title: Increased turnover of CCR5+ and redistribution of CCR5- CD4 T lymphocytes during primary human immunodeficiency virus type 1 infection.
abstract: CCR5 is the major coreceptor for human immunodeficiency virus (HIV) type 1 during primary infection. CCR5+ CD4 T lymphocytes were studied in subjects with primary HIV-1 infection (PHI) or acute Epstein-Barr virus (EBV) infection and in HIV-uninfected controls. The early decline of CD4 T lymphocytes during PHI resulted from depletion of CCR5- CD4 T lymphocytes. After antiretroviral therapy, Ki-67- CCR5- CD4 T cell counts rapidly increased in the circulation, which suggests that the initial decrease was due to an alteration in trafficking and/or sequestration. In the CCR5+ subset of CD4 T cells, there was an elevation in the proliferative (Ki-67+) fraction during PHI, yet their total number remained in the normal range. In contrast, in acute EBV infection, proliferating CCR5+ CD4 T cells accumulated to very high levels, suggesting they have an important role in the early antiviral response, which may be impaired in HIV-1 infection.
authors.affiliation: Centre for Immunology, St. Vincent's Hospital, Darlinghurst, NSW 2010, Australia. J.Zaunders@cfi.unsw.edu.au
authors.forename: J J
authors.initials: JJ
authors.lastname: Zaunders
authors.forename: G R
authors.initials: GR
authors.lastname: Kaufmann
authors.forename: P H
authors.initials: PH
authors.lastname: Cunningham
authors.forename: D
authors.initials: D
authors.lastname: Smith
authors.forename: P
authors.initials: P
authors.lastname: Grey
authors.forename: K
authors.initials: K
authors.lastname: Suzuki
authors.forename: A
authors.initials: A
authors.lastname: Carr
authors.forename: L E
authors.initials: LE
authors.lastname: Goh
authors.forename: D A
authors.initials: DA
authors.lastname: Cooper
mesh_terms: D000328:Adult; D019380:Anti-HIV Agents / Q000494:pharmacology / Q000627:therapeutic use*; D018791:CD4 Lymphocyte Count; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*; D002219:Carbamates; D015224:Dideoxynucleosides / Q000494:pharmacology / Q000627:therapeutic use; D020031:Epstein-Barr Virus Infections / Q000276:immunology; D005434:Flow Cytometry; D005663:Furans; D005838:Genotype; D015658:HIV Infections / Q000188:drug therapy / Q000276:immunology*; D015497:HIV-1 / Q000187:drug effects / Q000235:genetics / Q000276:immunology*; D006801:Humans; D007075:Immunoglobulin M / Q000097:blood; D019259:Lamivudine / Q000494:pharmacology / Q000627:therapeutic use; D008137:Longitudinal Studies; D008297:Male; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D019713:Receptors, CCR5 / Q000096:biosynthesis* / Q000235:genetics / Q000276:immunology; D013449:Sulfonamides / Q000494:pharmacology / Q000627:therapeutic use; D013997:Time Factors; D015215:Zidovudine / Q000494:pharmacology / Q000627:therapeutic use; D000099227:Abacavir
chemical_list: D019380:Anti-HIV Agents; D002219:Carbamates; D015224:Dideoxynucleosides; D005663:Furans; D007075:Immunoglobulin M; D019259:Lamivudine; D019253:Proto-Oncogene Proteins c-bcl-2; D019713:Receptors, CCR5; D013449:Sulfonamides; D015215:Zidovudine; D000099227:Abacavir; C095108:amprenavir