潜伏感染HIV的t细胞的细胞大小依赖性迁移。

Kathrin Bohn-Wippert, Roy D Dar
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摘要

人类免疫缺陷病毒(HIV)通过整合到宿主DNA并形成潜伏的转录沉默原病毒优先感染t淋巴细胞。如前所述,HIV-1通过与人C-X-C趋化因子受体-4 (CXCR4)共同调节病毒基因表达来改变t淋巴细胞的迁移模式。在这里,我们表明受感染的t淋巴细胞的运动性依赖于细胞大小。在细胞迁移试验中,迁移细胞始终比非迁移细胞大。这种效果与药物治疗无关。在先前生成的Jurkat潜伏期模型中观察到的细胞大小依赖性运动性与含有修饰的HIV-1全长构建体JLatd2GFP的原代人CD4+ t细胞的运动性相关。此外,潜伏感染HIV病毒的大型迁移t细胞,在潜伏期的再激活率略有下降。这些结果表明,HIV的再激活是细胞迁移依赖的,宿主细胞的大小是改变迁移速度的催化剂。我们认为,宿主细胞大小控制迁移揭示了细胞控制病毒命运决定的另一种机制,这对病毒传播和从潜伏期重新激活很重要。这一观察结果可能为病毒-宿主相互作用调节细胞迁移和从潜伏期重新激活提供更多的见解,并有助于设计和实施新的治疗策略。
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Cell size dependent migration of T-cells latently infected with HIV.

Human immunodeficiency virus (HIV) preferentially infects T-lymphocytes by integrating into host DNA and forming a latent transcriptionally silent provirus. As previously shown, HIV-1 alters migration modes of T-lymphocytes by co-regulating viral gene expression with human C-X-C chemokine receptor-4 (CXCR4). Here, we show that motility of infected T-lymphocytes is cell size dependent. In cell migration assays, migrating cells are consistently larger than non-migrating cells. This effect is drug-treatment independent. The cell size dependent motility observed in a previously generated Jurkat latency model correlates with the motility of primary human CD4+ T-cells containing a modified HIV-1 full-length construct JLatd2GFP. In addition, large migrating T-cells, latently infected with HIV, show a slightly decreased rate of reactivation from latency. these results demonstrate that HIV reactivation is cell migration-dependent, where host cell size acts as a catalyst for altered migration velocity. We believe that host cell size controlled migration uncovers an additional mechanism of cellular controlled viral fate determination important for virus dissemination and reactivation from latency. This observation may provide more insights into viral-host interactions regulating cell migration and reactivation from latency and helps in the design and implementation of novel therapeutic strategies.

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