Department of Medical Laboratory Science and Biotechnology, Kaohsiung Medical University, Kaohsiung 80708, Taiwan.
Center for Tropical Medicine and Infectious Disease, Kaohsiung Medical University, Kaohsiung 80708, Taiwan.
Viruses. 2022 Jul 13;14(7):1528. doi: 10.3390/v14071528.
Viral assembly and budding are the final steps and key determinants of the virus life cycle and are regulated by virus-host interaction. Several viruses are known to use their late assembly (L) domains to hijack host machinery and cellular adaptors to be used for the requirement of virus replication. The L domains are highly conserved short sequences whose mutation or deletion may lead to the accumulation of immature virions at the plasma membrane. The L domains were firstly identified within retroviral Gag polyprotein and later detected in structural proteins of many other enveloped RNA viruses. Here, we used HIV-1 as an example to describe how the HIV-1 virus hijacks ESCRT membrane fission machinery to facilitate virion assembly and release. We also introduce galectin-3, a chimera type of the galectin family that is up-regulated by HIV-1 during infection and further used to promote HIV-1 assembly and budding via the stabilization of Alix-Gag interaction. It is worth further dissecting the details and finetuning the regulatory mechanism, as well as identifying novel candidates involved in this final step of replication cycle.
病毒组装和出芽是病毒生命周期的最后步骤和关键决定因素，受病毒-宿主相互作用的调节。已知几种病毒利用其晚期组装（L）结构域劫持宿主机制和细胞衔接蛋白来满足病毒复制的需求。L 结构域是高度保守的短序列，其突变或缺失可能导致未成熟的病毒颗粒在质膜处积累。L 结构域最初在逆转录病毒 Gag 多蛋白中被鉴定，后来在许多其他包膜 RNA 病毒的结构蛋白中也被检测到。在这里，我们以 HIV-1 为例描述 HIV-1 病毒如何劫持 ESCRT 膜分裂机制来促进病毒组装和释放。我们还介绍了半乳糖凝集素-3，它是半乳糖凝集素家族的嵌合体类型，在感染过程中被 HIV-1 上调，并进一步通过稳定 Alix-Gag 相互作用来促进 HIV-1 组装和出芽。值得进一步剖析细节并微调调控机制，以及鉴定参与复制周期这最后一步的新候选物。
