Premium
Haemopoietic CD34+ progenitor cells are not infected by HIV‐1 in vivo but show impaired clonogenesis
Author(s) -
Luca Andrea De,
Teofili Luciana,
Antinori Andrea,
Iovino Michela Stefania,
Mencarini Paola,
Visconti Elena,
Tamburrini Enrica,
Leone Giuseppe,
Ortona Luigi
Publication year - 1993
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1993.tb08640.x
Subject(s) - cd34 , progenitor cell , haematopoiesis , bone marrow , clonogenic assay , in vivo , biology , peripheral blood mononuclear cell , immunology , virology , population , stem cell , medicine , in vitro , microbiology and biotechnology , environmental health , biochemistry
Summary. We evaluated the role of CD34 + bone marrow progenitor cells in vivo, in the pathogenesis of AIDS‐related haematological abnormalities. The clonogenic activity of CD34+ cells from seven patients with HIV‐1 infection, without bone marrow involving opportunistic infections or neoplasms, was assessed in semisolid cultures. The number of CFU‐GM was significantiy reduced as compared to the controls (P=0.017). independently from myelotoxic therapy, while the number of BFU‐E was not. The presence of retroviral sequences in CFU‐GM colonies from four patients and in the total population of CD34 + cells from six patients with advanced stage HIV infection was investigated using the polymerase chain reaction. The presence of HIV‐1 sequences was also searched for in a purified suspension of CD34 + cells after 3 weeks liquid culture. All these cells were always HIV‐1 negative, while viral sequences were always detected in bone marrow mononuclear cells from these and other patients. The number of HIV‐1 DNA copies decreased with increasing enrichment. At most 1:10000 CD34+ cells are infected in vivo . Other mechanisms than direct viral infection of progenitor cells must account for the defective haemopoiesis in HIV‐1 infected patients.