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 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.
Sciortino
Maria Teresa
MT
Department of Microbiological, Genetic and Molecular Sciences, University of Messina, Salita Sperone 31, 98166 Messina, Italy.
Perri
Donata
D
Medici
Maria Antonietta
MA
Grelli
Sandro
S
Serafino
Annalucia
A
Borner
Christoph
C
Mastino
Antonio
A
D000818:Animals; D017209:Apoptosis; D002522:Chlorocebus aethiops; D018258:Herpesvirus 2, Human / Q000472:pathogenicity*; D006801:Humans; D051379:Mice; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism* / Q000494:pharmacology; D020298:U937 Cells; D014709:Vero Cells; D014779:Virus Replication / Q000187:drug effects*
D019253:Proto-Oncogene Proteins c-bcl-2