美國和泰國研究人員9月10日在英國《自然》雜志網(wǎng)站上報告說,，他們發(fā)現(xiàn)了艾滋病病毒外殼上一個易被攻破的弱點,，這能夠解釋之前相關試驗中一種艾滋病疫苗的有效性問題，將有助于開發(fā)更有效的艾滋病疫苗,。
幾年前美國和泰國研究人員曾聯(lián)手進行一個代號為RV144的艾滋病疫苗試驗,，結果顯示這種疫苗能夠幫助部分人避免感染艾滋病病毒，但它的有效性只有31%,，這一問題讓研究人員百思不得其解,。
在本次研究中，研究人員對前述試驗中一些參與者感染艾滋病病毒的情況進行了仔細分析,，結果發(fā)現(xiàn),，艾滋病病毒的蛋白質(zhì)外殼上一個名為V1/V2的地方是疫苗有效與否的關鍵。在那些注射疫苗且起到保護效果的人群中,，疫苗會引起人體免疫系統(tǒng)對艾滋病病毒的這個部位進行攻擊,；而在那些注射疫苗但仍然感染了艾滋病病毒的人群中，他們感染的病毒多是在V2這個部位發(fā)生了變異,。
研究人員因此認為,，這個部位是艾滋病病毒易被攻破的弱點。據(jù)估計,，只要艾滋病病毒的這個部位沒有變異,，注射疫苗可以使感染艾滋病病毒的風險降低８0%,。而對于那些這個部位產(chǎn)生了變異以掩蓋自身弱點的艾滋病病毒，現(xiàn)在也可以更有針對性地研發(fā)新疫苗,，針對這個弱點窮追猛打,，幫助實現(xiàn)通過注射疫苗來有效控制艾滋病的夢想。（生物谷Bioon.com）
doi:10.1038/nature11519
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Increased HIV-1 vaccine efficacy against viruses with genetic signatures in Env V2
Morgane Rolland, Paul T. Edlefsen, Brendan B. Larsen, Sodsai Tovanabutra, Eric Sanders-Buell, Tomer Hertz, Allan C. deCamp, Chris Carrico, Sergey Menis, Craig A. Magaret, Hasan Ahmed, Michal Juraska, Lennie Chen, Philip Konopa, Snehal Nariya, Julia N. Stoddard, Kim Wong, Hong Zhao, Wenjie Deng, Brandon S. Maust, Meera Bose, Shana Howell, Adam Bates, Michelle Lazzaro, Annemarie O’Sullivan et al.
The RV144 trial demonstrated 31% vaccine efficacy at preventing human immunodeficiency virus (HIV)-1 infection1. Antibodies against the HIV-1 envelope variable loops 1 and 2 (Env V1 and V2) correlated inversely with infection risk2. We proposed that vaccine-induced immune responses against V1/V2 would have a selective effect against, or sieve, HIV-1 breakthrough viruses. A total of 936 HIV-1 genome sequences from 44 vaccine and 66 placebo recipients were examined. We show that vaccine-induced immune responses were associated with two signatures in V2 at amino acid positions 169 and 181. Vaccine efficacy against viruses matching the vaccine at position 169 was 48% (confidence interval 18% to 66%; P = 0.0036), whereas vaccine efficacy against viruses mismatching the vaccine at position 181 was 78% (confidence interval 35% to 93%; P = 0.0028). Residue 169 is in a cationic glycosylated region recognized by broadly neutralizing and RV144-derived antibodies. The predicted distance between the two signature sites (21?±?7??) and their match/mismatch dichotomy indicate that multiple factors may be involved in the protection observed in RV144. Genetic signatures of RV144 vaccination in V2 complement the finding of an association between high V1/V2-binding antibodies and reduced risk of HIV-1 acquisition, and provide evidence that vaccine-induced V2 responses plausibly had a role in the partial protection conferred by the RV144 regimen.
