Species-specific, postentry barriers to primate immunodeficiency virus infection

Species-specific, postentry barriers to primate immunodeficiency virus infection
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DOI:
10.1128/jvi.73.12.10020-10028.1999
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发表时间:
1999-12-01
影响因子:
5.4
通讯作者:
Sodroski, J
Sodroski, J
中科院分区:
医学2区
文献类型:
--
作者:
Hofmann, W;Schubert, D;Sodroski, J

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利用人类免疫缺陷病毒1型(HIV-1)、猿猴免疫缺陷病毒(SIVmac)和小鼠白血病病毒(MuLV)衍生的复制缺陷载体(均为假型),结合水疱性口炎病毒(VSV) G糖蛋白,在几种哺乳动物靶细胞中检测了进入后、早期感染事件的效率。在大多数旧大陆猴细胞系和原代细胞中,HIV-1载体的滴度明显低于SIVmac和MuLV载体。相比之下,大多数新世界猴细胞对SIVmac载体的滴度比HTV-1载体低得多。原猴细胞对HIV-1和SIVmac载体都有抵抗力,尽管MuLV载体能够感染这些细胞。来自其他哺乳动物物种的细胞对这三种载体的易感性大致相当,但兔子细胞对HIV-1载体具有特异性抗性。在啮齿动物、兔、牛和猪的转导细胞中,HIV-1载体的表达水平非常低。灵长类免疫缺陷病毒感染的早期入境后限制表现出与物种边界基本一致的模式,并适用于单个宿主内的多种细胞类型,这表明涉及物种特异性,广泛表达的细胞因子。
By using replication defective vectors derived from human immunodeficiency virus type 1 (HIV-1), simian immunodeficiency virus (SIVmac), and murine leukemia virus (MuLV), all of which were pseudotyped,vith the vesicular stomatitis virus (VSV) G glycoprotein, the efficiency of postentry, early infection events was examined in target cells of several mammalian species. Titers of HIV-1 vectors were significantly lower than those of SIVmac and MuLV vectors in most cell lines and primary cells from Old World monkeys. By contrast, most New World monkey cells exhibited much lower titers for the SIVmac vector compared with those of the HTV-1 vector. Prosimian cells were resistant to both HIV-1 and SIVmac vectors, although the MuLV vector was able to infect these cells. Cells from other mammalian species were roughly equivalent in susceptibility to the three vectors, with, the exception of rabbit cells, which were specifically resistant to the HIV-1 vector. The level of HIV-1 vector expression was very low in transduced cells of rodent, rabbit, cow, and pig origin. Early postentry restriction of primate immunodeficiency virus infection exhibits patterns largely coincident with species borders and applies to diverse cell types within an individual host, suggesting the involvement of species-specific, widely expressed cellular factors.