• 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

人类免疫缺陷病毒(HIV)进入MT-2,即人类T细胞白血病病毒携带细胞系。

Entry of human immunodeficiency virus (HIV) into MT-2, human T cell leukemia virus carrier cell line.

作者信息

Goto T, Harada S, Yamamoto N, Nakai M

机构信息

Department of Microbiology, Osaka Medical College, Japan.

出版信息

Arch Virol. 1988;102(1-2):29-38. doi: 10.1007/BF01315560.

DOI:10.1007/BF01315560
PMID:2904253
Abstract

The ultrastructural features of early events in human immunodeficiency virus (HIV) infection of HTLV-I-carrying MT-2 lymphocytes were investigated by electron microscopy. Within 10 min after virus inoculation at 37 degrees C, the virus entered the cell in two ways; (1) the virus attached to the lymphocyte membrane and the viral core entered the cell after fusion of the viral envelope with the cell membrane, and (2) part of the cell membrane to which the virus was attached became invaginated, the virus became trapped in a phagosome and the viral core entered after the fusion of viral membrane with the vacuolar membrane. Thereafter, some cells were observed to form syncytia with multiple nuclei. When the proportion of anti-HIV antibody-reactive cells present exceeded 90%, virus production was strongly activated, and budding on the cell membrane was frequently observed.

摘要

利用电子显微镜研究了携带人嗜T淋巴细胞病毒I型(HTLV-I)的MT-2淋巴细胞感染人类免疫缺陷病毒(HIV)早期事件的超微结构特征。在37℃接种病毒后10分钟内,病毒通过两种方式进入细胞:(1)病毒附着于淋巴细胞膜,病毒包膜与细胞膜融合后病毒核心进入细胞;(2)附着病毒的部分细胞膜内陷,病毒被困于吞噬体中,病毒膜与液泡膜融合后病毒核心进入。此后,观察到一些细胞形成多核巨细胞。当抗HIV抗体反应性细胞的比例超过90%时,病毒产生被强烈激活,且经常观察到细胞膜上有出芽现象。

相似文献

1
Entry of human immunodeficiency virus (HIV) into MT-2, human T cell leukemia virus carrier cell line.人类免疫缺陷病毒(HIV)进入MT-2,即人类T细胞白血病病毒携带细胞系。
Arch Virol. 1988;102(1-2):29-38. doi: 10.1007/BF01315560.
2
Electron microscopic analysis of HIV-host cell interactions.
Tissue Cell. 1994 Aug;26(4):539-50. doi: 10.1016/0040-8166(94)90006-x.
3
Factors affecting cellular tropism of human immunodeficiency virus.影响人类免疫缺陷病毒细胞嗜性的因素。
J Virol. 1990 Nov;64(11):5600-4. doi: 10.1128/JVI.64.11.5600-5604.1990.
4
Infection of monocyte-derived macrophages with human immunodeficiency virus type 1 (HIV-1). Monocyte-tropic and lymphocyte-tropic strains of HIV-1 show distinctive patterns of replication in a panel of cell types.人免疫缺陷病毒1型(HIV-1)感染单核细胞衍生的巨噬细胞。HIV-1的嗜单核细胞株和嗜淋巴细胞株在一组细胞类型中表现出独特的复制模式。
J Exp Med. 1989 Oct 1;170(4):1149-63. doi: 10.1084/jem.170.4.1149.
5
Human immunodeficiency virus (HIV) infection in CD4+ T lymphocytes genetically deficient in LFA-1: LFA-1 is required for HIV-mediated cell fusion but not for viral transmission.缺乏淋巴细胞功能相关抗原-1(LFA-1)的CD4 + T淋巴细胞中的人类免疫缺陷病毒(HIV)感染:HIV介导的细胞融合需要LFA-1,但病毒传播不需要。
J Exp Med. 1991 Feb 1;173(2):511-4. doi: 10.1084/jem.173.2.511.
6
Human immunodeficiency virus type 1 (HIV-1) and herpes simplex virus type 2 (HSV-2) can coinfect and simultaneously replicate in the same human CD4+ cell: effect of coinfection on infectious HSV-2 and HIV-1 replication.1型人类免疫缺陷病毒(HIV-1)和2型单纯疱疹病毒(HSV-2)可共同感染并在同一个人类CD4+细胞中同时复制:共同感染对HSV-2和HIV-1感染性复制的影响。
AIDS Res Hum Retroviruses. 1990 May;6(5):641-7. doi: 10.1089/aid.1990.6.641.
7
Compensatory link between fusion and endocytosis of human immunodeficiency virus type 1 in human CD4 T lymphocytes.人类CD4 T淋巴细胞中1型人类免疫缺陷病毒融合与胞吞作用之间的代偿性联系
J Virol. 2004 Feb;78(3):1375-83. doi: 10.1128/jvi.78.3.1375-1383.2004.
8
Establishment of an MT4 cell line persistently producing infective HIV-1 particles.
Acta Microbiol Hung. 1992;39(3-4):271-9.
9
Dendritic cells exposed to human immunodeficiency virus type-1 transmit a vigorous cytopathic infection to CD4+ T cells.
Science. 1992 Jul 17;257(5068):383-7. doi: 10.1126/science.1352913.
10
Membrane-fusing capacity of the human immunodeficiency virus envelope proteins determines the efficiency of CD+ T-cell depletion in macaques infected by a simian-human immunodeficiency virus.人类免疫缺陷病毒包膜蛋白的膜融合能力决定了感染猿猴-人类免疫缺陷病毒的猕猴中CD+ T细胞耗竭的效率。
J Virol. 2001 Jun;75(12):5646-55. doi: 10.1128/JVI.75.12.5646-5655.2001.

引用本文的文献

1
Lipid rafts and pathogens: the art of deception and exploitation.脂筏与病原体:欺骗与利用的艺术。
J Lipid Res. 2020 May;61(5):601-610. doi: 10.1194/jlr.TR119000391. Epub 2019 Oct 15.
2
Overexpression of the Interferon-Inducible Isoform 4 of Dissects the Entry Route of Enveloped Viruses and Demonstrates that HIV Enters Cells via Fusion at the Plasma Membrane.干扰素诱导的 4 型异构体的过表达解析了包膜病毒的进入途径,并证明 HIV 通过融合进入细胞膜进入细胞。
Viruses. 2019 Jan 29;11(2):121. doi: 10.3390/v11020121.
3
Simple mathematical models do not accurately predict early SIV dynamics.

本文引用的文献

1
On the entry of Semliki forest virus into BHK-21 cells.关于Semliki森林病毒进入BHK - 21细胞的过程。
J Cell Biol. 1980 Feb;84(2):404-20. doi: 10.1083/jcb.84.2.404.
2
Ultrastructural and immunofluorescence studies of early events in adenovirus-HeLa cell interactions.腺病毒与HeLa细胞相互作用早期事件的超微结构和免疫荧光研究。
J Gen Virol. 1983 May;64(Pt 5):1091-9. doi: 10.1099/0022-1317-64-5-1091.
3
Review article initial stages in infection with animal viruses.综述文章:动物病毒感染的初始阶段
简单的数学模型无法准确预测早期的猴免疫缺陷病毒动态。
Viruses. 2015 Mar 13;7(3):1189-217. doi: 10.3390/v7031189.
4
HIV-1 entry in SupT1-R5, CEM-ss, and primary CD4+ T cells occurs at the plasma membrane and does not require endocytosis.HIV-1进入SupT1-R5细胞、CEM-ss细胞和原代CD4+ T细胞是在质膜上发生的,且不需要内吞作用。
J Virol. 2014 Dec;88(24):13956-70. doi: 10.1128/JVI.01543-14. Epub 2014 Sep 24.
5
Mathematical modeling of escape of HIV from cytotoxic T lymphocyte responses.HIV逃避细胞毒性T淋巴细胞反应的数学建模。
J Stat Mech. 2013 Jan 1;2013:P01010. doi: 10.1088/1742-5468/2013/01/P01010.
6
HIV entry: a game of hide-and-fuse?HIV 进入:一场“躲猫猫”与“融合”的游戏?
Curr Opin Virol. 2014 Feb;4:1-7. doi: 10.1016/j.coviro.2013.09.004. Epub 2013 Nov 1.
7
Inhibition of lysosome and proteasome function enhances human immunodeficiency virus type 1 infection.抑制溶酶体和蛋白酶体功能可增强1型人类免疫缺陷病毒感染。
J Virol. 2005 May;79(9):5705-12. doi: 10.1128/JVI.79.9.5705-5712.2005.
8
Involvement of clathrin-mediated endocytosis in human immunodeficiency virus type 1 entry.网格蛋白介导的内吞作用在1型人类免疫缺陷病毒进入过程中的作用。
J Virol. 2005 Feb;79(3):1581-94. doi: 10.1128/JVI.79.3.1581-1594.2005.
9
Pathogenesis of human immunodeficiency virus infection.人类免疫缺陷病毒感染的发病机制
Microbiol Rev. 1993 Mar;57(1):183-289. doi: 10.1128/mr.57.1.183-289.1993.
10
HIV-particles in spermatozoa of patients with AIDS and their transfer into the oocyte.艾滋病患者精子中的HIV颗粒及其向卵母细胞的转移。
J Cell Biol. 1994 Nov;127(4):903-14. doi: 10.1083/jcb.127.4.903.
J Gen Virol. 1982 Mar;59(Pt 1):1-22. doi: 10.1099/0022-1317-59-1-1.
4
Uncoating of enveloped viruses.包膜病毒的脱壳
Cell. 1982 Jan;28(1):5-6. doi: 10.1016/0092-8674(82)90368-3.
5
Type C virus particles in a cord T-cell line derived by co-cultivating normal human cord leukocytes and human leukaemic T cells.通过将正常人脐带血白细胞与人类白血病T细胞共同培养而获得的脐带T细胞系中的C型病毒颗粒。
Nature. 1981 Dec 24;294(5843):770-1. doi: 10.1038/294770a0.
6
Isolation of lymphocytopathic retroviruses from San Francisco patients with AIDS.从旧金山艾滋病患者中分离淋巴细胞病变逆转录病毒。
Science. 1984 Aug 24;225(4664):840-2. doi: 10.1126/science.6206563.
7
Frequent detection and isolation of cytopathic retroviruses (HTLV-III) from patients with AIDS and at risk for AIDS.从艾滋病患者和有患艾滋病风险的人群中频繁检测和分离出细胞病变逆转录病毒(HTLV-III)。
Science. 1984 May 4;224(4648):500-3. doi: 10.1126/science.6200936.
8
Detection, isolation, and continuous production of cytopathic retroviruses (HTLV-III) from patients with AIDS and pre-AIDS.从艾滋病患者和艾滋病前期患者中检测、分离并持续生产细胞病变逆转录病毒(HTLV-III)。
Science. 1984 May 4;224(4648):497-500. doi: 10.1126/science.6200935.
9
Isolation of a T-lymphotropic retrovirus from a patient at risk for acquired immune deficiency syndrome (AIDS).从一名有获得性免疫缺陷综合征(艾滋病)风险的患者体内分离出一种嗜T淋巴细胞逆转录病毒。
Science. 1983 May 20;220(4599):868-71. doi: 10.1126/science.6189183.
10
T4 positive human neoplastic cell lines susceptible to and permissive for HTLV-III.对HTLV-III敏感且允许其感染的T4阳性人类肿瘤细胞系。
Lancet. 1984 Dec 22;2(8417-8418):1472-3. doi: 10.1016/s0140-6736(84)91666-0.