In human immunodeficiency virus type-1 (HIV-1) infected individuals, CD34+ hematopoietic stem/progenitor cells are profoundly impaired in their proliferation/differentiation capacities. The bulk of the available experimental evidence seems to indicate that hematopoietic progenitors are not susceptible to HIV-1 infection and their defects seem rather the consequence of direct or indirect negative influences of HIV-1-specific soluble proteins released by productively infected accessory cells. We have now shown that in the presence of a concurrent human herpesvirus-6 infection, two hematopoietic (TF-1 [erythromyeloid] and KG-1 [lymphomyeloid]) progenitor cell lines and human CD34+ hematopoietic progenitors isolated from the bone marrow of normal donors, became susceptible to HIV-1 infection and permissive to HIV-1 replication, although with a limited virus yield. These results suggest a further possible mechanism leading to hematopoietic derangement in HIV-1-infected subjects and may help to clarify the controversial issue of the susceptibility of human hematopoietic progenitors to HIV-1 infection.
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June 1, 1996
A concurrent human herpesvirus-6 infection renders two human hematopoietic progenitor (TF-1 and KG-1) cell lines susceptible to human immunodeficiency virus type-1
G Furlini,
G Furlini
Institute of Microbiology of the University of Bologna, Italy.
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M Vignoli,
M Vignoli
Institute of Microbiology of the University of Bologna, Italy.
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E Ramazzotti,
E Ramazzotti
Institute of Microbiology of the University of Bologna, Italy.
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MC Re,
MC Re
Institute of Microbiology of the University of Bologna, Italy.
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G Visani,
G Visani
Institute of Microbiology of the University of Bologna, Italy.
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Placa La
Placa La
Institute of Microbiology of the University of Bologna, Italy.
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Blood (1996) 87 (11): 4737–4745.
Citation
G Furlini, M Vignoli, E Ramazzotti, MC Re, G Visani, Placa La; A concurrent human herpesvirus-6 infection renders two human hematopoietic progenitor (TF-1 and KG-1) cell lines susceptible to human immunodeficiency virus type-1. Blood 1996; 87 (11): 4737–4745. doi: https://doi.org/10.1182/blood.V87.11.4737.bloodjournal87114737
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June 1 1996
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