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急性疟疾中携带爱泼斯坦-巴尔病毒的循环B细胞

Circulating Epstein-Barr virus-carrying B cells in acute malaria.

作者信息

Lam K M, Syed N, Whittle H, Crawford D H

机构信息

Department of Clinical Sciences, London School of Hygiene and Tropical Medicine, UK.

出版信息

Lancet. 1991 Apr 13;337(8746):876-8. doi: 10.1016/0140-6736(91)90203-2.

Abstract

Epstein-Barr virus (EBV) infection and Plasmodium falciparum malaria are two known cofactors in the aetiology of endemic Burkitt's lymphoma. To assess the relation between these factors, limiting dilution analysis was used to assess the number of EBV-carrying B cells in the circulation of Gambian children during and after acute malaria. Numbers of virus-carrying cells were five times higher in acute malaria patients and in UK patients with infectious mononucleosis than in convalescent malaria patients and in healthy control adults from the UK. Spontaneous outgrowth in limiting dilution cultures from acute malaria samples was inhibited by acyclovir, a viral DNA polymerase inhibitor. The mechanism of outgrowth, therefore, was virus release from the in-vivo infected cell, which led to infection and immortalisation of co-cultured normal B cells. The findings provide evidence that acute malaria is associated with an increase in the number of EBV-carrying B cells in the circulation. Because of this increase, there is a greater chance of a cytogenetic abnormality occurring in such a cell, with consequent evolution of Burkitt's lymphoma.

摘要

爱泼斯坦-巴尔病毒(EBV)感染和恶性疟原虫疟疾是地方性伯基特淋巴瘤病因学中两个已知的辅助因素。为评估这些因素之间的关系,采用有限稀释分析法评估冈比亚儿童急性疟疾期间及之后循环中携带EBV的B细胞数量。急性疟疾患者及英国传染性单核细胞增多症患者体内携带病毒的细胞数量,比疟疾康复患者及英国健康对照成年人高出五倍。来自急性疟疾样本的有限稀释培养物中的自发生长,受到病毒DNA聚合酶抑制剂阿昔洛韦的抑制。因此,生长机制是病毒从体内感染细胞释放,导致共培养的正常B细胞感染并永生化。这些发现提供了证据,表明急性疟疾与循环中携带EBV的B细胞数量增加有关。由于这种增加,此类细胞发生细胞遗传学异常的可能性更大,进而导致伯基特淋巴瘤的演变。

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