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Journal of Virology, November 1999, p. 9089-9097, Vol. 73, No. 11
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Human Immunodeficiency Virus Type 1-Induced Hematopoietic Inhibition Is Independent of Productive Infection of Progenitor Cells In Vivo

Prasad S. Koka,1 Beth D. Jamieson,1 David G. Brooks,2 and Jerome A. Zack1,2,*

Division of Hematology/Oncology, Department of Medicine, Jonsson Comprehensive Cancer Center, UCLA AIDS Institute,1 and Department of Microbiology, Immunology and Molecular Genetics,2 UCLA School of Medicine, Los Angeles, California 90095

Received 22 March 1999/Accepted 14 July 1999

Human immunodeficiency virus (HIV)-infected individuals exhibit a variety of hematopoietic dysfunctions. The SCID-hu mouse (severe combined immunodeficient mouse transplanted with human fetal thymus and liver tissues) can be used to model the loss of human hematopoietic precursor cell function following HIV infection and has a distinct advantage in that data can be obtained in the absence of confounding factors often seen in infected humans. In this study, we establish that HIV type 1 (HIV-1) bearing a reporter gene inserted into the viral vpr gene is highly aggressive in depleting human myeloid and erythroid colony-forming precursor activity in vivo. Human CD34+ progenitor cells can be efficiently recovered from infected implants yet do not express the viral reporter gene, despite severe functional defects. Our results indicate that HIV-1 infection alone leads to hematopoietic inhibition in vivo; however, this effect is due to indirect mechanisms rather than to direct infection of CD34+ cells in vivo.

* Corresponding author. Mailing address: Division of Hematology/Oncology, 11-934 Factor Bldg., 10833 LeConte Ave., UCLA School of Medicine, Los Angeles, CA 90095-1678. Phone: (310) 794-7765. Fax: (310) 825-6192. E-mail: jzack{at}ucla.edu.

Journal of Virology, November 1999, p. 9089-9097, Vol. 73, No. 11
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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