Vaccine and Gene Therapy Institute, Department of Molecular Microbiology, Oregon Health & Science University, Beaverton, Oregon 97006, USA.
Nature. 2011 May 26;473(7348):523-7. doi: 10.1038/nature10003. Epub 2011 May 11.
The acquired immunodeficiency syndrome (AIDS)-causing lentiviruses human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) effectively evade host immunity and, once established, infections with these viruses are only rarely controlled by immunological mechanisms. However, the initial establishment of infection in the first few days after mucosal exposure, before viral dissemination and massive replication, may be more vulnerable to immune control. Here we report that SIV vaccines that include rhesus cytomegalovirus (RhCMV) vectors establish indefinitely persistent, high-frequency, SIV-specific effector memory T-cell (T(EM)) responses at potential sites of SIV replication in rhesus macaques and stringently control highly pathogenic SIV(MAC239) infection early after mucosal challenge. Thirteen of twenty-four rhesus macaques receiving either RhCMV vectors alone or RhCMV vectors followed by adenovirus 5 (Ad5) vectors (versus 0 of 9 DNA/Ad5-vaccinated rhesus macaques) manifested early complete control of SIV (undetectable plasma virus), and in twelve of these thirteen animals we observed long-term (≥1 year) protection. This was characterized by: occasional blips of plasma viraemia that ultimately waned; predominantly undetectable cell-associated viral load in blood and lymph node mononuclear cells; no depletion of effector-site CD4(+) memory T cells; no induction or boosting of SIV Env-specific antibodies; and induction and then loss of T-cell responses to an SIV protein (Vif) not included in the RhCMV vectors. Protection correlated with the magnitude of the peak SIV-specific CD8(+) T-cell responses in the vaccine phase, and occurred without anamnestic T-cell responses. Remarkably, long-term RhCMV vector-associated SIV control was insensitive to either CD8(+) or CD4(+) lymphocyte depletion and, at necropsy, cell-associated SIV was only occasionally measurable at the limit of detection with ultrasensitive assays, observations that indicate the possibility of eventual viral clearance. Thus, persistent vectors such as CMV and their associated T(EM) responses might significantly contribute to an efficacious HIV/AIDS vaccine.
获得性免疫缺陷综合征(AIDS)致病的慢病毒包括人类免疫缺陷病毒(HIV)和猴免疫缺陷病毒(SIV),它们能够有效地逃避宿主免疫,而且一旦建立感染,这些病毒的感染通常很难通过免疫机制得到控制。然而,在黏膜暴露后的最初几天内,即在病毒传播和大量复制之前,初始感染可能更容易受到免疫控制。在这里,我们报告称,包含恒河猴巨细胞病毒(RhCMV)载体的 SIV 疫苗能够在恒河猴的潜在 SIV 复制部位建立持久的、高频的、SIV 特异性效应记忆 T 细胞(T(EM))反应,并在黏膜挑战后早期严格控制高致病性 SIV(MAC239)感染。在接受 RhCMV 载体单独或 RhCMV 载体加腺病毒 5(Ad5)载体的 24 只恒河猴中,有 13 只(9 只 DNA/Ad5 疫苗接种的恒河猴中没有)表现出早期完全控制 SIV(无法检测到血浆病毒),并且在这 13 只动物中有 12 只观察到长期(≥1 年)保护。其特征为:血浆病毒血症偶尔出现短暂波动,但最终减弱;血液和淋巴结单核细胞中主要无法检测到细胞相关病毒载量;效应部位 CD4+记忆 T 细胞没有耗竭;未诱导或增强 SIV Env 特异性抗体;诱导并随后丢失了对 RhCMV 载体中未包含的 SIV 蛋白(Vif)的 T 细胞反应。保护与疫苗阶段中 SIV 特异性 CD8+T 细胞反应的峰值幅度相关,并且无需记忆性 T 细胞反应即可发生。值得注意的是,长期 RhCMV 载体相关的 SIV 控制对 CD8+或 CD4+淋巴细胞耗竭不敏感,并且在尸检时,通过超敏检测仅偶尔在检测限下测量到细胞相关 SIV,这些观察结果表明最终可能实现病毒清除。因此,持续存在的病毒载体(如 CMV)及其相关的 T(EM)反应可能会显著促进有效的 HIV/AIDS 疫苗的开发。