Analysis of TCR antagonism on patients having variant HCV

在模型实验中，假设在野生型病毒中出现了少量的变异病毒，我们先前发现1/1000的变异病毒极大地抑制了CTL的诱导，并且剩余的CTL群体，如果有的话，不识别变异病毒本身。在这篇报道中，我们分析了变异病毒已经取代野生病毒的患者的CTL。在该患者中，我们发现了三个CTL群体。一种只识别变异病毒，另一种对变异病毒和野生病毒都识别得很弱，另一种只识别野生病毒。用变异病毒作为次优刺激因子，我们没有发现TCR拮抗作用。然而，在患者体内存在三个CTL群体，我们不能用变异病毒作为刺激因子来诱导识别变异株和野生株的CTL。

In the model experiment assuming that a subtle amount of variant HCV virus emerged in wild one, we previously showed that a 1/1000 amount of variant virus greatly inhibited CTL induction and the remaining CTL population, if any, did not recognize the variant virus itself.In this report, we analyzed the CTL in the patient in whom the variant virus had replaced the wild one already.In that patient, we found three CTL populations. One recognized only the variant virus, another did weakly both of the variant one and the wild one, and the other did only the wild one. And we could not find TCR antagonism using the variant virus as a sub optimal stimulator.Nevertheless, three CTL populations existed in the patient, we could not induce the CTL recognizing both the variant one and the wild one using the variant virus as a stimulator.