CD8 + T细胞对猿猴免疫缺陷病毒感染的恒河猴中病毒复制的抑制及Mamu - A*01限制性表位中突变出现的作用。
Contribution of CD8+ T cells to containment of viral replication and emergence of mutations in Mamu-A*01-restricted epitopes in Simian immunodeficiency virus-infected rhesus monkeys.
作者信息
Kim Eun-Young, Veazey Ronald S, Zahn Roland, McEvers Kimberly J, Baumeister Susanne H C, Foster Gabriel J, Rett Melisa D, Newberg Michael H, Kuroda Marcelo J, Rieber E Peter, Piatak Michael, Lifson Jeffrey D, Letvin Norman L, Wolinsky Steven M, Schmitz Jörn E
机构信息
Division of Infectious Diseases, The Feinberg School of Medicine, Northwestern University, 676 N. St. Clair St., Suite 200, Chicago, IL 60611, USA.
出版信息
J Virol. 2008 Jun;82(11):5631-5. doi: 10.1128/JVI.02749-07. Epub 2008 Mar 26.
Abstract
Here, we investigated the containment of virus replication in simian immunodeficiency virus (SIV) infection by CD8(+) lymphocytes. Escape mutations in Mamu-A*01 epitopes appeared first in SIV Tat TL8 and then in SIV Gag p11C. The appearance of escape mutations in SIV Gag p11C was coincident with compensatory changes outside of the epitope. Eliminating CD8(+) lymphocytes from rhesus monkeys during primary infection resulted in more rapid disease progression that was associated with preservation of canonical epitopes. These results confirm the importance of cytotoxic T cells in controlling viremia and the constraint on epitope sequences that require compensatory changes to go to fixation.
摘要
在此，我们研究了CD8(+)淋巴细胞对猿猴免疫缺陷病毒（SIV）感染中病毒复制的抑制作用。Mamu - A*01表位的逃逸突变首先出现在SIV Tat TL8中，然后出现在SIV Gag p11C中。SIV Gag p11C中逃逸突变的出现与表位外的补偿性变化同时发生。在恒河猴初次感染期间清除CD8(+)淋巴细胞会导致疾病进展更快，这与经典表位的保留有关。这些结果证实了细胞毒性T细胞在控制病毒血症中的重要性，以及对需要补偿性变化才能固定的表位序列的限制。
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