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. 2015 Jan 28;89(8):4058–4068. doi: 10.1128/JVI.03574-14

FIG 6.

FIG 6

Working model describing C18's role during SV40 infection. (A) At steady state, C18 binds to BAP31, which also interacts with the B12-B14 complex. (B) During ER membrane penetration of SV40, the VP2/3-exposed viral particle promotes C18, along with the B12-B14 complex and BAP31, to rearrange into foci in the bilayer of the ER membrane. Formation of foci requires both VP2 and VP3. While the precise mechanism by which C18 controls the recruitment of the B12-B14 complex and BAP31 to the foci remains unclear, it may be due to interaction of C18 with BAP31, which also binds to the B12-B14 complex. Regardless, focus formation likely serves to concentrate cytosolic Hsc70 machinery used to eject the virus into the cytosol, as suggested by our earlier study (31). Functional domains of C18, B12, and B14 essential for SV40-induced focus formation are colored in orange.