Abstract
BackgroundStudies examining herpesvirus-herpesvirus (cytomegalovirus (CMV)-Epstein-Barr virus (EBV)) interactions are limited, and many of the studies have been clinical observations suggesting such an interaction exists. This report aims to examine the in vitro susceptibilities of BJAB-B1 and P3HR-1 cells (EBV positive Burkitt's lymphoma B-cell lines) to a CMV superinfection; and show that EBV reactivation occurs after CMV superinfects these cell lines.ResultsThe BJAB-B1 and P3HR-1 cells were observed to be susceptible to a CMV superinfection by the detection of the major immediate early (MIE) viral transcript and protein (p52) expression. The BZLF1 transcript was observed in both cell lines superinfected with CMV, indicating EBV reactivation. BZLF1 protein was observed in the BJAB-B1 cells. Antigen detection was not performed in the P3HR-1 cells.ConclusionThe results from the in vitro superinfections support the in vivo studies suggesting a CMV infection is related to an EBV reactivation and suggests that CMV may be important as a co-factor in EBV pathogenesis in the immunocompromised patient.
Highlights
Studies examining herpesvirus-herpesvirus (cytomegalovirus (CMV)-Epstein-Barr virus (EBV)) interactions are limited, and many of the studies have been clinical observations suggesting such an interaction exists
BJAB-B1 and P3HR-1 cells that were exposed to UV-irradiated CMV had no presence of the CMV major immediate early (MIE) transcript, indicating that the virus was inactivated (Figures 1B and 2B, respectively)
The uninfected cell lines were negative for the CMV MIE transcript and show that the CMV primers do not cross-react with EBV
Summary
Studies examining herpesvirus-herpesvirus (cytomegalovirus (CMV)-Epstein-Barr virus (EBV)) interactions are limited, and many of the studies have been clinical observations suggesting such an interaction exists. Cytomegalovirus (CMV) and Epstein-Barr virus (EBV), in immunocompetent individuals, are etiologically associated with infectious mononucleosis as well as other disease presentations and malignancies [1,2]. The significance of CMV disease in transplant and HIV infected individuals goes much further than the direct pathological effects because CMV has been shown to be an immune modulator and may contribute significantly to the net immunosuppressive status of the patient [11]. This immunomodulation would (page number not for citation purposes)
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