Antibodies to platelet glycoproteins in haemophiliacs infected with HIV

Abstract

Summary The techniques of Western blotting and the monoclonal antibody specific immobilization of platelet antigen (MAIPA) assay were used to detect antibodies to platelet glycoproteins in 43 samples of serum from 23 anti‐HIV positive haemophiliacs (8 with severe thrombocytopenia, 6 with moderate thrombocytopenia, and 9 with a normal platelet count), six anti‐HIV negative haemophiliacs and ten controls. Antibodies were present in the majority of anti‐HIV positive patients' sera even before the onset of thrombocytopenia. Thrombocytopenia was associated with an increase in the incidence of antibodies to GPIIIa and GPIb, whereas the antigen most frequently recognized in patients without thrombocytopenia was GPIIb. Anti‐GPIIb and/or GPIIIa reactivity was also seen in three out of the six anti‐HIV negative patients. There was no correlation between the absolute platelet count and the detection of antibodies in either assay. Effective therapy for thrombocytopenia with zidovudine, interferon or splenectomy did not influence the presence of antibody. Eight of nine patients with AIDS were negative in the MAIPA assay, consistent with their depressed immune status. It is concluded that the production of antibodies to platelet membrane glycoprotein in anti‐HIV positive haemophiliacs is influenced by factors other than HIV. The presence of such antibodies is independent of the platelet count and is therefore unlikely to play a causative role in HIV‐related thrombocytopenia.

Platelet and HIV Interactions and Their Contribution to Non-AIDS Comorbidities

“…Indeed, immunoglobulins that recognize a common epitope between HIV p24 or GP120 and platelets [112][113][114], as well as those that recognize the platelet glycoprotein GPIb/IX and GP IIb/IIIa [115][116][117][118][119], have all been detected in the circulation of PLWH. These antibodies can be detected in HIV-seropositive patients even before the onset of symptoms or thrombocytopenia [120], suggesting that immune dysregulation develops in the earliest phases of HIV infection. Subsequent splenic sequestration of these immune complexes removes platelets from circulation [121].…”