Immunological Nonresponse to Highly Active Antiretroviral Therapy in HIV-Infected Subjects: Is the Bone Marrow Impairment Causing CD4 Lymphopenia?

摘要

In this issue of Clinical Infectious Diseases, Isgro et al. demonstrated that HIV-infected patients who were unable to achieve immunological reconstitution despite viral suppression during HAART demonstrated specific defects of bone marrow clonogenic function. In the pre-HAART era, it was already observed that some individuals, after acute HIV infection, developed accelerated CD4 cell depletion and cellular immunity impairment leading to AIDS. Indeed, AIDS patients display various degrees of bone marrow failure, including either monocytopenia affecting platelets, neutrophils, and RBCs or, most often, pancytopenia . Although these hematopoietic defects can be attributed to multiple causes, including in-tercurrent infections and illegal drug use, many studies have demonstrated that advanced HIV infection has a profound impact on bone marrow functions. Indeed, both multilineage and lineage-restricted hematopoietic progenitors are decreased in the bone marrow of HIV-infected#