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Journal of Virology, October 2004, p. 10906-10910, Vol. 78, No. 20
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.20.10906-10910.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Early Bone Marrow Hematopoietic Defect in Simian/Human Immunodeficiency Virus C2/1-Infected Macaques and Relevance to Advance of Disease

Kenji Yamakami,¹ Mitsuo Honda,^2* Masami Takei,¹ Yasushi Ami,³ Noboru Kitamura,¹ Susumu Nishinarita,⁴ Shigemasa Sawada,^1,5 and Takashi Horie⁶

Division of Hematology and Rheumatology,¹ Division of Respiratory Medicine, Nihon University School of Medicine,⁶ AIDS Research Center,² Division of Experimental Research, National Institute of Infectious Diseases,³ Akiru Municipal General Hospital,⁴ Nerima Hikarigaoka Nihon University Hospital, Tokyo, Japan⁵

Received 4 October 2003/ Accepted 28 June 2004

To clarify hematological abnormalities following infection with human immunodeficiency virus (HIV), we examined the hematopoietic capability of bone marrow by using cynomolgus monkeys infected with pathogenic simian/human immunodeficiency virus (SHIV) strain C2/1, an animal model of HIV infection. The relationship between the progress of the infection and the CD4/CD8 ratio of T lymphocytes or the amount of SHIV C2/1 viral load in the peripheral blood was also investigated. A colony assay was performed to assess the hematopoietic capability of bone marrow stem cells during the early and advanced phases of the infection. Colonies of granulocytes-macrophages (GM) were examined by PCR for the presence of the SIVmac239 gag region to reveal direct viral infection. There was a remarkable decrease in the CFU-GM growth on days 1 and 3 postinoculation, followed by recovery on day 56. During the more advanced stage, the CFU-GM growth decreased again. There was minimal evidence of direct viral infection of pooled cultured CFU-GM despite the continuously low CD4/CD8 ratios. These results indicate that the decrease in colony formation by bone marrow stem cells is reversible and fluctuates with the advance of the disease. This decrease was not due to direct viral infection of CFU-GM. Our data may support the concept that, in the early phase, production of inhibitory factors or deficiency of a stimulatory cytokine is responsible for some of the bone marrow defects described in the SHIV C2/1 model.

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* Corresponding author. Mailing address: National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku, Tokyo, Japan. Phone: 81-3-5285-1111. Fax: 81-3-5285-1183. E-mail: mhonda{at}nih.go.jp.

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Journal of Virology, October 2004, p. 10906-10910, Vol. 78, No. 20
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.20.10906-10910.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

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