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Differential Pathogenesis of Primary CCR5-Using Human Immunodeficiency Virus Type 1 Isolates in Ex Vivo Human Lymphoid Tissue

Unit of Virology, Division of Medical Microbiology, Department of Laboratory Medicine, Lund University, Lund, Sweden,¹ Laboratory of Cellular and Molecular Biophysics and National Institute of Child Health and Human Development,² NASA/NIH Center for Three-Dimensional Tissue Culture, National Institutes of Health, Bethesda, Maryland;,³ Venhälsan, Karolinska University Hospital, Stockholm, Sweden,⁴ Swedish Institute for Infectious Disease Control and Microbiology and Tumorbiology Center, Karolinska Institute, Stockholm, Sweden⁵

Received 23 February 2005/ Accepted 25 May 2005

In the course of human immunodeficiency virus (HIV) disease, CCR5-utilizing HIV type 1 (HIV-1) variants (R5), which typically transmit infection and dominate its early stages, persist in approximately half of the infected individuals (nonswitch virus patients), while in the other half (switch virus patients), viruses using CXCR4 (X4 or R5X4) emerge, leading to rapid disease progression. Here, we used a system of ex vivo tonsillar tissue to compare the pathogeneses of sequential primary R5 HIV-1 isolates from patients in these two categories. The absolute replicative capacities of HIV-1 isolates seemed to be controlled by tissue factors. In contrast, the replication level hierarchy among sequential isolates and the levels of CCR5⁺ CD4⁺ T-cell depletion caused by the R5 isolates seemed to be controlled by viral factors. R5 viruses isolated from nonswitch virus patients depleted more target cells than R5 viruses isolated from switch virus patients. The high depletion of CCR5⁺ cells by HIV-1 isolates from nonswitch virus patients may explain the steady decline of CD4⁺ T cells in patients with continuous dominance of R5 HIV-1. The level of R5 pathogenicity, as measured in ex vivo lymphoid tissue, may have a predictive value reflecting whether, in an infected individual, X4 HIV-1 will eventually dominate.

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