Abstract

Defective Epstein-Barr virus (EBV) has a deleted and rearranged genome (termed het DNA) that disrupts latency and induces standard EBV to replicate in vitro. We used the polymerase chain reaction to detect, in 2 of 10 patient samples, the junction of abnormally juxtaposed EBV DNA fragments BamHI W and Z, a genomic rearrangement responsible for the biologic activity of het DNA. By sequence analysis, the junction in wild-type defective DNA appears to be similar but not identical to the recombination in the DNA of laboratory strain P3HR-1. The presence of this marker for het DNA in the epithelial lesions of two patients suggests a role for defective EBV in a human pathologic process. J Virol. 1990 January; 64(1): 397-400