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Journal of Virology, February 2004, p. 2121-2130, Vol. 78, No. 4
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.4.2121-2130.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Induction of Simian AIDS in Infant Rhesus Macaques Infected with CCR5- or CXCR4-Utilizing Simian-Human Immunodeficiency Viruses Is Associated with Distinct Lesions of the Thymus

R. A. Reyes,1 Don R. Canfield,2 Ursula Esser,3 Lourdes A. Adamson,1 Charles R. Brown,4 Cecilia Cheng-Mayer,5 Murray B. Gardner,1 Janet M. Harouse,5 and Paul A. Luciw1,3*

Center for Comparative Medicine,1 California National Primate Research Center,2 Department of Medical Pathology, University of California, Davis, California 95616,3 Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland 20852,4 Aaron Diamond Research Center, The Rockefeller University, New York, New York 100165

Received 17 April 2003/ Accepted 27 October 2003

Newborn rhesus macaques were infected with two chimeric simian-human immunodeficiency virus (SHIV) strains which contain unique human immunodeficiency virus type 1 (HIV-1) env genes and exhibit distinct phenotypes. Infection with either the CCR5-specific SHIVSF162P3 or the CXCR4-utilizing SHIVSF33A resulted in clinical manifestations consistent with simian AIDS. Most prominent in this study was the detection of severe thymic involution in all SHIVSF33A-infected infants, which is very similar to HIV-1-induced thymic dysfunction in children who exhibit a rapid pattern of disease progression. In contrast, SHIVSF162P3 induced only a minor disruption in thymic morphology. Consistent with the distribution of the coreceptors CXCR4 and CCR5 within the thymus, the expression of SHIVSF162P3 was restricted to the thymic medulla, whereas SHIVSF33A was preferentially detected in the cortex. This dichotomy of tissue tropism is similar to the differential tropism of HIV-1 isolates observed in the reconstituted human thymus in SCID-hu mice. Accordingly, our results show that the SHIV-monkey model can be used for the molecular dissection of cell and tissue tropisms controlled by the HIV-1 env gene and for the analysis of mechanisms of viral immunopathogenesis in AIDS. Furthermore, these findings could help explain the rapid progression of disease observed in some HIV-1-infected children.

* Corresponding author. Mailing address: Center for Comparative Medicine, University of California, Davis, CA 95616. Phone: (530) 752-3430. Fax: (530) 752-7914. E-mail: paluciw{at}ucdavis.edu.

Journal of Virology, February 2004, p. 2121-2130, Vol. 78, No. 4
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.4.2121-2130.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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