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Human immunodeficiency virus infection, antiphospholipid antibodies, and the antiphospholipid syndrome.

Over recent years it has become evident that the spectrum of autoimmune and rheumatic diseases in patients with human immunodeficiency virus (HIV) infection is increasing1-4 and includes conditions such as polymyositis/myopathies5-7, Sjogren’s syndrome, Raynaud’s phenomenon4, psoriatic arthritis, as well as primary biliary cirrhosis8, HIV-related vasculitis9, and Behcet’s syndrome10. Systemic lupus erythematosus (SLE) and sarcoidosis, however, in the HIV-infected population, seem to have a lower incidence than would be expected in the general population, although several cases of sarcoidosis, which is associated with depressed cellular immunity, have been documented in patients with AIDS. It is possible that the development of an autoimmune diathesis is suppressed by HIV infection and could be restored with therapy and normalization of CD4 counts with functional T cells. Indeed this hypothesis has been verified by the documentation of several such cases. Erdal, et al11 reported a patient with HIV who developed SLE after the initiation of highly effective active retroviral treatment. Fox, et al12 documented a female patient with SLE who developed HIV infection followed by clinical improvement and disappearance of autoantibodies. Thyrotoxicosis and thyroid autoantibodies have also been reported in a patient with HIV after restoration of immune function13 as has sarcoidosis, which has been reported in 2 patients following potent anti-HIV therapy14,15. Antiphospholipid antibodies (aPL) may be demonstrated during the course of many infections in addition to occurring in conditions such as SLE, primary antiphospholipid syndrome (APS), and a wide variety of other rheumatic diseases. Syphilis was the first infection to be linked with aPL: one of the components of the VDRL reagent (cardiolipin) being responsible for the original finding that antibodies thought initially to be directed against cardiolipin, were, in fact, pivotal in the pathogenesis and for the diagnosis of the APS. It was subsequently found, however, that these antibodies were directed against a number of serum proteins, primarily ß2-glycoprotein I (ß2-GPI) and prothrombin, the phospholipids modifying the protein molecules to create a “cryptic epitope” or neoantigen on the protein molecules that were revealed or formed only when these proteins were bound to certain anionic surfaces, e.g., gamma-irradiated polystyrene or anionic phospholipid membranes. Recent work by Roubey, et al has shed some light and offers another explanation of the relationship between anticardiolipin (aCL) and ß2-GPI 16. Certain IgG aCL recognize ß2-GPI. Binding occurs when ß2-GPI is immobilized on gamma irradiated polystyrene, on cardiolipin-coated polystyrene (as in the standard aCL ELISA) or on cardiolipin-containing liposomes, but not when the antigen is immobilized on untreated polystyrene. Antibody binding to ß2-GPI coated on gamma-irradiated polystyrene seems to be dependent upon high antigen density and antibody valency. Autoantibodies to ß2-GPI are of relatively low intrinsic affinity and there are other examples of this phenomenon (e.g., binding of IgM rheumatoid factors to aggregated IgG). The major infection worldwide over the past 20 years has been HIV-induced infection and it is not surprising that this condition has been so extensively studied by immunologists and rheumatologists in view of its eventual destruction of the patient’s immune system with resultant major “autoimmune” complications.