Mode of replication and pathogenicity of human herpesvirus 7
人疱疹病毒7型的复制方式和致病性
基本信息
- 批准号:06670329
- 负责人:
- 金额:$ 1.09万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for General Scientific Research (C)
- 财政年份:1994
- 资助国家:日本
- 起止时间:1994 至 1995
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Human Herpesvirus 7 (HHV-7), a new T-lymphotropic herpesvirus, is related to, but significantly different from HHV-6. We isolated several clinical isolates from saliva samples of healthy adults, and they were identified as HHV-7. We established a method for infectious titration and a method to obtain high titer cell-free virus preparation using cord blood lymphocytes. One-step growth curves of HHV-6A,6B,and 7 were comparatively analyzed. Among 21 hematopoietic cell lines, a CD4+ CD8+ T cell line, SUP-T1, was the only cell line that supported HHV-7 replication. Virus titers of HHV-7 in SUP-T1 cells were comparable to those in cord blood lymphocytes.Persistent production of infectious virus was observed after infection of SUP-T1 cells with HHV-7. The culture was the mixture of infected and uninfected cells with the ratio of the infected cells ranging around 10 to 20%. Interferon activity was not detected in the supernatant. However, the treatment of the culture with exogenous interferon beta dramatically reduced the production of virus and cured the culture of the persistent infection. No virus production, infected cell, or HHV-7 genome was detectable.We studied the interaction of HIV-1 and HHV-7 using the SUP-T1 cell line and a HIV carrier cell line established from SUP-T1. Expression of the CD4 antigen was completely downregulated in the HIV-1 carrier cell line. While superinfection of HIV-1 carrier SUP-T1 cells with HHV-6 was readily accomplished, the same cells were completely resistant to superinfection with HHV-7. Furthermore, treatment of SUP-T1 cells with anti-CD4 monoclonal antibodies inhibited the growth of HHV-7. These results suggest that resistance of HIV-1 carrier SUP-T1 cells to HHV-7 is due to the absence of the CD4 antigen on the cell surface and that HIV-1 and HHV-7 use the same molecule, the CD4 antigen, as the virus receptor.
人类疱疹病毒7型(HHV-7)是一种新的T淋巴细胞疱疹病毒,与HHV-6既有亲缘关系,又有显著不同。我们从健康成人的唾液标本中分离到几株临床分离株,经鉴定为HHV-7。我们建立了一种感染性滴定的方法和一种利用脐带血淋巴细胞获得高滴度无细胞病毒制剂的方法。比较分析了HHV-6A、6B、7株的一步生长曲线。在21个造血细胞系中,CD4+CD8+T细胞系SUP-T1是唯一支持HHV-7复制的细胞系。HHV-7在SUP-T1细胞中的病毒滴度与脐血淋巴细胞中的HHV-7病毒滴度相当,感染SUP-T1细胞后可持续产生传染性病毒。培养物为感染细胞和未感染细胞的混合物,感染细胞比例约为10%~20%。培养上清液中未检测到干扰素活性。然而,外源干扰素β处理显著减少了病毒的产生,并治愈了持续感染的培养。未检测到病毒产生、感染细胞或HHV-7基因组。我们利用SUP-T1细胞系和由SUP-T1建立的HIV载体细胞系研究了HIV-1和HHV-7的相互作用。在HIV-1携带者细胞系中,CD4抗原的表达完全下调。虽然HIV-1携带者SUP-T1细胞很容易与HHV-6重叠感染,但相同的细胞对HHV-7重叠感染完全具有抵抗力。此外,用抗CD4单抗处理SUP-T1细胞可抑制HHV-7的生长。这些结果表明,HIV-1携带者SUP-T1细胞对HHV-7的抵抗力是由于细胞表面缺乏CD4抗原,并且HIV-1和HHV-7使用相同的分子,即CD4抗原作为病毒受体。
项目成果
期刊论文数量(50)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Yamada M: "Resistance of HIV-1 carrier SUP-T1 cells to superinfection with human herpesvirus 7" AIDS Research Newsletter. 37. (1994)
Yamada M:“HIV-1 携带者 SUP-T1 细胞对人类疱疹病毒 7 重复感染的抵抗力”艾滋病研究通讯。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Hayashi K: "HTLV-II non-integrated malignant lymphoma induction in japanese white rabbits following intravenous inoculation of HTLV-II-infected simian leukocyte cell line (Si-IIA)." Japanese.Journal of Cancer Research. 85. 808-818 (1994)
Hayashi K:“静脉注射 HTLV-II 感染的猿白细胞系 (Si-IIA) 后,日本白兔体内诱导 HTLV-II 非整合性恶性淋巴瘤。”
- DOI:
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- 影响因子:0
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Hayase Y: "Ultrahigh-resolution scanning electron microscopy of MDCK cells infected with influenza viruses." Journal of Electron Microscopy. 44. 281-288 (1995)
Hayase Y:“用超高分辨率扫描电子显微镜观察感染流感病毒的 MDCK 细胞。”
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Hayashi K.: "HTLV-II non-integrated malignant lymphoma induction in Japanese white rabbits following intravenous inoculation of HTLV-II-infected simian leukocyte cell line(Si-IIA)" Jap.J Cancer Res.86(8). 808-818 (1994)
Hayashi K.:“静脉内接种 HTLV-II 感染的猿白细胞系 (Si-IIA) 后,日本白兔中诱导 HTLV-II 非整合性恶性淋巴瘤”Jap.J Cancer Res.86(8)。
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- 发表时间:
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- 影响因子:0
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Nakamura J: "Analysis of molluscum contagiosum virus genomes isolated in Japan." Journal of Medical Virology. 46. 339-348 (1995)
Nakamura J:“日本分离的传染性软疣病毒基因组分析。”
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- 影响因子:0
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YAMADA Masao其他文献
YAMADA Masao的其他文献
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{{ truncateString('YAMADA Masao', 18)}}的其他基金
Alternative splicing in disease genes
疾病基因中的选择性剪接
- 批准号:
18590318 - 财政年份:2006
- 资助金额:
$ 1.09万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Inhibitory Effects of Beta-herpesviruses on Hematopoiesis
β-疱疹病毒对造血的抑制作用
- 批准号:
13670299 - 财政年份:2001
- 资助金额:
$ 1.09万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Analysis of antigenic properties of human herpesvirus 7 and the host immune responses
人疱疹病毒7型抗原特性及宿主免疫反应分析
- 批准号:
10670285 - 财政年份:1998
- 资助金额:
$ 1.09万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Dynamic mutations in genome, like triplet repeat expansion
基因组中的动态突变,例如三联体重复扩增
- 批准号:
07458253 - 财政年份:1995
- 资助金额:
$ 1.09万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
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