Skip to main content
. 2022 Jul 14;14(7):1538. doi: 10.3390/v14071538

Figure 8.

Figure 8

Cartoon depicting the response of NK cells to HCV infection following IL-2/IL-15 or IFN-α activation. The activation of NK cells with IFN-α induces the secretion of IFN-γ and galectin-9. IFN-γ drives the up-regulation of MX1 and IFIT1 by target hepatocytes, which contain/inhibit HCV replication. Extracellularly, Galectin-9 reduces HCV infectivity, putatively through its binding to viral-surface glycoprotein. This binding not only likely prevents the re-infection of target cells but also inhibits HCV ligation to receptors on NK-cell surface, thus interfering with the impairment of effector cells by the virus. The activation of NK cells with IL-2/IL-15 primarily induces the release of antiviral cytokines TNF-α and IFN-γ and only partially contains HCV infection. Galectin-9 is not secreted by NK cells upon activation with IL-2/IL-15. Figure was created with BioRender.com.