The white lesion, which cannot be scraped off, is benign and does not require any treatment, although its appearance may have diagnostic and prognostic implications for the underlying condition.

[6] The virus also causes lytic infection in the oropharynx, but is kept in check by a normal, functioning immune system.

[5] Rarely are other causes of immunocompromise associated with OHL, but it has been reported in people who have received transplants and are taking immunosuppressive medication.

Diagnosis of OHL is mainly clinical, but can be supported by proof of EBV in the lesion (achieved by in situ hybridization, polymerase chain reaction, immunohistochemistry, Southern blotting, or electron microscopy) and HIV serotesting.

[7] When clinical appearance alone is used to diagnose OHL, there is a false positive rate of 17% compared to more objective methods.

The condition often resolves rapidly with high dose acyclovir or desiclovir but recurs once this therapy is stopped, or as the underlying immunocompromise worsens.

[clarification needed][5] Recurrence of the lesion may also signify that highly active antiretroviral therapy (HAART) is becoming ineffective.

[8] The incidence rises as the CD4 count falls,[8] and the appearance of OHL may signify progression of HIV to AIDS.

[10] A study from 2001 reported a significant decrease in the incidence of some oral manifestations of AIDS (including OHL and necrotizing ulcerative periodontitis), which was attributed to the use of HAART, whilst the incidence of other HIV-associated oral lesions did not alter significantly.