T cell telomere length in HIV-1 infection: No evidence for increased CD4+ T cell turnover

Science

Volumn 274, Issue 5292, 1996, Pages 1543-1547

  Wolthers, Katja C ^a   Wisman, G Bea A ^b   Otto, Sigrid A ^a   De Roda Husman, Ana Maria ^a   Schaft, Niels ^a   De Wolf, Frank ^a   Goudsmit, Jaap ^a   Coutinho, Roel A ^c   Van Der Zee, Ate G J ^b   Meyaard, Linde ^a   Miedema, Frank ^a,d  

^a UNIVERSITY OF AMSTERDAM   (Netherlands)

^b UNIVERSITY MEDICAL CENTER GRONINGEN   (Netherlands)

^c MUNICIPAL HEALTH SERVICE   (Netherlands)

^d CENTRAL LABORATORY   (Netherlands)

Author keywords

[No Author keywords available]

Indexed keywords

CD4 ANTIGEN; CD8 ANTIGEN;

ACQUIRED IMMUNE DEFICIENCY SYNDROME; ARTICLE; CELL DIVISION; CELL POPULATION; CELL RENEWAL; CLINICAL ARTICLE; CONTROLLED STUDY; DISEASE COURSE; HUMAN; HUMAN CELL; HUMAN IMMUNODEFICIENCY VIRUS 1; HUMAN IMMUNODEFICIENCY VIRUS INFECTION; LYMPHOCYTE COUNT; LYMPHOCYTE DEPLETION; MALE; MONONUCLEAR CELL; PRIORITY JOURNAL; RESTRICTION FRAGMENT; SEROCONVERSION; T LYMPHOCYTE; TELOMERE;

ACQUIRED IMMUNODEFICIENCY SYNDROME; CD4 LYMPHOCYTE COUNT; CD4-POSITIVE T-LYMPHOCYTES; CD8-POSITIVE T-LYMPHOCYTES; CELL DEATH; CELL DIVISION; CROSS-SECTIONAL STUDIES; DISEASE PROGRESSION; HIV INFECTIONS; HIV-1; HUMANS; LEUKOCYTES, MONONUCLEAR; LYMPHOCYTE COUNT; MALE; MATCHED-PAIR ANALYSIS; TELOMERASE; TELOMERE;

HUMAN IMMUNODEFICIENCY VIRUS; HUMAN IMMUNODEFICIENCY VIRUS 1;

EID: 10544220422     PISSN: 00368075     EISSN: None     Source Type: Journal    
DOI: 10.1126/science.274.5292.1543     Document Type: Article

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57. This study was performed as part of the Amsterdam Cohort Studies on AIDS, a collaboration between the Municipal Health Service, the Academic Medical Centre, and the Central Laboratory of the Netherlands Red Cross Blood Transfusion Service, Amsterdam, Netherlands, and was supported by grants from the Netherlands Foundation for Preventive Medicine, the Netherlands Organization for Scientific Research (NWO), and the Dutch AIDS Foundation. We thank H. Schuitemaker, R. van Lier, M. Klein, and D. Hamann for valuable suggestions and critical reading of the manuscript and N. Pakker for statistical analysis. K. Prowse, P. Lansdorp (Terry Fox Laboratory, Vancouver), and R. Dee are thanked for technical advice and helpful discussions. The HIV-negative blood bank donor samples were kindly provided by B. Breur-Vriesendorp and J. Vingerhoed. We thank our colleagues at the Municipal Health Service R. Keet. J. Maas, and N. Albrecht for providing us with fresh blood samples from cohort participants. The pTH2Δ probe was a kind gift of T. de Lange. Rockefeller University, New York.