Autoimmunity in human immunodeficiency virus infection and the use of thalidomide.

Although it is usually accepted that the pathogeny of HIV infection is related to the direct cytotoxic effect of the virus or indirectly by the invasion of T4 cells altering the T4/T8 ratio, clinical and serological and biochemical manifestations of the B cell polyclonal activation were described early in HIV infection epidemy. It is postulated that the central pathophysiologic mechanism in HIV infection is a high and inefficient production of interferon-gamma, genetically determined, leading to a production of autoantibodies that blocks the target organs even the immune system as well as a progressive interleukins levels increase, including tumor necrosis factor-alpha (TNF-alpha), responsible for many of the symptoms of these patients like fever, headache, fatigue, myalgia, hypotension, seizure and other neurological disorders, hematologic and hepatic disorders. Thalidomide reduces polyclonal hypergammaglobulinemia, that is associated with a clinical and laboratorial improvement, in a dose dependent manner as well as TNF-alpha levels. It seems that HIV infection is more a disease of abnormal host response triggered by HIV than an HIV disease.