Chisari F V, Curtiss L K, Jensen F C
J Clin Invest. 1981 Aug;68(2):329-36. doi: 10.1172/jci110260.
Epstein-Barr virus (EBV)-induced immortalization of adult human B lymphocytes is suppressed by physiologic concentrations of human plasma lipoproteins. Several inhibitory mechanisms appear to be operative. First, low density lipoproteins (LDL) directly reduce the ability of EBV to transform human B cells. Second, LDL as well as intermediate and very low density lipoproteins modulate early inductive events rendering the B cell refractory to transforming signals from EBV. Third, LDL also selectively inhibit an EBV-inducible step that occurs within 24 h after transformation. Finally, very low density lipoproteins can abrogate the ongoing, cellular proliferation of EBV-transformed, established B cell lines. The plasma lipoproteins may therefore prevent the emergence of EBV-transformed malignant B cell clones in vivo. Conceivably, on this basis, environmental and genetic influences on plasma lipoprotein concentrations may affect the global distribution of Burkitt's lymphoma, a lymphoid malignancy putatively caused by EBV.
生理浓度的人血浆脂蛋白可抑制爱泼斯坦-巴尔病毒(EBV)诱导的成人人类B淋巴细胞永生化。几种抑制机制似乎在起作用。首先,低密度脂蛋白(LDL)直接降低EBV转化人类B细胞的能力。其次,LDL以及中密度脂蛋白和极低密度脂蛋白调节早期诱导事件,使B细胞对来自EBV的转化信号产生抗性。第三,LDL还选择性抑制转化后24小时内发生的EBV诱导步骤。最后,极低密度脂蛋白可以消除EBV转化的已建立B细胞系正在进行的细胞增殖。因此,血浆脂蛋白可能会阻止体内EBV转化的恶性B细胞克隆的出现。可以想象,在此基础上,环境和遗传对血浆脂蛋白浓度的影响可能会影响伯基特淋巴瘤的全球分布,伯基特淋巴瘤是一种推测由EBV引起的淋巴恶性肿瘤。