Role of Bcl-2 expression for productive herpes simplex virus 2 replication

Herpes simplex viruses infect a variety of cells in vitro. However, not all infected cells sustain a fully productive replication of these viruses. We have shown that, in U937 monocytoid cells, herpes simplex virus 2 (HSV-2) causes a low-productive infection characterized by apoptosis as cytopathic...

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Published in:Virology (New York, N.Y.) N.Y.), 2006-12, Vol.356 (1), p.136-146
Main Authors: Sciortino, Maria Teresa, Perri, Donata, Medici, Maria Antonietta, Grelli, Sandro, Serafino, Annalucia, Borner, Christoph, Mastino, Antonio
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Bcl-2
Cercopithecus aethiops
Herpes simplex
Herpes simplex virus 2
Herpesvirus 2, Human - pathogenicity
Humans
Mice
Proto-Oncogene Proteins c-bcl-2 - metabolism
Proto-Oncogene Proteins c-bcl-2 - pharmacology
U937 Cells
Vero Cells
Virus infection
Virus replication
Virus Replication - drug effects
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Summary:Herpes simplex viruses infect a variety of cells in vitro. However, not all infected cells sustain a fully productive replication of these viruses. We have shown that, in U937 monocytoid cells, herpes simplex virus 2 (HSV-2) causes a low-productive infection characterized by apoptosis as cytopathic effect at a late stage of infection. This effect was associated with a down-regulation of the Bcl-2 protein. We therefore asked whether destabilization of Bcl-2 expression could act as a limiting factor for the productive HSV-2 infection. We found that overexpression of Bcl-2 in U937 cells dramatically increased the capability of these cells to sustain a fully productive infection, while protecting against apoptosis induced by HSV-2. Overall, our data indicate that Bcl-2 expression acts as a regulator of HSV-2 replication.
ISSN:0042-6822
1096-0341
DOI:10.1016/j.virol.2006.08.001