Lifson J D, Rossio J L, Piatak M, Parks T, Li L, Kiser R, Coalter V, Fisher B, Flynn B M, Czajak S, Hirsch V M, Reimann K A, Schmitz J E, Ghrayeb J, Bischofberger N, Nowak M A, Desrosiers R C, Wodarz D
Retroviral Pathogenesis Laboratory, AIDS Vaccine Program, SAIC Frederick, National Cancer Institute at Frederick, Frederick, Maryland 21702, USA.
J Virol. 2001 Nov;75(21):10187-99. doi: 10.1128/JVI.75.21.10187-10199.2001.
Transient antiretroviral treatment with tenofovir, (R)-9-(2-phosphonylmethoxypropyl)adenine, begun shortly after inoculation of rhesus macaques with the highly pathogenic simian immunodeficiency virus (SIV) isolate SIVsmE660, facilitated the development of SIV-specific lymphoproliferative responses and sustained effective control of the infection following drug discontinuation. Animals that controlled plasma viremia following transient postinoculation treatment showed substantial resistance to subsequent intravenous rechallenge with homologous (SIVsmE660) and highly heterologous (SIVmac239) SIV isolates, up to more than 1 year later, despite the absence of measurable neutralizing antibody. In some instances, resistance to rechallenge was observed despite the absence of detectable SIV-specific binding antibody and in the face of SIV lymphoproliferative responses that were low or undetectable at the time of challenge. In vivo monoclonal antibody depletion experiments demonstrated a critical role for CD8(+) lymphocytes in the control of viral replication; plasma viremia rose by as much as five log units after depletion of CD8(+) cells and returned to predepletion levels (as low as <100 copy Eq/ml) as circulating CD8(+) cells were restored. The extent of host control of replication of highly pathogenic SIV strains and the level of resistance to heterologous rechallenge achieved following transient postinoculation treatment compared favorably to the results seen after SIVsmE660 and SIVmac239 challenge with many vaccine strategies. This impressive control of viral replication was observed despite comparatively modest measured immune responses, less than those often achieved with vaccination regimens. The results help establish the underlying feasibility of efforts to develop vaccines for the prevention of AIDS, although the exact nature of the protective host responses involved remains to be elucidated.
在恒河猴接种高致病性猿猴免疫缺陷病毒(SIV)毒株SIVsmE660后不久开始用替诺福韦((R)-9-(2-膦酰甲氧基丙基)腺嘌呤)进行短暂抗逆转录病毒治疗,促进了SIV特异性淋巴细胞增殖反应的发展,并在停药后持续有效控制感染。接种后短暂治疗后能控制血浆病毒血症的动物,对随后用同源(SIVsmE660)和高度异源(SIVmac239)SIV毒株进行静脉再攻击显示出显著抗性,即使在没有可测量的中和抗体的情况下,这种抗性可持续长达1年多。在某些情况下,尽管在攻击时没有可检测到的SIV特异性结合抗体且SIV淋巴细胞增殖反应很低或无法检测到,但仍观察到对再攻击的抗性。体内单克隆抗体清除实验证明CD8(+)淋巴细胞在控制病毒复制中起关键作用;CD8(+)细胞清除后血浆病毒血症上升多达5个对数单位,随着循环CD8(+)细胞恢复,病毒血症回到清除前水平(低至<100拷贝当量/毫升)。与许多疫苗策略在SIVsmE660和SIVmac239攻击后看到的结果相比,接种后短暂治疗后对高致病性SIV毒株复制的宿主控制程度和对异源再攻击的抗性水平更优。尽管测得的免疫反应相对适度,低于疫苗接种方案通常达到的水平,但仍观察到对病毒复制的这种显著控制。这些结果有助于确立开发预防艾滋病疫苗努力的潜在可行性,尽管所涉及的保护性宿主反应的确切性质仍有待阐明。