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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 n-Barr virus (EBV) replication characterizes hairy leukoplakia, an oral epithelial lesion typically o
8 and patients with either oral candidiasis or hairy leukoplakia and a low CD4:CD8 cell ratio should be
13 sis (EC), pseudomembranous candidiasis (PC), hairy leukoplakia (HL), and warts was computed over foll
14 ent membrane protein (LMP)-1 is expressed in hairy leukoplakia (HL), but data on LMP-1 sequence varia
15 immunodeficiency virus (HIV)-associated oral hairy leukoplakia (HLP) and Epstein-Barr virus (EBV) rep
16 his study, EBV strains were identified in 25 hairy leukoplakia (HLP) biopsies and six matched periphe
17 F-7 protein expression in vivo in lesions of hairy leukoplakia (HLP) in which there is abundant EBV r
23 immunodeficiency virus (HIV)-candidiasis and hairy leukoplakia-in 152 HIV-infected blood transfusion
24 s, such as nasopharyngeal carcinoma and oral hairy leukoplakia, indicating that the virus can infect
25 ence of HHV-8 DNA in both the EBV-associated hairy leukoplakia lesions and in the EBV-associated AIDS
26 cells lytically infected with EBV (from oral hairy leukoplakia lesions) express much more FAS than un
28 as nasopharyngeal carcinoma (NPC), and oral hairy leukoplakia (OHL) lesions that have lytic infectio
29 ses are due to lytic infection (such as oral hairy leukoplakia) or latent infection (such as nasophar
30 roduce diverse pathologies ranging from oral hairy leukoplakia to nasopharyngeal carcinoma, from infe
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