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Journal of Virology, September 2001, p. 8390-8399, Vol. 75, No. 18
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.18.8390-8399.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

A Preponderance of CCR5+ CXCR4+ Mononuclear Cells Enhances Gastrointestinal Mucosal Susceptibility to Human Immunodeficiency Virus Type 1 Infection

Michael A. Poles,* Julie Elliott, Philip Taing, Peter A. Anton, and Irvin S. Y. Chen

Department of Medicine, UCLA School of Medicine, UCLA Center for HIV and Digestive Diseases, and UCLA AIDS Institute, Los Angeles, California 90095

Received 2 April 2001/Accepted 5 June 2001

The gastrointestinal mucosa harbors the majority of the body's CD4+ cells and appears to be uniquely susceptible to human immunodeficiency virus type 1 (HIV-1) infection. We undertook this study to examine the role of differences in chemokine receptor expression on infection of mucosal mononuclear cells (MMCs) and peripheral blood mononuclear cells (PBMCs) by R5- and X4-tropic HIV-1. We performed in vitro infections of MMCs and PBMCs with R5- and X4-tropic HIV-1, engineered to express murine CD24 on the infected cell's surface, allowing for quantification of HIV-infected cells and their phenotypic characterization. A greater percentage of MMCs than PBMCs are infected by both R5- and X4-tropic HIV-1. Significant differences exist in terms of chemokine receptor expression in the blood and gastrointestinal mucosa; mucosal cells are predominantly CCR5+ CXCR4+, while these cells make up less than 20% of the peripheral blood cells. It is this cell population that is most susceptible to infection with both R5- and X4-tropic HIV-1 in both compartments. Regardless of whether viral isolates were derived from the blood or mucosa of HIV-1-infected patients, HIV-1 p24 production was greater in MMCs than in PBMCs. Further, the chemokine receptor tropism of these patient-derived viral isolates did not differ between compartments. We conclude that, based on these findings, the gastrointestinal mucosa represents a favored target for HIV-1, in part due to its large population of CXCR4+ CCR5+ target cells and not to differences in the virus that it contains.

* Corresponding author. Mailing address: Center for HIV and Digestive Diseases, Division of Digestive Diseases, Department of Medicine, UCLA School of Medicine, 1529 McDonald Research Laboratories, 675 Charles E. Young Dr. South, Los Angeles, CA 90095. Phone: (310) 794-7195. Fax: (310) 267-0289. E-mail: mpoles{at}ucla.edu.

Journal of Virology, September 2001, p. 8390-8399, Vol. 75, No. 18
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.18.8390-8399.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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