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. 2018 Jun 13;92(13):e00240-18. doi: 10.1128/JVI.00240-18

FIG 11.

FIG 11

(A) Proposed scheme showing UL49.5 C42 and CT residue interactions with gM and VP22, respectively, and their functional implications. Double-headed solid arrows indicate the interaction between the two proteins, and single-headed solid arrows link the specific protein or its interactions to known functions. The dashed arrow indicates a putative noncovalent mutant UL49.5/gM interaction. A 13% increase in MHC-I cell surface expression due to UL49.5 CT-null mutation (15) is also indicated (*). (B) Schematic summary of UL49.5 and gM virion incorporation of different UL49.5, gM, and VP22 mutant viruses. Note that covalently linked UL49.5/gM complex is essential for gM maturation and cell-to-cell spread of virus but not for UL49.5-mediated MHC-I downregulation. Note that in the absence of covalently linked UL49.5 and gM complex (UL49.5 C42S mutation), virion incorporation of UL49.5 C42S and immature gM proteins is not affected. However, simultaneous UL49.5 C42S/CT-null mutation or UL49.5 C42S mutation in the backbone of VP22Δ virus affected the mutant UL49.5 C42S and immature gM incorporation in the virion. This indicates that in the absence of covalently linked UL49.5/gM complex, UL49.5 CT-VP22 interaction was required for UL49.5 C42S virion incorporation. As predicted, in the gM-deleted virus, UL49.5 was incorporated in the virion because in the absence of gM, UL49.5 CT interaction with VP22 promoted UL49.5 virion incorporation. The horizontal gray bars indicate the UL49.5-gM interaction, a red cross indicates the disruption of the UL49.5-gM interaction due to the C42S mutation, a black cross on the arrow indicates no virion incorporation, and a light gray cross on the arrow indicates either no or markedly reduced virion incorporation.