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摘要
免疫缺陷小鼠与人类CD4 + T细胞重组可以通过转移成熟细胞或未成熟的祖细胞来实现,这是研究体内淋巴细胞HIV-1感染的唯一动物模型。然而,这些模型大多数免疫功能低下,以至于其不能用于疫苗研究。然而,该模型可能非常适合于HIV-1的基因治疗研究,因为引起有效的抗病毒免疫反应并不是主要终点。相反,HIV-1基因治疗应该保护的CD4 + T细胞,使其免受HIV-1诱导的缺失和/或病毒复制的减少。本文描述了HIV-1基因治疗领域的最新进展,注重于在人性化小鼠模型得到验证的工具和靶点。通过研究表明,通过中和抗体或融合抑制剂以针对病毒进入的方法是目前为止最有效的。事实上,针对病毒进入的方法在临床临床试验中得到很好的结果。因此,人性化的小鼠可作为制定安全和最有效的HIV-1基因治疗策略的主要模型。
关键词: HIV-1
Current Gene Therapy
Title:Lessons From HIV-1 Gene Therapy in Humanized Mice: Is Targeting Viral Entry the Road to Success?
Volume: 16 Issue: 1
Author(s): Nicolas Petit and Gilles Marodon
Affiliation:
关键词: HIV-1
摘要: Immunodeficient mice reconstituted with human CD4+ T cells, which can be achieved either by transfer of mature cells or immature progenitors, represent the only animal model to study HIV-1 infection of human lymphocytes in vivo. However, the immunocompromised status of most of these models currently rule out their use for vaccine studies. Nevertheless, the model might be ideally suited for HIV-1 gene therapy studies since eliciting an efficient anti-viral immune response is not the primary end-point. Rather, HIV-1 gene therapy should protect CD4+ T cells from HIV-1- induced deletion and/or reduced viral replication. Here, we describe recent advancements in the field of HIV-1 gene therapy, focusing on tools and targets validated in various models of humanized mice. From the analysis of this literature, it appears that strategies targeting viral entry, by means of neutralizing antibodies or fusion inhibitors, are the most promising so far. Indeed, strategies targeting viral entry have moved to the clinic with encouraging results. Thus, humanized mice should be considered as the prime model to devise the safer and most effective HIV-1 gene therapy strategy.
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Cite this article as:
Nicolas Petit and Gilles Marodon , Lessons From HIV-1 Gene Therapy in Humanized Mice: Is Targeting Viral Entry the Road to Success?, Current Gene Therapy 2016; 16 (1) . https://dx.doi.org/10.2174/1566523216666160104141644
DOI https://dx.doi.org/10.2174/1566523216666160104141644 |
Print ISSN 1566-5232 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5631 |
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