1 f oral epithelial EBV in the pathogenesis of oral hairy leukoplakia.

2 y but not sufficient for the pathogenesis of oral hairy leukoplakia.

3 layer of the tongue epithelium in lesions of oral hairy leukoplakia.

4 atment of EBV-associated diseases other than oral hairy leukoplakia.

5 (HIV)-seropositive subjects with and without oral hairy leukoplakia, a replicative EBV-associated epi

6 sted odds ratio (OR) = 0.68, p = 0.0035) and oral hairy leukoplakia (adjusted OR = 0.67, p = 0.033) w

7 ranscription from Zp, with all Z(+) cells in oral hairy leukoplakia being BLIMP1(+).

8 uman immunodeficiency virus (HIV)-associated oral hairy leukoplakia (HLP) and Epstein-Barr virus (EBV

9 -Barr virus (EBV) replicates productively in oral hairy leukoplakia (HLP).

10 fy genes associated with the pathogenesis of oral hairy leukoplakia (HLP).

11 an induce epithelial cell lesions resembling oral hairy leukoplakia in AIDS patients.

12 logies, such as nasopharyngeal carcinoma and oral hairy leukoplakia, indicating that the virus can in

13 ngue cells lytically infected with EBV (from oral hairy leukoplakia lesions) express much more FAS th

14  such as nasopharyngeal carcinoma (NPC), and oral hairy leukoplakia (OHL) lesions that have lytic inf

15 diseases are due to lytic infection (such as oral hairy leukoplakia) or latent infection (such as nas

16 can produce diverse pathologies ranging from oral hairy leukoplakia to nasopharyngeal carcinoma, from

17                                              Oral hairy leukoplakia tongue tissue, which contains the