Evidence for a Role of the Membrane-Proximal Region of Herpes Simplex Virus Type 1 Glycoprotein H in Membrane Fusion and Virus Inhibition

ChemBioChem ◽  
2007 ◽  
Vol 8 (8) ◽  
pp. 885-895 ◽  
Author(s):  
Stefania Galdiero ◽  
Annarita Falanga ◽  
Mariateresa Vitiello ◽  
Marina D'Isanto ◽  
Craig Collins ◽  
...  
2012 ◽  
Vol 93 (2) ◽  
pp. 319-329 ◽  
Author(s):  
Yudan Ren ◽  
Susanne Bell ◽  
Helen L. Zenner ◽  
S.-Y. Kathy Lau ◽  
Colin M. Crump

Herpes simplex virus type 1 glycoprotein M (gM) is a type III membrane protein conserved throughout the family Herpesviridae. However, despite this conservation, gM is classed as a non-essential protein in most alphaherpesviruses. Previous data have suggested that gM is involved in secondary envelopment, although how gM functions in this process is unknown. Using transfection-based assays, we have previously shown that gM is able to mediate the internalization and subcellular targeting of other viral envelope proteins, suggesting a possible role for gM in localizing herpesvirus envelope proteins to sites of secondary envelopment. To investigate the role of gM in infected cells, we have now analysed viral envelope protein localization and virion incorporation in cells infected with a gM-deletion virus or its revertant. In the absence of gM expression, we observed a substantial inhibition of glycoprotein H–L (gH–L) internalization from the surface of infected cells. Although deletion of gM does not affect expression of gH and gL, virions assembled in the absence of gM demonstrated significantly reduced levels of gH–L, correlating with defects of the gM-negative virus in entry and cell-to-cell spread. These data suggest an important role of gM in mediating the specific internalization and efficient targeting of gH–L to sites of secondary envelopment in infected cells.


2001 ◽  
Vol 120 (5) ◽  
pp. A136-A137
Author(s):  
K TSAMAKIDES ◽  
E PANOTOPOULOU ◽  
D DIMITROULOPOULOS ◽  
M CHRISTOPOULO ◽  
D XINOPOULOS ◽  
...  

1994 ◽  
Vol 75 (11) ◽  
pp. 3127-3135 ◽  
Author(s):  
H. S. Marsden ◽  
M. Murphy ◽  
G. L. McVey ◽  
K. A. MacEachran ◽  
A. M. Owsianka ◽  
...  

2008 ◽  
Vol 283 (44) ◽  
pp. 29993-30009 ◽  
Author(s):  
Stefania Galdiero ◽  
Annarita Falanga ◽  
Mariateresa Vitiello ◽  
Luca Raiola ◽  
Roberto Fattorusso ◽  
...  

Intervirology ◽  
2001 ◽  
Vol 44 (4) ◽  
pp. 232-242 ◽  
Author(s):  
E.U. Lorentzen ◽  
B.R. Eing ◽  
W. Hafezi ◽  
R. Manservigi ◽  
J.E. Kühn

2006 ◽  
Vol 87 (12) ◽  
pp. 3483-3494 ◽  
Author(s):  
Sven Hoppe ◽  
Mario Schelhaas ◽  
Verena Jaeger ◽  
Timo Liebig ◽  
Philipp Petermann ◽  
...  

The aim of this study was to understand how molecular determinants of epithelial cells influence initial infection by herpes simplex virus type 1 (HSV-1). Upon infection of the epithelial MDCKII cell line, enhanced association of virus particles with cells forming actin protrusions was observed, suggesting a putative role of actin dynamics in HSV-1 infection. Thus, the impact of the small Rho-like GTPases Rac1, Cdc42 and RhoA acting as key regulators of actin dynamics was addressed. Endogenous Rac1 and Cdc42 were temporarily activated at 15 and 30 min after HSV-1 infection. When constitutively active Cdc42 or Rac1 mutants were expressed transiently, a significant decrease in infectivity was observed, whereas expression of RhoA mutants had no influence. Furthermore, dominant-negative Cdc42 led to decreased infectivity, whereas dominant-negative Rac1 had no effect. So far, the study of potential effectors indicated that Rac1/Cdc42 mutants inhibited infectivity independently of p21-activated kinase (Pak1). The inhibitory effect of Rac1/Cdc42 mutant expression on HSV-1 infection was characterized further and it was found that binding, internalization and transport of HSV-1 were not affected by expression of Rac1/Cdc42 mutants. Thus, these results provide the first evidence for a role of Rac1/Cdc42 signalling during early HSV-1 infection and suggest a mechanism relying on virus-induced regulation of Rac1/Cdc42 activities.


Eye ◽  
1994 ◽  
Vol 8 (3) ◽  
pp. 298-306 ◽  
Author(s):  
Richard R Tamesis ◽  
Elisabeth M Messmer ◽  
Beverly A Rice ◽  
James E Dutt ◽  
C Stephen Foster

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