Müller W E, Schröder H C, Reuter P, Sarin P S, Hess G, Meyer zum Büschenfelde K H, Kuchino Y, Nishimura S
Abt. Angewandte Molekularbiologie, Universität Mainz, West Germany.
AIDS Res Hum Retroviruses. 1988 Aug;4(4):279-86. doi: 10.1089/aid.1988.4.279.
HTLV-IIIB-infected H9 cells are shown to contain a high level of the natural UAG suppressor glutamine tRNA(UmUG Gln); this tRNA has been demonstrated to be required for the synthesis of Moloney murine leukemia virus (Mo-MuLV)-encoded protease. After cultivation of HTLV-IIIB-infected H9 cells with Avarol at a concentration (1 microgram/ml), previously found to protect the cells against the cytopathic effects of HTLV-III, an almost complete inhibition of the synthesis of the tRNA(UmUG Gln) was observed. Moreover, we obtained some evidence that the processing of the HTLV-III precursor protein p53 to p24 is inhibited by Avarol in infected cells, suggesting that the compound interferes with the expression of the viral protease gene.
研究表明,感染HTLV-IIIB的H9细胞含有高水平的天然UAG抑制性谷氨酰胺tRNA(UmUG Gln);已证明这种tRNA是莫洛尼鼠白血病病毒(Mo-MuLV)编码的蛋白酶合成所必需的。先前发现浓度为1微克/毫升的阿伐他汀可保护细胞免受HTLV-III的细胞病变效应,在用其培养感染HTLV-IIIB的H9细胞后,观察到tRNA(UmUG Gln)的合成几乎完全受到抑制。此外,我们获得了一些证据表明,阿伐他汀在感染细胞中可抑制HTLV-III前体蛋白p53加工成p24,这表明该化合物干扰了病毒蛋白酶基因的表达。