Schneidewind Arne, Brumme Zabrina L, Brumme Chanson J, Power Karen A, Reyor Laura L, O'Sullivan Kristin, Gladden Adrianne, Hempel Ursula, Kuntzen Thomas, Wang Yaoyu E, Oniangue-Ndza Cesar, Jessen Heiko, Markowitz Martin, Rosenberg Eric S, Sékaly Rafick-Pierre, Kelleher Anthony D, Walker Bruce D, Allen Todd M
Partners AIDS Research Center, Massachusetts General Hospital, Boston, MA, USA.
J Virol. 2009 Apr;83(8):3993-7. doi: 10.1128/JVI.01108-08. Epub 2008 Dec 17.
Human immunodeficiency virus effectively evades CD8(+) T-cell responses through the development of CD8 escape mutations. Recent reports documenting reversion of transmitted mutations and the impact of specific escape mutations upon viral replication suggest that complex forces limit the accumulation of CD8 escape mutations at the population level. However, the presence of compensatory mutations capable of alleviating the impact of CD8 escape mutations on replication capacity may enable their persistence in an HLA-mismatched host. Herein, we illustrate the long-term stability of stereotypic escape mutations in the immunodominant HLA-B27-restricted epitope KK10 in p24/Gag following transmission when accompanied by a specific compensatory mutation.
人类免疫缺陷病毒通过产生CD8逃逸突变有效地逃避CD8(+) T细胞反应。最近有报告记录了传播突变的逆转以及特定逃逸突变对病毒复制的影响，这表明复杂的力量在群体水平上限制了CD8逃逸突变的积累。然而，能够减轻CD8逃逸突变对复制能力影响的补偿性突变的存在，可能使它们在HLA不匹配的宿主中持续存在。在此，我们说明了在传播时，p24/Gag中免疫显性的HLA - B27限制性表位KK10中的典型逃逸突变，在伴有特定补偿性突变时的长期稳定性。
