Does HIV infection have a direct role in the pathogenesis of rheumatic syndromes?
A wide spectrum of rheumatic syndromes/diseases has been described in HIV-positive individuals, but a direct role of HIV has not been well established. Although the specific mechanism is unclear, many of the rheumatic syndromes (polymyositis [PM], vasculitis, HIV-associated arthritis, and DILS) occur in the presence of profound immunodeficiency. Decreasing frequencies of some rheumatic syndromes/diseases in HIV-infected individuals treated with ART suggest at least an indirect role of HIV infection. In addition, with CD4+ T-cell depletion, diseases in which CD8+ T cells are predominant such as psoriasis, ReA, and DILS are more commonly seen. T regulatory cells, a subset of CD4+ T cells with the main function of maintaining self-tolerance and avoiding the development of autoimmunity, are depleted in patients with HIV infection. The depletion of these regulatory cells and the production of various cytokines is believed to play an important role in the pathogenesis of HIV and may contribute to the development of autoantibodies and autoimmune complications. As CD4+ T cell numbers decline (<300/μL), the risk of opportunistic infections rises. Viral particles have been identified in the synovium and synovial fluid of patients with arthritis, suggesting a direct inflammatory effect.