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Analysis of HTLV-I infection mechanisms using cell-free virus

利用无细胞病毒分析HTLV-I感染机制

基本信息

批准号：
11470075
负责人：
HOSHINO Hiroo
金额：
$ 7.74万
依托单位：
Gunma University School of Medicine
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B).
财政年份：
1999
资助国家：
日本
起止时间：
1999 至 2000
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-11470075/
关键词：
HTLV-I HSC70 cell fusion oligopeptide synovial cell GFP Tax pseudotype 脾腫好中球増多症 BLV 滑膜細胞突症性サイトカイン合胞体合成ペプチド

项目摘要

1) We showed that the expression of HSC70 enhanced HTLV-I-induced cell fusion but did not affect the efficiency of cell-free HTLV-I plating, suggesting that HSC7O binds to HTLV-I but is not its receptor.2) When 8C cells expressing Tax of HTLV-I were infected with cell-free HTLV-I, numerous syncytia were formed in these cells and production of progeny HTLV-I was detected in culture supernatants.3) Pseudotype virus, namely, chimeric vesicular stomatitis virus (VSV) containing GFP gene that bears envelope proteins of HTLV-I, was formed efficiently when HTLV-I-producing cells were infected with chimeric VSV.4) We found that HTLV-I was highly sensitive to ultraviolet light irradiation and that it was not so stable at 37℃, as compared with bovine leukemia virus (BLV).5) When human synovial cells were infected with HTLV-I or BLV, both viruses were detected shortly after infection. The cells infected with BLV but not HTLV-I grew more than one year in tissue culture.6) One of oligopeptides encompassing gp21 inhibited HTLV-I infection at a step after virus adsorption.7) Sera of HTLV-I-infected subjects inhibited HTLV-I infection in vitro after virus adsorption step.8) HTLV-I produced from cells treated with glycosylation inhibitors, especially inhibitors at early steps of glycosylation showed reduced infectivities. In contrast, sialidase enhanced its infectivity.9) Injection of human osetosarcoma cells infected with HTLV-I or transduced with tax into nude mice induced rapid tumor formation, splenomegaly and neutrophilia. G-CSF or GM-CSF was detected in their sera at high levels.

1）我们发现HSC70的表达增强了HTLV-I诱导的细胞融合，但不影响无细胞HTLV-I铺板的效率，表明HSC7O与HTLV-I结合但不是其受体。2）当表达HTLV-I Tax的8C细胞被无细胞HTLV-I感染时，在这些细胞中形成大量合胞体并产生后代在培养上清液中检测到HTLV-I。3)当产生HTLV-I的细胞被嵌合VSV感染时，有效地形成了假型病毒，即含有带有HTLV-I包膜蛋白的GFP基因的嵌合水泡性口炎病毒(VSV)。4)我们发现HTLV-I对与牛白血病病毒(BLV)相比，它在37℃下不太稳定。5)当人类滑膜细胞感染HTLV-I或BLV时，两种病毒在感染后不久就被检测到。感染 BLV 而不是 HTLV-I 的细胞在组织培养中生长超过一年。6) 一种包含 gp21 的寡肽在病毒吸附步骤后抑制 HTLV-I 感染。7) HTLV-I 感染受试者的血清在病毒吸附步骤后在体外抑制 HTLV-I 感染。8) 从处理的细胞产生 HTLV-I 使用糖基化抑制剂，特别是糖基化早期阶段的抑制剂，显示出感染性降低。相反，唾液酸酶增强了其感染性。9)将感染HTLV-I或用tax转导的人骨肉瘤细胞注射到裸鼠体内，诱导了快速肿瘤形成、脾肿大和中性粒细胞增多。他们的血清中检测到高水平的 G-CSF 或 GM-CSF。