Gayama S, Vaupel B A, Kanagawa O
Department of Pathology and Medicine, Washington University School of Medicine, St Louis, MO 63110, USA.
Int Immunol. 1995 May;7(5):861-8. doi: 10.1093/intimm/7.5.861.
A defective murine leukemia virus is the causative agent of murine acquired immunodeficiency syndrome (MAIDS). We have cloned cDNAs from both virus infected and non-infected cells using the PCR methods with primers corresponding to the franking sequence of the unique p12 gag gene. Sequence analysis of these cDNA clones revealed: (i) the presence of endogenous virus related to MAIDS virus in C57BL/6 mice, (ii) B cell lineage specific expression of endogenous virus and (iii) extensive heterogeneity of MAIDS virus recovered from virus infected cells due to the recombination of the related viruses (defective pathogenic virus, ecotropic virus and endogenous virus). These findings suggest that the creation of virus variants in infected cells may play an important role in virus pathogenesis and escape from immune attack during the development of MAIDS.
一种有缺陷的鼠白血病病毒是鼠获得性免疫缺陷综合征(MAIDS)的病原体。我们使用与独特的p12 gag基因的侧翼序列相对应的引物,通过PCR方法从病毒感染细胞和未感染细胞中克隆了cDNA。对这些cDNA克隆的序列分析显示:(i)C57BL/6小鼠中存在与MAIDS病毒相关的内源性病毒,(ii)内源性病毒的B细胞谱系特异性表达,以及(iii)由于相关病毒(缺陷致病病毒、亲嗜性病毒和内源性病毒)的重组,从病毒感染细胞中回收的MAIDS病毒具有广泛的异质性。这些发现表明,感染细胞中病毒变体的产生可能在MAIDS发展过程中的病毒发病机制和逃避免疫攻击中起重要作用。