“…Although now generally accepted, there is evidence arguing against the infection of CD4+ cells with HIV be ing the sole mechanism for the development of immuno deficiency: depletion of L3T4 lymphocytes (the analogue of human CD4+ lymphocytes) in the mouse does not lead to immunodeficiency [15], The latent disease-free period with a mean of more than 5 years is very long, although the virus needs only days to weeks for replication [16,17], On the other hand, autoimmune phenomena, such as an in crease of anti-CD4+ autoantibodies and autoantibodyproducing CD5+ B cells, are associated with the devel opment of AIDS [18][19][20][21], Viruses have been implicated as triggers for autoim mune diseases in which an antiviral antibody cross-reacts with the host's own tissue [22,23], A retroviral cause was discussed in Sjogren's syndrome, systemic lupus erythe matosus and Graves' disease, because antibodies directed against the pl7 and p24 gag proteins of HIV-1 and HIV-2 were detectable in some patients [24,25] HIV+ hemophilia patients with platelet counts <50,000/pl had significantly higher IgM-anti-F(ab')2Y and IgM-anti-Fc,, activities than patients with platelet counts >50,000/pl. No significant associ ation was found between IgG-anti-F(ab')2Y, IgG-anti-Fc,, and throm bocytopenia.…”