Abstract
BackgroundPoly(ADP-ribosylation) is a post-translational modification of nuclear proteins involved in several cellular events as well as in processes that characterize the infective cycle of some viruses. In the present study, we investigated the role of poly(ADP-ribosylation) on Epstein-Barr Virus (EBV) lytic cycle activation.ResultsInhibition of PARP-1 by 3-aminobenzamide (3-ABA) during EBV induction, diminished cell damage and apoptosis in the non-productive Raji cell line while markedly reducing the release of viral particles in the productive Jijoye cells. Furthermore, incubation with 3-ABA up-regulated the levels of LMP1 and EBNA2 latent viral proteins. At the same time, it slightly affected the expression of the immediate early BZLF1 gene, but largely down-regulated the levels of the early BFRF1 protein. The modulation of the expression of both latent and lytic EBV genes appeared to be post-transcriptionally regulated.ConclusionTaken together the data indicate that PARP-1 plays a role in the progression of EBV lytic cycle and therefore, PARP inhibitors might represent suitable pharmacological adjuncts to control viral spread in EBV productive infection.
Highlights
Poly(ADP-ribosylation) is a post-translational modification of nuclear proteins involved in several cellular events as well as in processes that characterize the infective cycle of some viruses
The effect of PARP inhibition on EpsteinBarr Virus (EBV) early antigen expression was evaluated on Raji cells induced in the presence or in the absence of 3-ABA and on latentlyinfected Raji cells used as controls
At 72 hours, a 34% of apoptotic cells was observed in induced Raji cells, while only a 20% was measured when lytic cycle activation was carried out in the presence of 3-ABA
Summary
Poly(ADP-ribosylation) is a post-translational modification of nuclear proteins involved in several cellular events as well as in processes that characterize the infective cycle of some viruses. We investigated the role of poly(ADP-ribosylation) on EpsteinBarr Virus (EBV) lytic cycle activation. Epstein Barr Virus (EBV), the ethiological agent of infectious mononucleosis (IM) is associated with a number of tumors such as Burkitt's lymphoma (BL), Hodgkin's disease (HD), nasopharingeal carcinoma (NPC) and with lymphoproliferative diseases in the immunocompromised individuals [1]. A limited number of genes is differentially expressed. These include six nuclear antigens, designated as EBNA-1 to -6, three membrane proteins, indicated as LMP-1, -2A, and -2B and two small non-polyadenylated RNAs (EBERs). EBV nuclear antigen EBNA1 is required for latent replication, episomal mainteinance and viral genome segregation [2]. With the exception of EBNA-3B, they all concurr with the EBERs to B cell transformation [3]
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