Retroviruses and psoriasis.
Psoriasis occurs with at least undiminished frequency in HIV infected individuals. The behaviour of psoriasis in HIV disease is of interest, both in terms of pathogenesis and therapy, because of the background of profound immunodysregulation. It is paradoxical that, while drugs that target T lymphocytes are effective in psoriasis, the condition should be exacerbated by HIV infection. Antiretroviral therapy may improve psoriasis in tandem with improvement in the overall clinical and virological condition of the patient. The aetiopathogenesis of psoriasis is unknown but genetic and environmental factors are thought to be involved. There are controversial issues regarding the immunological basis of psoriasis and the role of CD4+ versus CD8+ T lymphocytes. Current opinion favours an autoimmune basis for psoriasis, although the precipitating activating signal(s) within psoriatic plaques remains unknown. The immunodysregulation resulting from HIV infection may trigger psoriasis in those genetically predisposed by the Cw*0602 allele. Since CD8+ T cells recognize antigen in the context of class I molecules, the identification of a human leucocyte antigen class I association in HIV-associated psoriasis strengthens the argument for an important role for CD8+ T lymphocytes in the immunopathogenesis of psoriasis. HLA-Cw*0602 could act as a cross-reactive target for cytotoxic T lymphocytes responding to processed peptides from microorganisms. Human retrovirus-5 is a recently described, partially characterized retrovirus and has been implicated in the pathogenesis of psoriatic arthropathy but not psoriasis.
Mallon
Eleanor
E