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Proliferation of HIV-infected renal epithelial cells following virus acquisition from infected macrophages
Author(s) -
Kelly T. Hughes,
Güray Akturk,
Sacha Gnjatic,
Benjamin Chen,
Mary E. Klotman,
Maria Di Blasi
Publication year - 2020
Publication title -
aids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.195
H-Index - 216
eISSN - 1473-5571
pISSN - 0269-9370
DOI - 10.1097/qad.0000000000002589
Subject(s) - kidney , flow cytometry , biology , macrophage , virus , nephropathy , monocyte , immunology , virology , in vitro , biochemistry , diabetes mellitus , endocrinology
HIV-1 can infect and persist in different organs and tissues, resulting in the generation of multiple viral compartments and reservoirs. Increasing evidence supports the kidney as such a reservoir. Previous work demonstrated that HIV-1 infected CD4 T-cells transfer virus to renal tubule epithelial (RTE) cells through cell-to-cell contact. In addition to CD4 T cells, macrophages represent the other major target of HIV-1. Renal macrophages induce and regulate inflammatory responses and are critical to homeostatic regulation of the kidney environment. Combined with their ability to harbour virus, macrophages may also play an important role in the spread of HIV-1 infection in the kidney.

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