在猴免疫缺陷病毒传播后，三级突变稳定了与 CD8+T 淋巴细胞逃逸相关的补偿性突变。
Tertiary mutations stabilize CD8+ T lymphocyte escape-associated compensatory mutations following transmission of simian immunodeficiency virus.
机构信息
Vaccine & Gene Therapy Institute, Oregon Health & Science University, Portland, Oregon, USA.
出版信息
J Virol. 2014 Mar;88(6):3598-604. doi: 10.1128/JVI.03304-13. Epub 2013 Dec 26.
Abstract
Compensatory mutations offset fitness defects resulting from CD8(+) T lymphocyte (CD8(TL))-mediated escape, but their impact on viral evolution following transmission to naive hosts remains unclear. Here, we investigated the reversion kinetics of Gag(181-189)CM9 CD8(TL) escape-associated compensatory mutations in simian immunodeficiency virus (SIV)-infected macaques. Preexisting compensatory mutations did not result in acute-phase escape of the SIVmac239 CD8(TL) epitope Gag(181-189)CM9 and instead required a tertiary mutation for stabilization in the absence of Gag(181-189)CM9 escape mutations. Therefore, transmitted compensatory mutations do not necessarily predict rapid CD8(TL) escape.
摘要
补偿突变抵消了 CD8(+)T 淋巴细胞（CD8(TL)）介导的逃逸导致的适应性缺陷，但它们对传播到未感染宿主后的病毒进化的影响尚不清楚。在这里，我们研究了感染猴免疫缺陷病毒（SIV）的猕猴中 Gag(181-189)CM9 CD8(TL)逃逸相关补偿突变的回复动力学。预先存在的补偿突变并没有导致 SIVmac239 CD8(TL)表位 Gag(181-189)CM9 的急性逃逸，而是需要在没有 Gag(181-189)CM9 逃逸突变的情况下稳定存在的三级突变。因此，传播的补偿突变不一定预示着快速的 CD8(TL)逃逸。
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