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. 2018 Jun 15;9:2358. doi: 10.1038/s41467-018-04792-7

Fig. 8.

Fig. 8

Schematic model of antiviral mechanism of TAT-P1/DIG-3 in one viral life cycle. When cells are transfected with TAT-P1/DIG-3 and infected with influenza virus, a TAT/P1-DIG-3 are internalized into cells by endocytosis; b Virus can be bound with TAT-P1 and internalized into cells by endocytosis. TAT-P1 can prevent endosomal acidification to block the release of viral RNP into the cytoplasm  and then  nuclei; c Some virus particles that are not bound by TAT-P1 might be internalized into cells by endocytosis and undergo endosomal acidification. d TAT-P1/DIG-3 released from endosomes are imported into nuclei (d1) and viral RNPs released from endosomes are imported into nuclei (d2). e Viral DIG and wild-type genes (WTG) replicate in nuclei. f Newly produced DIG and WTG are exported to cytoplasm. g Viral DIG and WTG are reassorted in cytoplasm and move to the cell membrane to be incorporated into new virions. Seven types of DIV and one type of wild-type virus (WTV) are released from cells to start new virus life cycle. The newly generated DIV can have sustained antiviral activity to competitively inhibit WTV replication in non-transfected cells