Fig. 1: Schematic illustration of the mechanisms of TME reprogramming and virus replication modulation by HSV-1/Navoximod-loaded silk-hydrogels (V-Navo@gel) in the HCC model. | Communications Biology

Fig. 1: Schematic illustration of the mechanisms of TME reprogramming and virus replication modulation by HSV-1/Navoximod-loaded silk-hydrogels (V-Navo@gel) in the HCC model.

From: Navoximod modulates local HSV-1 replication to reshape tumor immune microenvironment for enhanced immunotherapy via an injectable hydrogel

Fig. 1

After intratumoral injection, hydrogels could limit HSV-1 at the tumor site to reduce the systemic toxicity. HSV-1 at the tumor site could induce the expression of the immunosuppressive protein IDO1, which impaired the therapeutic effect. Navoximod releasing from V-Navo@gel could therefore inhibit the enzymatic activity of IDO1, and subsequently enhance the virus replication and the antitumor immune responses at the same time.

Back to article page