV)基因组的逆转录,但仅TCR结合不足以刺激SIV DNA转移至细胞核并形成长末端重复序列(LTR)环。单独的TCR或CD28受体连接以及单独的白细胞介素2(IL-2)均不能诱导LTR环的形成;然而,TCR连接与CD28连接或IL-2剂量的联合使用则可以。抗IL-2血清可抑制由CD3和CD28交联诱导的LTR环的形成,但对病毒逆转录增加的诱导没有影响。因此,免疫缺陷病毒转移至T细胞核似乎需要两个信号,一个来自TCR以促进病毒基因组的逆转录,另一个通过依赖IL-2的过程导致LTR环的形成。