• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

人恶性滋养层细胞系JAR被1型人类免疫缺陷病毒(HIV-1)进行体外生产性感染。

In vitro productive infection of human malignant trophoblastic cell line JAR with human immunodeficiency virus type 1 (HIV-1).

作者信息

Zachar V, Ebbesen P

机构信息

Danish Cancer Society, Department of Virus and Cancer, Aarhus.

出版信息

Acta Virol. 1991 Sep;35(5):464-8.

PMID:1688080
Abstract

Human choriocarcinoma cells of the JAR line, with no demonstrable surface CD4 receptor were infected with human immunodeficiency virus type 1 (HIV-1), strain RF. Primer-directed enzymatic DNA amplification (polymerase chain reaction, PCR) detected the presence of viral DNA when the cultures were investigated at day 5 post-infection (p.i.). The absence of cytopathic changes attributable to virus replication suggested silent infection of these malignant trophoblastic cells. Neither reverse transcriptase (RT) activity nor HIV-specific antigens were found in the culture nutrient medium during JAR cell propagation. However, when the HIV-carrier JAR cells were continuously cultured and the cocultivation was initiated with CEM-SS lymphoblastoid cells after two subsequent passages, rescue of infectious virus was observed.

摘要

用人免疫缺陷病毒1型(HIV-1)RF株感染了无明显表面CD4受体的JAR系人绒毛膜癌细胞。在感染后第5天(p.i.)对培养物进行检测时,引物介导的酶促DNA扩增(聚合酶链反应,PCR)检测到了病毒DNA的存在。未观察到由病毒复制引起的细胞病变变化,提示这些恶性滋养层细胞发生了潜伏感染。在JAR细胞增殖过程中,培养营养培养基中未发现逆转录酶(RT)活性和HIV特异性抗原。然而,当持续培养携带HIV的JAR细胞,并在随后传代两次后与CEM-SS淋巴母细胞系进行共培养时,观察到了感染性病毒的释放。

相似文献

1
In vitro productive infection of human malignant trophoblastic cell line JAR with human immunodeficiency virus type 1 (HIV-1).人恶性滋养层细胞系JAR被1型人类免疫缺陷病毒(HIV-1)进行体外生产性感染。
Acta Virol. 1991 Sep;35(5):464-8.
2
Human immunodeficiency virus type 1 infection of choriocarcinoma-derived trophoblasts.
Acta Virol. 1993 Feb;37(1):21-8.
3
Infection of baboons with simian/human immunodeficiency viruses.狒狒感染猿猴/人类免疫缺陷病毒。
J Acquir Immune Defic Syndr Hum Retrovirol. 1995 Aug 15;9(5):429-41.
4
Susceptibility of cultured human trophoblasts to infection with human immunodeficiency virus type 1.培养的人滋养层细胞对1型人类免疫缺陷病毒感染的易感性。
J Gen Virol. 1991 Jun;72 ( Pt 6):1253-60. doi: 10.1099/0022-1317-72-6-1253.
5
Inhibition of HIV-1 replication by cyclopentenone prostaglandins in acutely infected human cells. Evidence for a transcriptional block.环戊烯酮前列腺素对急性感染人细胞中HIV-1复制的抑制作用。转录阻滞的证据。
J Clin Invest. 1996 Apr 15;97(8):1795-803. doi: 10.1172/JCI118609.
6
Human immunodeficiency virus type 1 infection of human uterine epithelial cells: viral shedding and cell contact-mediated infectivity.人类子宫上皮细胞的1型人类免疫缺陷病毒感染:病毒脱落与细胞接触介导的传染性。
J Infect Dis. 2003 May 15;187(10):1522-33. doi: 10.1086/374782. Epub 2003 Apr 23.
7
Human transformed trophoblast-derived cells lacking CD4 receptor exhibit restricted permissiveness for human immunodeficiency virus type 1.缺乏CD4受体的人转化滋养层来源细胞对1型人类免疫缺陷病毒的易感性有限。
J Virol. 1991 Apr;65(4):2102-7. doi: 10.1128/JVI.65.4.2102-2107.1991.
8
Productive human immunodeficiency virus type 1 infection in peripheral blood predominantly takes place in CD4/CD8 double-negative T lymphocytes.外周血中1型人类免疫缺陷病毒的有效感染主要发生在CD4/CD8双阴性T淋巴细胞中。
J Virol. 2007 Sep;81(18):9693-706. doi: 10.1128/JVI.00492-07. Epub 2007 Jul 3.
9
Inhibition of human immunodeficiency virus type 1 replication by siRNA targeted to the highly conserved primer binding site.靶向高度保守引物结合位点的小干扰RNA对1型人类免疫缺陷病毒复制的抑制作用
Virology. 2004 Dec 5;330(1):221-32. doi: 10.1016/j.virol.2004.09.027.
10
Infection of CD8+ T lymphocytes with HIV. Requirement for interaction with infected CD4+ cells and induction of infectious virus from chronically infected CD8+ cells.HIV对CD8+ T淋巴细胞的感染。与受感染的CD4+细胞相互作用的必要性以及从慢性感染的CD8+细胞中诱导产生传染性病毒。
J Immunol. 1991 Apr 1;146(7):2220-6.