Unité Virus et Immunite, Institut Pasteur, URA CNRS 3015, Paris, France.
J Virol. 2010 May;84(10):5314-28. doi: 10.1128/JVI.02329-09. Epub 2010 Mar 10.
Poxvirus-based human immunodeficiency virus (HIV) vaccine candidates are currently under evaluation in preclinical and clinical trials. Modified vaccinia virus Ankara (MVA) vectors have excellent safety and immunogenicity records, but their behavior in human cell cultures remains only partly characterized. We studied here various virological and immunological aspects of the interactions of MVA-HIV, a vaccine candidate developed by the French National Agency for AIDS Research (ANRS), with primary human cells. We report that MVA-HIV infects and drives Gag expression in primary macrophages, dendritic cells (DCs), and epithelial and muscle cells. MVA-HIV-infected DCs matured, efficiently presented Gag, Pol, and Nef antigens, and activated HIV-specific cytotoxic T lymphocytes (CTLs). As expected with this type of vector, infection was cytopathic and led to DC apoptosis. Coculture of MVA-HIV-infected epithelial cells or myotubes with DCs promoted efficient Gag antigen major histocompatibility complex class I (MHC-I) cross-presentation without inducing direct infection and death of DCs. Antigen-presenting cells (APCs) infected with MVA-HIV also activated HIV-specific CD4(+) T cells. Moreover, exposure of DCs to MVA-HIV or to MVA-HIV-infected myotubes induced type I interferon (IFN) production and inhibited subsequent HIV replication and transfer to lymphocytes. Altogether, these results show that MVA-HIV promotes efficient MHC-I and MHC-II presentation of HIV antigens by APCs without facilitating HIV replication. Deciphering the immune responses to MVA in culture experiments will help in the design of innovative vaccine strategies.
痘病毒载体的人类免疫缺陷病毒(HIV)候选疫苗目前正在进行临床前和临床试验评估。改良安卡拉牛痘病毒(MVA)载体具有出色的安全性和免疫原性记录,但它们在人类细胞培养物中的行为仅部分得到了描述。我们在此研究了法国国家艾滋病研究署(ANRS)开发的候选疫苗 MVA-HIV 与原代人细胞相互作用的各种病毒学和免疫学方面。我们报告称,MVA-HIV 可感染并驱动原代巨噬细胞、树突状细胞(DC)、上皮细胞和肌肉细胞中的 Gag 表达。MVA-HIV 感染的 DC 成熟,有效呈递 Gag、Pol 和 Nef 抗原,并激活 HIV 特异性细胞毒性 T 淋巴细胞(CTL)。与这种类型的载体一样,感染具有细胞病变作用,并导致 DC 凋亡。将 MVA-HIV 感染的上皮细胞或肌管与 DC 共培养可促进 Gag 抗原主要组织相容性复合体 I 类(MHC-I)交叉呈递,而不会直接感染和导致 DC 死亡。感染了 MVA-HIV 的抗原呈递细胞(APC)也可激活 HIV 特异性 CD4(+)T 细胞。此外,DC 暴露于 MVA-HIV 或 MVA-HIV 感染的肌管可诱导 I 型干扰素(IFN)的产生,并抑制随后的 HIV 复制和向淋巴细胞的转移。总之,这些结果表明,MVA-HIV 可促进 APC 有效呈递 HIV 抗原的 MHC-I 和 MHC-II,而不促进 HIV 复制。解析在培养实验中对 MVA 的免疫反应将有助于设计创新的疫苗策略。