Oral hairy leukoplakia is not a specific sign of HIV‐infection but related to immunosuppression in general

Syrjänen, Stina; Laine, Pekka; Niemelä, Mika; Rp, Happonen

doi:10.1111/j.1600-0714.1989.tb00728.x

Cited by 110 publications

(53 citation statements)

References 15 publications

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“…However, previous cases of OHL with hematologic malignancies have been reported in patients after chemotherapy, whose state of immunosuppression would be more severe than a malignancy per se 5,16,25 .…”

Section: Discussionmentioning

confidence: 96%

“…However, OHL has been reported in other immunosuppressed patients, including those with ulcerative colitis, pemphigus vulgaris, bullous pemphigoid, Behcet's syndrome, multiple myeloma, and leukemia 5,6,16,17,25 . Although rare cases of OHL in healthy people have been reported, OHL is believed to occur in immunosuppression as a rule 14,15 .…”

Section: Discussionmentioning

confidence: 99%

“…It can also be associated with other immunosuppressed conditions, such as an organ or bone marrow transplantation, chemotherapy, hematological malignancies and the long term use of systemic steroid 5,6 .…”

Section: Introductionmentioning

confidence: 99%

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Oral Hairy Leukoplakia Which Occurred as a Presenting Sign of Acute Myeloid Leukemia in a Child

et al. 2010

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Oral hairy leukoplakia (OHL) is caused by the reactivation of a previous Epstein-Barr virus (EBV) infection in the epithelium of the tongue. Most lesions are characterized by corrugated whitish patches on the lateral border of the tongue. It is frequently associated with AIDS, but cases in patients with other immunosuppressed states have also been reported. In leukemia patients, OHL is rarely encountered, and appears only after chemotherapy. We report a case of OHL which occurred as a presenting sign of acute myeloid leukemia (AML) in a previously healthy 15-year-old child. A 15-year-old boy presented with a whitish patch on the left lateral border of the tongue. The biopsy specimen revealed papillomatosis, hyperkeratosis, acanthosis and ballooning degeneration in the stratum spinosum. The patient was EBV seropositive, and PCR analysis of EBV DNA in the lesional tissue was positive. After the diagnosis of OHL in dermatologic department, the patient was referred to pediatrics due to the abnormal peripheral blood smear, and was diagnosed with AML. (Ann Dermatol 22(1) 73∼76, 2010)

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

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Oral Hairy Leukoplakia Which Occurred as a Presenting Sign of Acute Myeloid Leukemia in a Child

et al. 2010

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“…Recent individual reports have shown that the lytic cycle of EBV replication in OHL is not limited to immunocompromised patients under HIV infection (32). OHL is therefore not a specific sign of HIV infection, but is related to immunosuppression in general (33).…”

Section: Resultsmentioning

confidence: 99%

Expression of proteins encoded by Epstein-Barr virus trans-activator genes depends on the differentiation of epithelial cells in oral hairy leukoplakia.

Becker

Leser

Marschall

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

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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...

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“…Some authors suggest that the term 'oral hairy leukoplakia' should be abandoned, since it has a particular determined histological pattern [2] and this is not a premalignant one. Initially OHL was considered to be an oral pathognomonic sign of infection by human immunodeficiency virus (HIV), but the presence of this lesion in patients with other types of immune suppression has been described [3]. Nonetheless, cases of OHL in immunocompetent individuals have also been observed [4], although in the majority of these the presence of EBV has not been demonstrated.…”

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confidence: 99%

Morsicatio linguarum versus Oral Hairy Leukoplakia

et al. 2000

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Oral hairy leukoplakia is not a specific sign of HIV‐infection but related to immunosuppression in general

Cited by 110 publications

References 15 publications

Oral Hairy Leukoplakia Which Occurred as a Presenting Sign of Acute Myeloid Leukemia in a Child

Oral Hairy Leukoplakia Which Occurred as a Presenting Sign of Acute Myeloid Leukemia in a Child

Expression of proteins encoded by Epstein-Barr virus trans-activator genes depends on the differentiation of epithelial cells in oral hairy leukoplakia.

Morsicatio linguarum versus Oral Hairy Leukoplakia

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