Many pts with SLE have elevated EBV serologies against viral capsid (VCA) and early antigens (EA), but it is not known whether these antibody responses are secondary to EBV infection or the immunosuppression associated with SLE or its therapy. We examined the EBV burden in 12 children with SLE (mean age 15.5 yrs, range 10-20 yrs) who did not have symptoms compatible with infectious mononucleosis. All children were taking prednisone; two each were also on azathioprine or cyclophosphamide. All had EBV serologies performed and EBV burdens assessed via immortalization assays and DNA amplification of blood and saliva.

One pt had a positive IgM titer to VCA, while three pts had elevated IgG anti-VCA titers and negative titers to EBV nuclear antigen (EBNA); in healthy pts these serologic patterns are often indicative of a primary EBV infection. The remaining eight pts had elevated IgG anti-VCA and IgG anti-EA titers, in the presence of elevated titers against EBNA, which are often indicative of a reactivated EBV infection; one of these eight pts was the only one in whom a small amount of biologically active EBV was detected. Thus, in our series, virologic evidence of active EBV infection was not seen, despite serologic data which could be interpreted as evidence of a primary or reactivated infection. We conclude that the serologic profiles observed in our pts were a consequence of immune dysregulation secondary to SLE or its therapy, and not due to active infection with EBV.