The HIVs have evolved by selecting means to hijack numerous host cellular factors. HIVs exploit the transcription factor NF-κB to ensure efficient LTR-driven gene transcription. However, NF-κB is primarily known to act as a key regulator of the proinflammatory and antiviral responses. Interestingly, retroviruses activate NF-κB during early stages of infection to initiate proviral genome expression while suppressing it at later stages to restrain expression of antiviral genes. During HIV-1 infection, diverse viral proteins such as Env, Nef and Vpr have been proposed to activate NF-κB activity, whereas Vpu has been shown to inhibit NF-κB activation. It is still unclear how HIV-2 regulates NF-κB signaling pathway during its replication cycle. Here we confirm that human BST-2 and HIV-1 Env proteins can trigger potent activation of NF-κB. Importantly, we demonstrate for the first time that the HIV-2 Env induces NF-κB activation in HEΚ293T cells. Furthermore, the anti-BST-2 activity of the HIV-2 Env is not sufficient to completely inhibit NF-κB activity.

通过选择劫持大量宿主细胞因子的手段，艾滋病病毒已经进化。HIV利用转录因子NF-κB来确保有效的LTR驱动的基因转录。但是，主要已知NF-κB是促炎和抗病毒反应的关键调节剂。有趣的是，逆转录病毒在感染的早期激活NF-κB以启动前病毒基因组表达，而在后期抑制它，从而抑制抗病毒基因的表达。在HIV-1感染期间，已提出了多种病毒蛋白（例如Env，Nef和Vpr）来激活NF-κB活性，而Vpu已被证明可以抑制NF-κB激活。尚不清楚HIV-2在其复制周期中如何调节NF-κB信号通路。在这里，我们证实人类BST-2和HIV-1 Env蛋白可以触发NF-κB的有效激活。重要的，我们首次证明HIV-2 Env诱导HEK293T细胞中NF-κB活化。此外，HIV-2 Env的抗BST-2活性不足以完全抑制NF-κB活性。