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鼠逆转录病毒感染性进入小鼠细胞:酸性pH抑制吸附后步骤的证据。

Infectious entry of murine retroviruses into mouse cells: evidence of a postadsorption step inhibited by acidic pH.

作者信息

Portis J L, McAtee F J, Evans L H

出版信息

J Virol. 1985 Sep;55(3):806-12. doi: 10.1128/JVI.55.3.806-812.1985.

Abstract

The entry into cells by many enveloped RNA viruses is accomplished by endocytosis and subsequent penetration of the endosomal membrane by an acidic pH-dependent fusion event. In the current study, we examined early events in the infectious entry of mouse retroviruses, using as a framework the observation that infection of a mouse tail skin cell line by the ecotropic virus Friend murine leukemia virus was inhibited at mildly acidic pH (pH 6). This inhibition operated on a postadsorption step, since binding of virus was unaffected at this pH. The rate of penetration of preadsorbed virus, which displayed first-order kinetics, was markedly affected by changes in the pH of the medium. The half-time for disappearance of infectious cell surface virus at 37 degrees C was approximately 10 min at pH 7.6. At pH 6.0, however, greater than 98% of the adsorbed infectivity remained at the cell surface after 45 min. This cell surface virus, though not infecting the cell at pH 6.0, retained its capacity to enter and infect the cell when the pH of the medium was raised. Acidic pH had little effect on the rate of fluid uptake by the cells, as measured by internalization of [3H]sucrose, indicating that global inhibition of endocytosis had not occurred. In contrast, cell fusion induced by Friend murine leukemia virus was optimal at pH 7.6 but markedly inhibited at a pH of less than 6.4. This inhibitory effect of acidic pH on membrane fusion is unique among the enveloped viruses which have been studied and would preclude entry of Friend murine leukemia virus from within acidified endocytic vesicles. Entry of other members of the ecotropic, mink cell focus-forming, and xenotropic host range groups displayed similar pH sensitivity. However, one xenotropic virus was relatively resistant to the effect of acidic pH, suggesting that differences might exist in the requirements for entry of different retroviruses.

摘要

许多有包膜的RNA病毒进入细胞是通过内吞作用以及随后在酸性pH依赖的融合事件中穿透内体膜来完成的。在本研究中,我们以嗜亲性病毒弗氏鼠白血病病毒感染小鼠尾部皮肤细胞系在轻度酸性pH(pH 6)下受到抑制这一观察结果为框架,研究了小鼠逆转录病毒感染性进入的早期事件。这种抑制作用发生在吸附后步骤,因为在此pH下病毒的结合不受影响。预吸附病毒的穿透速率呈一级动力学,显著受培养基pH变化的影响。在37℃时,pH 7.6条件下感染性细胞表面病毒消失的半衰期约为10分钟。然而,在pH 6.0时,45分钟后超过98%的吸附感染力仍保留在细胞表面。这种细胞表面病毒虽然在pH 6.0时不感染细胞,但当培养基pH升高时仍保留其进入并感染细胞的能力。通过[3H]蔗糖的内化测定,酸性pH对细胞液体摄取速率影响很小,表明内吞作用未受到整体抑制。相比之下,弗氏鼠白血病病毒诱导的细胞融合在pH 7.6时最佳,但在pH小于6.4时显著受到抑制。酸性pH对膜融合的这种抑制作用在已研究的有包膜病毒中是独特的,这将阻止弗氏鼠白血病病毒从酸化的内吞小泡中进入。嗜亲性、貂细胞集落形成和异嗜性宿主范围组的其他成员的进入表现出类似的pH敏感性。然而,一种异嗜性病毒对酸性pH的影响相对抗性较强,这表明不同逆转录病毒进入的要求可能存在差异。

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