Under GCRV-I infection, gcTrim47 wild-type, ΔRING, and ΔBbox mutants (all retaining an intact SPRY domain) significantly reduced p62 levels, indicative of enhanced autophagic flux, whereas the ΔSPRY mutant—lacking the SPRY domain—exhibited no significant effect on p62 degradation (Figure 3E). Here, SQSTM1 is linked to infection.