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Defective viral DNA in Epstein-Barr virus-associated oral hairy leukoplakia
Author(s) -
Donna Patton,
Pamela S. Shirley,
Nancy RaabTraub,
Lionel Resnick,
John W. Sixbey
Publication year - 1990
Publication title -
journal of virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.617
H-Index - 292
eISSN - 1070-6321
pISSN - 0022-538X
DOI - 10.1128/jvi.64.1.397-400.1990
Subject(s) - biology , dna , virology , virus , polymerase chain reaction , epstein–barr virus , microbiology and biotechnology , genome instability , genome , dna polymerase , gene , genetics , dna damage
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.

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