In addition, our team found that PGS, a sulfated derivative of alginate, can effectively inhibit the expression and secretion of HBsAg and HBeAg in HepG2.2.15cells. The anti-HBV mechanism of PGS may be associated with appropriate activation of NF-κB and Raf/MEK/ERK signaling pathways to enhance the interferon system, and interfere with HBV transcription (Fig. 7 ). This study suggested that PGS merits further investigation as a novel anti-HBV agent aimed at modulating the host innate immune system in the future [42]. These studies bring new ideas to the development of current anti-novel coronavirus drugs.
Fig. 7 The molecular mechanisms of PGS inhibits HBV replication. Cellular NF-κB and Raf/MEK/ERK signaling pathways are associated with the activation of innate immune system such as interferon system. PGS can bind and enter into HepG2.2.15 cells to activate the NF-κB and Raf/MEK/ERK pathways to enhance the interferon system, and indirectly suppress HBV transcription [42].