Megakaryocytes of human immunodeficiency virus-infected individuals express viral RNA.
The pathogenesis of thrombocytopenia associated with human immunodeficiency virus (HIV) infection is not fully understood. Immune mechanisms provide a partial explanation but fail to account for a lack of compensatory megakaryocytosis, the rapid reversal after treatment with azidothymidine, and the ultrastructural aberrations seen in the megakaryocytes of patients with acquired immunodeficiency syndrome. Therefore, a direct effect of HIV on megakaryocytes was investigated. The bone marrow of HIV seropositive individuals was analyzed ultrastructurally, and the megakaryocytes of 10 thrombocytopenic patients were subjected to in situ hybridization with a HIV RNA probe. The structural aberrations in HIV megakaryocytes were distinct from those in HIV-negative immune thrombocytopenias, and the megakaryocytes of 10 of 10 patients examined by in situ hybridization unambiguously expressed viral RNA. Therefore, it is likely that direct infection of megakaryocytes with HIV-1 is one mechanism for the decrease in platelet production.
Zucker-Franklin
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New York University Medical Center, NY 10016.
Cao
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YZ
D000163:Acquired Immunodeficiency Syndrome / Q000382:microbiology*; D001853:Bone Marrow / Q000473:pathology; D015497:HIV-1 / Q000235:genetics* / Q000302:isolation & purification; D006801:Humans; D008533:Megakaryocytes / Q000276:immunology* / Q000648:ultrastructure; D008854:Microscopy, Electron; D012367:RNA, Viral / Q000235:genetics / Q000302:isolation & purification*; D014617:Vacuoles / Q000648:ultrastructure
D012367:RNA, Viral