Richard Longnecker (Northwestern University, USA)
“EBV Entry into Host”
Lindsey Hutt-Fletcher retires last year. Give all the reagents to Longnecker.
Cell-cell fusion
gp42 and MHC II structure.
Soluble gb42 stimulates fusion with B cells but inhibits fusion with epithelials.
From Ming-Han
Longnecker: EBV entry
gp350 gHgL gB BMRF2
gB( gp110) is highly conserved in Herpesvirus
gHgL against avb6)
gHgL+gp42: against MHCII 3D structure
(Mbio 2012)
KGD motif, blocking ab to gHgL also block fusion of eli cells (E1D1, CL40, CL59)
gB of EBV is more hydrophobic at C terminal domain
Conclusion:
gHgLgp42: B cell
gHgL: epi cells
soluble gp42: inhibit infection of B cells
Important domain of gHgL by protein striation.
Q: try to pull down receptor? A: try to do IP/Mass but nothing.
Q: B/epi cell infection? A: B cell use endocytosis as vesicle; epi cell firstly need to fused with plasma membrane then enter.
Q: virus entry cytosol; how many entry nucleus?
Q: integrin KO-> EBV infection can elevate or not; A: depend on cell type.