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 Blood, 1 July 2006, Vol. 108, No. 1, pp. 141-151.
Prepublished online as a Blood First Edition Paper on March 16, 2006; DOI 10.1182/blood-2005-04-1697.

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HEMATOPOIESIS

KSHV/HHV-8 infection of human hematopoietic progenitor (CD34+) cells: persistence of infection during hematopoiesis in vitro and in vivo

William Wu, Jeffrey Vieira, Nancy Fiore, Prabal Banerjee, Michelle Sieburg, Rosemary Rochford, William Harrington, Jr, and Gerold Feuer

From the Department of Microbiology and Immunology, State University New York (SUNY) Upstate Medical University, Syracuse, NY; the Department of Laboratory Medicine, University of Washington, and Program in Infectious Diseases, Fred Hutchinson Cancer Research Center, Seattle, WA; and the Division of Hematology/Oncology, Sylvester Comprehensive Cancer Center, University of Miami School of Medicine, Miami, FL.

The cellular reservoir for Kaposi sarcoma-associated herpesvirus (KSHV) infection in the hematopoietic compartment and mechanisms governing latent infection and reactivation remain undefined. To determine susceptibility of human CD34+ hematopoietic progenitor cells (HPCs) to infection with KSHV, purified HPCs were exposed to KSHV, and cells were differentiated in vitro and in vivo. Clonogenic colony-forming activity was significantly suppressed in KSHV-infected CD34+ cells, and viral DNA was predominantly localized to granulocyte-macrophage colonies differentiated in vitro. rKSHV.219 is a recombinant KSHV construct that expresses green fluorescent protein from a cellular promoter active during latency and red fluorescent protein from a viral lytic promoter. Infection of CD34+ HPCs with rKSHV.219 showed similar patterns of infection, persistence, and hematopoietic suppression in vitro in comparison with KSHV. rKSHV.219 infection was detected in human CD14+ and CD19+ cells recovered from NOD/SCID mouse bone marrow and spleen following reconstitution with rKSHV.219-infected CD34+ HPCs. These results suggest that rKSHV.219 establishes persistent infection in NOD/SCID mice and that virus may be disseminated following differentiation of infected HPCs into the B-cell and monocyte lineages. CD34+ HPCs may be a reservoir for KSHV infection and may provide a continuous source of virally infected cells in vivo. (Blood. 2006;108:141-151)


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