Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA.
Hum Gene Ther. 2012 May;23(5):473-83. doi: 10.1089/hum.2011.165. Epub 2012 Jan 26.
Small antisense RNAs targeted to the HIV-1 promoter have been shown to remodel the surrounding chromatin to a state unfavorable for transcriptional activation, yet transcriptional gene silencing (TGS) of HIV-1 has, to date, not been shown in primary human cells. We demonstrate here that TGS can reduce viral transcription in primary human CD4(+) T cells; however, increasing viral burden results in the loss of this antiviral effect. This observation suggests a critical level at which viral RNA can dilute out effective targeting by TGS-based RNAs. Furthermore, studies into off-target effects have identified a potential interaction between the small nucleolar RNA pathway and the TGS-based antisense RNA, resulting in activation of p53. Although not overtly toxic to primary cells, this represents a novel interaction between antisense RNAs and a cellular pathway that should be considered when pursuing small antisense RNA-based therapeutics.
针对 HIV-1 启动子的小反义 RNA 已被证明可以重塑周围染色质,使其不利于转录激活,但迄今为止,尚未在原代人细胞中显示出 HIV-1 的转录基因沉默 (TGS)。我们在这里证明,TGS 可以降低原代人 CD4(+) T 细胞中的病毒转录;然而,病毒负担的增加导致这种抗病毒作用的丧失。这一观察结果表明,在这个关键水平上,病毒 RNA 可以稀释基于 TGS 的 RNA 的有效靶向。此外,对非靶向效应的研究已经确定了小核仁 RNA 途径与基于 TGS 的反义 RNA 之间的潜在相互作用,导致 p53 的激活。虽然对原代细胞没有明显的毒性,但这代表了反义 RNA 与细胞途径之间的一种新的相互作用,在追求基于小反义 RNA 的治疗方法时应该考虑到这一点。