Modulation of the NF-κB signaling pathway by the HIV-2 envelope glycoprotein and its incomplete BST-2 antagonism
Abstract 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. Highlights HIV-2 envelope glycoprotein activates the NF-κB signaling pathway. The HIV-1 Vpu protein nearly abolishes the activation of NF-κB during the HIV-1 viral cycle. In contrast, the HIV-2 Env-mediated BST-2 antagonism is not sufficient to completely inhibit NF-κB activity. This study highlights the importance of an efficient anti-BST-2 activity in the regulation of NF-κB and could provide new insights in the understanding of the enhanced immune antiviral responses in HIV-2 disease. Graphical abstract [DISPLAY OMISSION]
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