Anti-VZV gH Recombinant Antibody (206) (CAT#: MRO-1155LC)

Figure 1 Replication of VZV in human skin xenografts in SCIDhu mice treated with anti-gH MAb 206 for 0 to 12 days or 4 to 12 dayspostinoculation.

Neutralization capacity of MAb 206 within xenografthomogenates against a standard inoculum of 10 PFU/ml of VZV.

Anti-Glycoprotein H Antibody Impairs the Pathogenicity ofVaricella-Zoster Virus in Skin Xenografts in theSCID Mouse Model

Figure 2 Formation of lesions in VZV-infected human skin xenografts treated with anti-gH MAb 206 for 0 to 12 days or 4 to 12 dayspostinoculation.

Lesions in skin xenografts inoculated with pOka-infected HELFs were identified by VZV gE expression (red) and werecounterstained with hematoxylin (blue). Representative lesions are shown at each time point, as follows: 7 dpi, panels A, G, and M; 14 dpi, panelsB, H, and N; 21 dpi, panels C, I, and O; 28 dpi, panels D, J, and P; 35 dpi, panels E, K, and Q; and 42 dpi, panels F, L, and R. The total numberof xenografts with lesions is shown in the lower left of each panel. Lesions were identified in xenografts from the PBS (A to F) and Ab-4-12 (Mto R) groups at all time points. Lesions were observed in xenografts from the Ab-0-12 group (G to L) only at 7, 21, 35, and 42 dpi. Representativeuninfected xenografts are shown for the Ab-0-12 group at 14 and 28 dpi. Syncytia were seen in all lesions. Magnification, ⫻50.

Anti-Glycoprotein H Antibody Impairs the Pathogenicity ofVaricella-Zoster Virus in Skin Xenografts in theSCID Mouse Model

Figure 3 Cell-cell spread of VZV in vitro in the presence of anti-gH MAb 206.

HELFs were mock treated (A to D) or treated with antibody (Eto H) and then fixed and stained with polyclonal sera against VZV at 24-h intervals. (A and E) 24 hpi; (B and F) 48 hpi; (C and G) 72 hpi; (Dand H) 96 hpi. Magnification, ⫻50.

Anti-Glycoprotein H Antibody Impairs the Pathogenicity ofVaricella-Zoster Virus in Skin Xenografts in theSCID Mouse Model

Figure 4 Localization of gH and MAb 206 relative to VZV gE and ORF23 proteins in fibroblasts in vitro.

HELFs inoculated with pOka weremock treated (A and C) or antibody treated (B and D) for 48 h, fixed, permeabilized, stained, and examined by confocal microscopy. UninfectedHELFs were also mock treated (A and C) or antibody treated (B and D) for 48 h, fixed, permeabilized, stained, and examined. (A) gH, red; gE,blue; TGN46, green; nuclei, gold. (B) MAb 206, red; gE, blue; TGN46, green; nuclei, gold. (C) gH, red; ORF23, blue; TGN46, green; nuclei, gold.(D) MAb 206, red; ORF23, blue; TGN46, green; nuclei, gold. Bar, 5 um.

Anti-Glycoprotein H Antibody Impairs the Pathogenicity ofVaricella-Zoster Virus in Skin Xenografts in theSCID Mouse Model

Figure 5 Localization of gH and MAb 206 relative to EEA1 and Vps4 in fibroblasts in vitro.

HELFs inoculated with pOka were mock treated (A to D, K to N) or antibody treated (F to I, P to S) for 48 h, fixed, permeabilized, stained, and examined by confocal microscopy. Uninfected HELFs were mock treated (E and O) or antibody treated (J and T) for 48 h, fixed, permeabilized, stained, and examined. Arrowheads highlight colocalization. (A) gH, red; EEA1, blue; TGN46, green; nuclei, gold. (B) MAb 206, red; EEA1, blue; TGN46, green; nuclei, gold. (C) gH, red; Vps4, blue; TGN46, green; nuclei, gold. (D) MAb 206, red; Vps4, blue; TGN46, green; nuclei, gold. Bar, 5 um.

Anti-Glycoprotein H Antibody Impairs the Pathogenicity ofVaricella-Zoster Virus in Skin Xenografts in theSCID Mouse Model