Epitopes of Herpes Simplex Virus Type 1 Glycoprotein B that Bind Type-Common Neutralizing Antibodies Elicit Type-Specific Antibody-Dependent Cellular Cytotoxicity

1992 ◽  
Vol 166 (3) ◽  
pp. 623-627 ◽  
Author(s):  
L. Sanchez-Pescador ◽  
P. Paz ◽  
D. Navarro ◽  
L. Pereira ◽  
S. Kohl
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Specific Antibody ◽  
Herpes Simplex Virus Type ◽  
Neutralizing Antibodies ◽  
Cellular Cytotoxicity ◽  
Antibody Dependent Cellular Cytotoxicity ◽  
Simplex Virus

Herpes simplex virus type 1-encoded glycoprotein C enhances coagulation factor VIIa activity on the virus

2004 ◽  
Vol 92 (11) ◽  
pp. 947-955 ◽  
Author(s):  
Michael Sutherland ◽  
Harvey Friedman ◽  
Edward Pryzdial
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Specific Antibody ◽  
Herpes Simplex Virus Type ◽  
Factor Viia ◽  
Virus Surface ◽  
Glycoprotein C ◽  
Simplex Virus

SummaryTissue factor (TF) is the blood coagulation initiator, whose cofactor function is required for physiological factor VIIa (FVIIa)-mediated activation of factor X (FX) to FXa. A previous study reported TF on herpes simplex virus type 1 (HSV1), but this explained only part of FVIIa-dependent FXa generation observed on the virus surface (Sutherland et al. (1997) Proc. Natl. Acad. Sci. USA. 94:13510-14). In the current study, we investigated the role of HSV1-encoded glycoprotein C (gC) in this process. Purified gC-deficient HSV1 facilitated several fold less FX activation by FVIIa than either wild type or gC-rescued strains.To confirm the implication of gC in FVIIa-dependent FX activation, purified soluble gC (sgC) enhanced FXa production in the absence of TF. sgC required FVIIa, calcium and anionic phospholipid to participate in FX activation, suggesting similarity to TF. When purified virus was combined with sgC, the sgC-dependent FXa generation was enhanced three orders of magnitude, suggesting synergy with an additional HSV1 component and explaining the relatively low activity of purified sgC compared to the viral counterpart. FX activation on gC-competent HSV1 was inhibited 20% by a gC-specific antibody, inhibited 40% by a TF-specific antibody, inhibited 65% by combining the gCand TF-specific antibodies, and nearly completely inhibited by the TF antibody alone on gC-deficient HSV-1. Cumulatively, these observations show that two pathways initiating FX activation function in parallel on the virus surface. In addition to the previously described TF-dependent pathway, HSV-1-encoded gC also enhances FXa generation, and like TF, requires FVIIa.

Role of herpes simplex virus type 1 (HSV-1) in the pathogenesis of peptic ulcer disease

2001 ◽  
Vol 120 (5) ◽  
pp. A136-A137
Author(s):  
K TSAMAKIDES ◽  
E PANOTOPOULOU ◽  
D DIMITROULOPOULOS ◽  
M CHRISTOPOULO ◽  
D XINOPOULOS ◽  
...  
Keyword(s):  
Peptic Ulcer ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Peptic Ulcer Disease ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Ulcer Disease ◽  
Simplex Virus
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