van der Noordaa J, van Strien A, Sol C J
J Gen Virol. 1986 Jul;67 ( Pt 7):1485-90. doi: 10.1099/0022-1317-67-7-1485.
High multiplicity BK virus (BKV) infection of primary cells derived from human foetal pancreas resulted in massive cytopathology and subsequent outgrowth of cells. Intranuclear BKV T-antigen was present in all cells and viral antigen was detected in 10 to 30% of these cells. The subcultured cells yielded BKV in the supernatant (approx. 10(5) TCID50/ml) and in the cells free viral DNA was present (approx. 10% of total cellular DNA content). Analysis of the viral DNA indicated the presence of deleted and rearranged BKV DNA molecules. Although all cells continuously expressed BKV T-antigen they did not exhibit the transformed phenotype. This persistent infection of human foetal pancreas cells represents a novel type of in vitro interaction between BKV and human cells which may correspond to the in vivo findings on BKV tropism for pancreatic cells.
源自人胎儿胰腺的原代细胞受到高复制率的BK病毒(BKV)感染后,出现了大规模细胞病理学变化以及随后的细胞生长。所有细胞中均存在核内BKV T抗原,并且在这些细胞的10%至30%中检测到病毒抗原。传代培养的细胞在上清液中产生BKV(约10⁵组织培养感染剂量50%/毫升),并且细胞中存在游离病毒DNA(约占细胞总DNA含量的10%)。对病毒DNA的分析表明存在缺失和重排的BKV DNA分子。尽管所有细胞持续表达BKV T抗原,但它们并未表现出转化表型。人胎儿胰腺细胞的这种持续感染代表了BKV与人类细胞之间一种新型的体外相互作用,这可能与BKV对胰腺细胞的嗜性的体内研究结果相符。