Lentiviruses are a class of genetically unique retroviruses that share similar features, despite their wide variety of host species. Transactivator of transcription (Tat) proteins of lentiviruses are critical for the regulation of viral transcription and replication. Recent studies demonstrate that in addition to mediating transactivation, Tat binds to the microtubule cytoskeleton of the host cell and interferes with microtubule dynamics, ultimately triggering apoptosis. This non-canonical function of Tat appears to be critical for the pathogenesis of lentiviral diseases, such as acquired immunodeficiency syndrome. Here, we compare the structure and activity of Tat proteins from three different types of lentiviruses, focusing on the roles of these proteins in the alteration of host microtubule dynamics and induction of apoptosis. We propose that further investigation of the Tat-microtubule interaction will provide important insight into the process of lentiviral pathogenesis and elucidate new avenues for the development of antiviral therapies.

慢病毒是一类遗传上独特的逆转录病毒，尽管它们具有多种宿主物种，但它们具有相似的特征。慢病毒的转录反式激活蛋白（Tat）对病毒转录和复制的调控至关重要。最近的研究表明，除了介导反式激活外，Tat还与宿主细胞的微管细胞骨架结合并干扰微管动力学，最终触发凋亡。Tat的这种非经典功能对于慢病毒疾病（如获得性免疫缺陷综合症）的发病机制似乎至关重要。在这里，我们比较三种不同类型的慢病毒的Tat蛋白的结构和活性，重点是这些蛋白在改变宿主微管动力学和诱导细胞凋亡中的作用。