The Epstein-Barr virus (EBV) immediate early gene product BZLF1 was localized by indirect immunofluorescence to the cytoplasm of the basal epithelial layer at the lateral border and dorsum of tongue in human immunodeficiency virus-infected and -seronegative patients. Two biopsies of oral hairy leukoplakia revealed a sporadic cytoplasmic staining of the BHRF1 and BRLF1 gene products in the basal epithelial layer. The widespread presence ofBZLF1 in the basal epithelial layer indicated that this cell layer contained EBV DNA and was probably directly infected by EBV. Nuclear localization of the immediate early and early gene products BZLF1, BHRF1, BRLF1, and BMLF1 was limited to oral hairy leukoplakia in human immunodeficiency virus-seropositive patients and revealed a codistribution with the virus capsid antigen. Our results indicate that the epithelium of the tongue is a potential reservoir for EBV and that in heavily immunocompromised patients EBV may move from the cytoplasm to the nucleus with increasing differentiation and be coactivated there during the terminal differentiation ofepithelial cells at the lateral border and dorsum of tongue. The cellular and viral factors that determine whether EBV infection is latent or productive are mainly unknown and depend on the host cell (10). EpsteinThe concept of strict B-lymphocyte tropism has been central to discussion of the biology of EBV since the discovery of this herpesvirus. The observation that epithelial cells in nasopharyngeal carcinoma are latently infected with EBV and that lytic expression of EBV occurs in epithelial cells of the parotid gland (11) and other sites of the human body (12) clearly points to a complex biology of this herpesvirus.Virus binding to B cells occurs via a specific interaction between the major envelope glycoprotein gp340 and the C3d receptor molecule (CD21; refs. 13 and 14) and it seems that the specificity of gp340-CD21 binding plays a major role in determining the viral B lymphotropism (15).The presence of EBV in the upper two-thirds of the epithelium in oral hairy leukoplakia (OHL) was originally described by Greenspan et al. (16) and was later confirmed by ultrastructural studies (17), immunohistochemistry, and in situ hybridization (18)(19)(20).The means by which EBV gains access to epithelial cells in general and the questions of which epithelial cell layer in OHL could be infected by EBV and of how the virus reaches the replicating cells in OHL have been the subject of numerous studies (15,(21)(22)(23)(24). Different modes of infection have been suggested: Receptor molecules similar but not identical to CD21 have been reported from undifferentiated epithelial cells of the oropharynx (22,25). It is possible that basal epithelial cells in OHL could be infected through such receptors or via cell fusion (21) by EBV-infected B lymphocytes from peripheral blood. Production of EBV in OHL could be initiated later as a consequence of cellular differentiation (26). It has been shown that human epithelial cells of normal nasopha...

No abstract

No abstract

Oral ulcerations associated with disseminated cytomegalovirus (CMV) infection were observed in four patients with AIDS manifestations showing low CD4 counts. Virus cultures of urine and saliva samples were positive for CMV in all cases. The lesions were characterized by a punched-out appearance, non-indurated borders, low bleeding tendency and lack of inflammatory wall. Light microscopy revealed granulation tissue containing "owl's eye" like cells in all specimens. Presence of CMV was confirmed by immunohistochemistry and in situ hybridization. The ulcerations were infiltrated with T-lymphocytes of the helper, suppressor and cytotoxic subset, most were positive for HLA DR. Despite the local invasion with immunocytes and high serum titers of serum antibodies the patients experienced progressive CMV disease.

Oral hairy leukoplakia; observations in 95 cases and review of the literature, J Oral Pathol Med 1989; 18; 410-415. Oral hairy leukoplakia (HL) was observed in 25.4% of 373 HIV-seropositive patients (« = 95). 87 were men of an average age of 37.1 yr, 8 were women (30,3 yr). 71.6% of the patients were male homosexuals. At initial diagnosis of HL the majority of cases was elassified as CDC IVc, (45,3%) and CDC II (22,1%), Average CD4/CD8 ratio {n = 19) was 0,24 with a range of 0,04-1,0, Thirty biopsies of HL revealed some of the histologic features thought to be characteristic. In only 20 of 30 biopsies EB-virus-specific-capsid antigen was detected. The problems of clinical and histological diagnosis of HL are discussed. Further strict criteria are necessary in order to define HL more ' distinctly. Three years after the first patients with acquired immunodeficiency syndrome (AIDS) were reported in 1981, oral hairy leukoplakia (HL) was described (1). Clinical features and epidemiologyOral hairy leukoplakia is clinically characterized as a white lesion of the lateral border of the tongue, occasionally also occurring in the buccal mucosa with slightly raised, poorly demarcated and corrugated "hairy" surface. Lesions cannot be rubbed off and are reported to be usually symptomless. Hairy leukoplakia has so far not been observed in other mucosal areas than the oral (2), During recent years a number of HL cases either as case reports or larger series have been reported from various areas of the USA, , While HL was initially observed in male homo-or bisexual men, it has now been shown to occur, though less often, in all HIV risk groups; hemophiliacs (4, 8, 21), drug abusers (6, 10, 17), blood transfusion recipients (21) and female partners of HIV-infected men (21). Recently, HL has been described in an HIV-negative patient with acute myeIoblastic leukemia (22) and an HIVnegative renal transplant patient (23), suggesting that HL is not a specific lesion associated to the HIV-infection, but may be a sign of immunosuppression in general.Prevalence rates of HL vary considerably. Four out of 23 patients with antibodies against HIV revealed HL (17.5%) (24), Among 115 HIV-seropositive patients 13% revealed HL (25). Among HIV-seronegative male homosexuals {n = 492) 1% demonstrated HL (25). Of a total of 375 homosexual men 28% had developed HL; it occurred in 23% of the AIDS cases, in 9% of the ARC cases and 47% in high risk persons (9), In a study from Berlin, 26% of ARC patients had HL (6). In Copenhagen, 32% of 69 seropositive asymptomatic patients, 36% and 46% of ARC and AIDS patients revealed HL (26), Low prevalenee rates were reported from New York (5%) and Frankfurt (4,8%) (28), None of 30 hemophiliac patients with factor VIII or IX deficiencies revealed HL (29), In contrast, 23 of 120 consecutive patients belonging to the i.v, drug abusing risk group (19%) had developed HL (17), In a study on oral manifestations of AIDS in Tanzania 35% of 58 patients had developed HL, The male; female ratio in this cohort was 1,6 ; 1,0...