Wyand M S, Manson K H, Garcia-Moll M, Montefiori D, Desrosiers R C
TSI Mason Laboratory, Worcester, Massachusetts, USA.
J Virol. 1996 Jun;70(6):3724-33. doi: 10.1128/JVI.70.6.3724-3733.1996.
Twelve rhesus monkeys were vaccinated with SIVmac316 delta nef (lacking nef sequences), and 12 were vaccinated with SIVmac239 delta3 (lacking nef, vpr, and upstream sequences in U3). SIVmac316 and SIVmac239 differ by only eight amino acids in the envelope; these changes render SIVmac316 highly competent for replication in macrophages. Seventeen of the animals developed persistent infections with the vaccine viruses. Seven of the 24 vaccinated animals, however, developed infections that were apparently transient in nature. Six of these seven yielded virus from peripheral blood when tested at weeks 2 and/or 3, three of the seven had transient antibody responses, but none of the seven had persisting antibody responses. The 24 monkeys were challenged in groups of four with 10 rhesus monkey infectious doses of wild-type, pathogenic SIVmac251 at weeks 8, 20, and 79 following receipt of vaccine. None of the seven with apparently transient infections with vaccine virus were protected upon subsequent challenge. Analysis of cell-associated viral loads, CD4+ cell counts, and viral gene sequences present in peripheral blood in the remainder of the monkeys following challenge allowed a number of conclusions. (i) There was a trend toward increased protection with length of time of vaccination. (ii) Solid vaccine protection was achieved by 79 weeks with the highly attenuated SIV239 delta3. (iii) Solid long-term protection was achieved in at least two animals in the absence of complete sterilizing immunity. (iv) Genetic backbone appeared to influence protective capacity; animals vaccinated with SIV239 delta3 were better protected than animals receiving SIV316 delta nef. This better protection correlated with increased levels of the replicating vaccine strain. (v) The titer of virus-neutralizing activity in serum on the day of challenge correlated with protection when measured against a primary stock of SIVmac251 but not when measured against a laboratory-passaged stock. The level of binding antibodies to whole virus by enzyme-linked immunosorbent assay also correlated with protection.
12只恒河猴接种了SIVmac316 delta nef(缺少nef序列),12只接种了SIVmac239 delta3(缺少nef、vpr以及U3中的上游序列)。SIVmac316和SIVmac239在外膜上仅相差8个氨基酸;这些变化使SIVmac316在巨噬细胞中具有高度的复制能力。17只动物感染了疫苗病毒并持续存在感染。然而,24只接种疫苗的动物中有7只发生了明显为短暂性的感染。这7只中的6只在第2周和/或第3周检测时外周血中产生了病毒,7只中的3只产生了短暂的抗体反应,但7只中没有一只具有持续的抗体反应。在接种疫苗后的第8周、第20周和第79周,将24只猴子分成每组4只,用10个恒河猴感染剂量的野生型致病性SIVmac251进行攻击。7只感染疫苗病毒且感染明显短暂的猴子在随后的攻击中均未得到保护。对攻击后其余猴子外周血中细胞相关病毒载量、CD4+细胞计数和病毒基因序列的分析得出了一些结论。(i)随着接种时间的延长,有保护作用增强的趋势。(ii)到79周时,使用高度减毒的SIV239 delta3可实现可靠的疫苗保护。(iii)在至少两只动物中,在没有完全无菌免疫的情况下实现了可靠的长期保护。(iv)基因骨架似乎影响保护能力;接种SIV239 delta3的动物比接种SIV316 delta nef的动物受到更好的保护。这种更好的保护与复制疫苗株水平的提高相关。(v)攻击当天血清中病毒中和活性的滴度在针对SIVmac251的原始毒株进行检测时与保护作用相关,但针对实验室传代毒株检测时则不相关。通过酶联免疫吸附测定法检测的与全病毒结合的抗体水平也与保护作用相关。