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Updated: Aug 30, 2026

Generation of Multivirus-specific T Cells to Prevent/treat Viral Infections after Allogeneic Hematopoietic Stem Cell Transplant
Published on: May 27, 2011
Susceptibility of hematopoietic stem cells to pathogens: role in virus/bacteria tropism and pathogenesis
Annette Kolb-Mäurer1, Werner Goebel
1Department of Dermatology, University of Würzburg, Würzburg, Germany. ankolb@biozentrum.uni-wuerzburg.de
Human hematopoietic stem cells (HSCs) are generated in the bone marrow and differentiate into erythrocytes, granulocytes, monocytes, megacaryocytes, and lymphocytes. HSCs may be manipulated under different conditions. Advances in cell biology result in a better understanding of the relationship between viruses/bacteria and hematopoietic cells. Microbial infections can lead to profound disturbance of hematopoiesis. Infection may augment the production of cytokines, with proliferation and differentiation of the stem cells. Alternatively, infection may lead to destruction of progenitor cells. This results in defective hematopoiesis in certain infections. Since circulating CD34+ cells represent a distinct progenitor pool responsible for seeding extramedullary sites of hematopoiesis, infected peripheral blood-derived CD34+ progenitor cells may serve to disseminate pathogens into diverse anatomic sites. Therefore, progenitor cell infection may additionally effect long-term functional consequences within extramedullary sites of lymphopoiesis. A variety of viruses have been reported to target HSCs, whereas quiescent human HSCs are fully resistant to infection by different bacteria. For susceptibility of HSCs to infectious agents pathogen-receptor interaction plays an important role in virus/bacteria tropism and pathogenesis.
Human hematopoietic stem cells (HSCs) are generated in the bone marrow and differentiate into erythrocytes, granulocytes, monocytes, megacaryocytes, and lymphocytes. HSCs may be manipulated under different conditions. Advances in cell biology result in a better understanding of the relationship between viruses/bacteria and hematopoietic cells. Microbial infections can lead to profound disturbance of hematopoiesis. Infection may augment the production of cytokines, with proliferation and differentiation of the stem cells. Alternatively, infection may lead to destruction of progenitor cells. This results in defective hematopoiesis in certain infections. Since circulating CD34+ cells represent a distinct progenitor pool responsible for seeding extramedullary sites of hematopoiesis, infected peripheral blood-derived CD34+ progenitor cells may serve to disseminate pathogens into diverse anatomic sites. Therefore, progenitor cell infection may additionally effect long-term functional consequences within extramedullary sites of lymphopoiesis. A variety of viruses have been reported to target HSCs, whereas quiescent human HSCs are fully resistant to infection by different bacteria. For susceptibility of HSCs to infectious agents pathogen-receptor interaction plays an important role in virus/bacteria tropism and pathogenesis.
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