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1 l epithelial EBV in the pathogenesis of oral hairy leukoplakia.
2 not sufficient for the pathogenesis of oral hairy leukoplakia.
3 of the tongue epithelium in lesions of oral hairy leukoplakia.
4 t of EBV-associated diseases other than oral hairy leukoplakia.
6 -seropositive subjects with and without oral hairy leukoplakia, a replicative EBV-associated epitheli
7 odds ratio (OR) = 0.68, p = 0.0035) and oral hairy leukoplakia (adjusted OR = 0.67, p = 0.033) when c
8 n-Barr virus (EBV) replication characterizes hairy leukoplakia, an oral epithelial lesion typically o
9 and patients with either oral candidiasis or hairy leukoplakia and a low CD4:CD8 cell ratio should be
14 sis (EC), pseudomembranous candidiasis (PC), hairy leukoplakia (HL), and warts was computed over foll
15 ent membrane protein (LMP)-1 is expressed in hairy leukoplakia (HL), but data on LMP-1 sequence varia
16 immunodeficiency virus (HIV)-associated oral hairy leukoplakia (HLP) and Epstein-Barr virus (EBV) rep
17 his study, EBV strains were identified in 25 hairy leukoplakia (HLP) biopsies and six matched periphe
18 F-7 protein expression in vivo in lesions of hairy leukoplakia (HLP) in which there is abundant EBV r
24 immunodeficiency virus (HIV)-candidiasis and hairy leukoplakia-in 152 HIV-infected blood transfusion
25 s, such as nasopharyngeal carcinoma and oral hairy leukoplakia, indicating that the virus can infect
26 ence of HHV-8 DNA in both the EBV-associated hairy leukoplakia lesions and in the EBV-associated AIDS
27 cells lytically infected with EBV (from oral hairy leukoplakia lesions) express much more FAS than un
29 as nasopharyngeal carcinoma (NPC), and oral hairy leukoplakia (OHL) lesions that have lytic infectio
30 ses are due to lytic infection (such as oral hairy leukoplakia) or latent infection (such as nasophar
31 roduce diverse pathologies ranging from oral hairy leukoplakia to nasopharyngeal carcinoma, from infe