Differential down-modulation of HLA-G and HLA-A2 or -A3 cell surface expression following human cytomegalovirus infection

2004 ◽  
Vol 62 (1-2) ◽  
pp. 3-15 ◽  
Author(s):  
Nathalie Pizzato ◽  
Barbara Garmy-Susini ◽  
Philippe Le Bouteiller ◽  
Françoise Lenfant
Keyword(s):  
Cell Surface ◽  
Human Cytomegalovirus ◽  
Cytomegalovirus Infection ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Human Cytomegalovirus Infection

Down-Regulation of HLA-G1 Cell Surface Expression in Human Cytomegalovirus Infected Cells

2003 ◽  
Vol 50 (4) ◽  
pp. 328-333 ◽  
Author(s):  
Nathalie Pizzato ◽  
Barbara Garmy-Susini ◽  
Philippe Le Bouteiller ◽  
Francoise Lenfant
Keyword(s):  
Cell Surface ◽  
Human Cytomegalovirus ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Down Regulation ◽  
Infected Cells

scholarly journals Human cytomegalovirus suppresses Fas expression and function

2014 ◽  
Vol 95 (4) ◽  
pp. 933-939 ◽  
Author(s):  
Sepehr Seirafian ◽  
Virginie Prod’homme ◽  
Daniel Sugrue ◽  
James Davies ◽  
Ceri Fielding ◽  
...  
Keyword(s):  
Cell Surface ◽  
Human Cytomegalovirus ◽  
De Novo ◽  
Late Phase ◽  
Surface Expression ◽  
Productive Infection ◽  
Cell Surface Expression ◽  
Trail Receptor ◽  
Infected Cells ◽  
High Level

Human cytomegalovirus (HCMV) is known to evade extrinsic pro-apoptotic pathways not only by downregulating cell surface expression of the death receptors TNFR1, TRAIL receptor 1 (TNFRSF10A) and TRAIL receptor 2 (TNFRSF10B), but also by impeding downstream signalling events. Fas (CD95/APO-1/TNFRSF6) also plays a prominent role in apoptotic clearance of virus-infected cells, so its fate in HCMV-infected cells needs to be addressed. Here, we show that cell surface expression of Fas was suppressed in HCMV-infected fibroblasts from 24 h onwards through the late phase of productive infection, and was dependent on de novo virus-encoded gene expression but not virus DNA replication. Significant levels of the fully glycosylated (endoglycosidase-H-resistant) Fas were retained within HCMV-infected cells throughout the infection within intracellular membranous structures. HCMV infection provided cells with a high level of protection against Fas-mediated apoptosis. Downregulation of Fas was observed with HCMV strains AD169, FIX, Merlin and TB40.

scholarly journals Peptide-derivatized dendrimers inhibit human cytomegalovirus infection by blocking virus binding to cell surface heparan sulfate

2010 ◽  
Vol 85 (3) ◽  
pp. 532-540 ◽  
Author(s):  
Anna Luganini ◽  
Andrea Giuliani ◽  
Giovanna Pirri ◽  
Lorena Pizzuto ◽  
Santo Landolfo ◽  
...  
Keyword(s):  
Cell Surface ◽  
Heparan Sulfate ◽  
Human Cytomegalovirus ◽  
Cytomegalovirus Infection ◽  
Virus Binding ◽  
Human Cytomegalovirus Infection

scholarly journals THY-1 Cell Surface Antigen (CD90) Has an Important Role in the Initial Stage of Human Cytomegalovirus Infection

2015 ◽  
Vol 11 (7) ◽  
pp. e1004999 ◽  
Author(s):  
Qingxue Li ◽  
Adrian R. Wilkie ◽  
Melodie Weller ◽  
Xueqiao Liu ◽  
Jeffrey I. Cohen
Keyword(s):  
Cell Surface ◽  
Human Cytomegalovirus ◽  
Surface Antigen ◽  
Cytomegalovirus Infection ◽  
Cell Surface Antigen ◽  
Initial Stage ◽  
Human Cytomegalovirus Infection

scholarly journals Human Cytomegalovirus UL40 Signal Peptide Regulates Cell Surface Expression of the NK Cell Ligands HLA-E and gpUL18

2012 ◽  
Vol 188 (6) ◽  
pp. 2794-2804 ◽  
Author(s):  
Virginie Prod’homme ◽  
Peter Tomasec ◽  
Charles Cunningham ◽  
Marius K. Lemberg ◽  
Richard J. Stanton ◽  
...  
Keyword(s):  
Cell Surface ◽  
Human Cytomegalovirus ◽  
Signal Peptide ◽  
Nk Cell ◽  
Surface Expression ◽  
Cell Surface Expression

scholarly journals Human cytomegalovirus UL141 promotes efficient downregulation of the natural killer cell activating ligand CD112

2010 ◽  
Vol 91 (8) ◽  
pp. 2034-2039 ◽  
Author(s):  
Virginie Prod'homme ◽  
Daniel M. Sugrue ◽  
Richard J. Stanton ◽  
Akio Nomoto ◽  
James Davies ◽  
...  
Keyword(s):  
Natural Killer Cell ◽  
Cell Surface ◽  
Natural Killer ◽  
Human Cytomegalovirus ◽  
Killer Cell ◽  
Surface Expression ◽  
Productive Infection ◽  
Cell Surface Expression ◽  
Poliovirus Receptor ◽  
Activating Receptor

Human cytomegalovirus (HCMV) UL141 induces protection against natural killer cell-mediated cytolysis by downregulating cell surface expression of CD155 (nectin-like molecule 5; poliovirus receptor), a ligand for the activating receptor DNAM-1 (CD226). However, DNAM-1 is also recognized to bind a second ligand, CD112 (nectin-2). We now show that HCMV targets CD112 for proteasome-mediated degradation by 48 h post-infection, thus removing both activating ligands for DNAM-1 from the cell surface during productive infection. Significantly, cell surface expression of both CD112 and CD155 was restored when UL141 was deleted from the HCMV genome. While gpUL141 alone is sufficient to mediate retention of CD155 in the endoplasmic reticulum, UL141 requires assistance from additional HCMV-encoded functions to suppress expression of CD112.

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