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SU和TM包膜蛋白均决定了猴免疫缺陷病毒SIVmac对猴细胞的嗜性。

Both SU and TM env proteins are responsible for monkey cell tropism of simian immunodeficiency virus SIV mac.

作者信息

Sakuragi S, Sakuragi J, Adachi A

机构信息

Institute for Virus Research, Kyoto University, Japan.

出版信息

Arch Virol. 1995;140(12):2255-60. doi: 10.1007/BF01323244.

Abstract

While simian immunodeficiency virus (SIV) derived from an infectious molecular clone pMA239 is tropic and pathogenic for monkeys, the virus derived from another infectious clone pMA142 does not replicate in monkey cells. To determine genetic sequences responsible for this tropism, a series of recombinant clones were constructed from pMA142 and pMA239. The determinant in pMA239 was mapped within regions encompassing the env gene. Viruses, which carry the 239 env gene encoding surface and/or transmembrane proteins, were tropic for monkey cells.

摘要

虽然源自感染性分子克隆pMA239的猿猴免疫缺陷病毒(SIV)对猴子具有嗜性且具有致病性,但源自另一个感染性克隆pMA142的病毒在猴细胞中不复制。为了确定负责这种嗜性的基因序列,从pMA142和pMA239构建了一系列重组克隆。pMA239中的决定因素定位在包含env基因的区域内。携带编码表面和/或跨膜蛋白的239 env基因的病毒对猴细胞具有嗜性。

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