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无辅助缺陷型逆转录病毒诱导的免疫缺陷及靶细胞的克隆性生长。

Immunodeficiency and clonal growth of target cells induced by helper-free defective retrovirus.

作者信息

Huang M, Simard C, Jolicoeur P

机构信息

Laboratory of Molecular Biology, Clinical Research Institute of Montreal, Quebec, Canada.

出版信息

Science. 1989 Dec 22;246(4937):1614-7. doi: 10.1126/science.2480643.

Abstract

The murine acquired immunodeficiency syndrome is induced by a defective retrovirus. To study the role of virus replication in this disease, helper-free stocks of defective Duplan virus were produced. These stocks were highly pathogenic in absence of detectable replicating murine leukemia viruses (MuLVs) other than xenotropic MuLV. They induced expansion of the infected cell population (over 1000-fold), and this cell expansion was oligoclonal in origin and, most likely, arose through cell division. These results suggest that this defective virus is oncogenic, inducing a primary neoplasia associated with an acquired immunodeficiency syndrome as a paraneoplastic syndrome. These data emphasize the need to determine whether virus replication is necessary for the progression of other immunodeficiency diseases, including acquired immunodeficiency syndrome, and whether these diseases also represent paraneoplastic syndromes.

摘要

鼠获得性免疫缺陷综合征是由一种缺陷型逆转录病毒引起的。为了研究病毒复制在该疾病中的作用,制备了不含辅助病毒的缺陷型杜普兰病毒毒株。这些毒株在除嗜异性小鼠白血病病毒(MuLV)外未检测到有复制活性的鼠白血病病毒(MuLV)的情况下具有高度致病性。它们诱导受感染细胞群体扩增(超过1000倍),并且这种细胞扩增起源于寡克隆,很可能是通过细胞分裂产生的。这些结果表明这种缺陷型病毒具有致癌性,可诱发与获得性免疫缺陷综合征相关的原发性肿瘤,作为副肿瘤综合征。这些数据强调需要确定病毒复制对于包括获得性免疫缺陷综合征在内的其他免疫缺陷疾病的进展是否必要,以及这些疾病是否也代表副肿瘤综合征。

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