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脂质体可调节人类免疫缺陷病毒的感染性。

Liposomes modulate human immunodeficiency virus infectivity.

作者信息

Konopka K, Davis B R, Larsen C E, Alford D R, Debs R J, Düzgüneş N

机构信息

Cancer Research Institute, University of California, San Francisco 94143-0128.

出版信息

J Gen Virol. 1990 Dec;71 ( Pt 12):2899-907. doi: 10.1099/0022-1317-71-12-2899.

Abstract

We have investigated the effects of the fusion of liposomes with human immunodeficiency virus type 1 (HIV-1LVA) on the ability of the virus to infect CD4+ and CD4- cells. Fluorescence dequenching measurements indicated that HIV-1 fuses with liposomes composed of either cardiolipin (CL) or N-[2,3-(dioleyloxy) propyl]-N,N,N-trimethyl ammonium chloride (DOTMA) but not appreciably with dioleoylphosphatidylcholine (DOPC) liposomes. Pre-incubation of HIV-1 with DOTMA liposomes enhanced virus production (measured by p24 gag antigen production in the culture medium and in situ) in CD4+ A3.01 and H9 cells in a concentration-dependent manner, but did not mediate the infection of the CD4- cell line, K562. Preincubation of HIV-1 with between 10 and 30 microM-DOTMA liposomes, and subsequent incubation with A3.01 cells, resulted in the production of about 30-fold greater levels of virus than controls. The presence of DOTMA liposomes during the incubation of A3.01 cells with HIV-1 enhanced the infectivity of the virus up to 90-fold compared to controls. Conversely, preincubation of HIV-1 with CL liposomes inhibited infection of A3.01 cells, dependent on the concentration of liposomes; DOPC liposomes did not alter the infectivity of the virus under any of the incubation conditions. Our results thus indicate that fusion of HIV-1 with liposomes alters the ability of the virus to infect its target cells.

摘要

我们研究了脂质体与1型人类免疫缺陷病毒(HIV-1LVA)融合对该病毒感染CD4+和CD4-细胞能力的影响。荧光猝灭测量表明,HIV-1可与由心磷脂(CL)或N-[2,3-(二油酰氧基)丙基]-N,N,N-三甲基氯化铵(DOTMA)组成的脂质体融合,但与二油酰磷脂酰胆碱(DOPC)脂质体的融合不明显。HIV-1与DOTMA脂质体预孵育后,可使CD4+ A3.01和H9细胞中的病毒产量(通过培养基中及原位的p24 gag抗原产量测定)呈浓度依赖性增加,但不能介导CD4-细胞系K562的感染。HIV-1与10至30 microM的DOTMA脂质体预孵育,随后与A3.01细胞孵育,产生的病毒水平比对照高约30倍。在A3.01细胞与HIV-1孵育期间存在DOTMA脂质体,与对照相比,可使病毒的感染性增强达90倍。相反,HIV-1与CL脂质体预孵育会抑制A3.01细胞的感染,这取决于脂质体的浓度;在任何孵育条件下,DOPC脂质体均不会改变病毒的感染性。因此,我们的结果表明,HIV-1与脂质体的融合改变了该病毒感染其靶细胞的能力。

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