CD4+ T-cell-epitope escape mutant virus selected in vivo
CD4+ T-cell-epitope escape mutant virus selected in vivo
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DOI：
10.1038/89915
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发表时间：
2001-07-01
期刊：
影响因子：
82.9
通讯作者：
Zinkernagel, RM
中科院分区：
文献类型：
--
作者：
Ciurea, A;Hunziker, L;Zinkernagel, RM
在持续性病毒感染期间，影响CD 8（+）细胞毒性T淋巴细胞识别T细胞受体的病毒基因组突变可使病毒逃避免疫监视。虽然CD 4（+）T辅助细胞在维持有效的细胞毒性T淋巴细胞和中和抗体应答中起着关键作用，但它们在病毒清除中的作用以及因此对病毒施加类似的选择性压力的作用尚不清楚。我们在这里表明，转基因病毒特异性CD 4（+）T细胞，转移到小鼠持续感染淋巴细胞性脉络丛脑膜炎病毒，选择辅助T细胞表位突变病毒，不被识别。结合在感染的孔形成蛋白缺陷型C57 BL/6小鼠的多克隆CD 4（+）T细胞应答过程中观察到的相同T辅助细胞表位的抗原变异，这一发现表明病毒从CD 4（+）T淋巴细胞逃逸是病毒持续存在的可能机制。
Mutations in viral genomes that affect T-cell-receptor recognition by CD8(+) cytotoxic T lymphocytes have been shown to allow viral evasion from immune surveillance during persistent viral infections. Although CD4(+) T-helper cells are crucially involved in the maintenance of effective cytotoxic T-lymphocyte and neutralizing-antibody responses, their role in viral clearance and therefore in imposing similar selective pressures on the virus is unclear. We show here that transgenic virus-specific CD4(+) T cells, transferred into mice persistently infected with lymphocytic choriomeningitis virus, select for T-helper epitope mutant viruses that are not recognized. Together with the observed antigenic variation of the same T-helper epitope during polyclonal CD4(+) T-cell responses in infected pore-forming protein-deficient C57BL/6 mice, this finding indicates that viral escape from CD4(+) T lymphocytes is a possible mechanism of virus persistence.