Presence of human herpes virus-8 in saliva and non-lesional oral mucosa in HIV-infected and oncologic immunocompromised patients
Background/Aim: Human Herpes Virus‐8 (HHV‐8) is a recently identified virus etiologically associated with Kaposi's sarcoma. Studies regarding its presence in the oral cavity have given variable results. This study attempted to determine the oral presence of HHV‐8 in an area where classic Kapos...
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Veröffentlicht in: | Oral microbiology and immunology 2004-06, Vol.19 (3), p.201-204 |
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Sprache: | eng |
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Zusammenfassung: | Background/Aim: Human Herpes Virus‐8 (HHV‐8) is a recently identified virus etiologically associated with Kaposi's sarcoma. Studies regarding its presence in the oral cavity have given variable results. This study attempted to determine the oral presence of HHV‐8 in an area where classic Kaposi's sarcoma is primarily found such as Greece.
Methods: Three groups of patients were studied: 10 immunocompromised with hematologic malignancies, 10 immunocompromised with HIV infection and 20 immunocompetent as controls. Whole unstimulated saliva and scrapes from the lingual and the buccal mucosa were collected and polymerase chain reaction was applied to amplify HHV‐8 DNA.
Results: None of the patients in any group had oral lesions. In the control group, all samples tested negative (0/60). HHV‐8 DNA was detected in 5/30 (17%) of all samples from HIV‐positive patients (the mean value of their CD4+ T‐lymphocytes being 385/mm3) and in 13/30 (43%) of all samples from oncologic patients (mean CD4+ T‐lymphocytes 51/mm3). HHV‐8 DNA was found in 10% of saliva samples and 40% of lingual and buccal scrapes both of HIV‐infected and of oncologic patients.
Conclusion: HHV‐8 is present in the saliva and the non‐lesional oral mucosa (not simultaneously) of patients with impaired immunity, with or without HIV co‐infection. The oral epithelium seems to represent an independent location of viral residency and may be of viral replication; the clinical implications need further clarification. |
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ISSN: | 0902-0055 1399-302X |
DOI: | 10.1111/j.0902-0055.2002.00131.x |