Rheumatic aspects of acquired immunodeficiency syndrome

Infection with HIV-1 continues to provide important insights into autoimmunity and rheumatic diseases. Studies on the mechanisms of B cell hyperreactivity in HIV-infected persons suggest a primary role for B cell complement receptor engagement by circulating immune complexes in the production of autoantibodies. Delineation of the epitopes recognized by antiphospholipid antibodies induced by HIV-1 offers insight into the mechanism of thrombosis associated with antiphospholipid antibodies found in the rheumatic diseases. Several reports have documented the coexistence of rheumatoid arthritis and HIV-1 infection, emphasizing the importance of both T cell-dependent and -independent mechanisms in the pathogenesis and clinical manifestations of rheumatoid arthritis. The mechanisms of host-virus interactions leading to rheumatic disease continue to be studied in HIV-infected persons with diffuse infiltrative lymphocytosis syndrome, a disease in which host immunogenetics appear to be the determining factor, and in persons with polymyositis. In both diseases, tissue cell damage appears to be a consequence of the host immune response to viral proteins present within macrophages in the target tissues. Because similar mechanisms appear to be involved in polymyositis associated with HTLV-I (human T cell lymphoma virus type I) infection, studies into a primate model of polymyositis induced by HTLV-I may be particularly informative. The clinical management of HIV-associated arthritides remains difficult, likely reflecting the role of HIV-1 gene products in initiating or amplifying inflammatory joint disease. Two anti-inflammatory drugs frequently used to treat patients with rheumatic diseases, indomethacin and hydroxychloroquine, can directly inhibit HIV-1 replication and may provide a rational therapeutic approach in combination with conventional antiviral agents.