OBJECTIVE: To determine the influence of pol replication capacity on the natural history of HIV-1 infection. DESIGN: Pol replication capacity was measured using a recombinant virus single cycle assay on baseline plasma specimens from subjects enrolled in the Hemophilia Growth and Development Study. SETTING: Children and adolescents with hemophilia and HIV-1 infection were enrolled at multiple sites across the USA into a natural history study. PARTICIPANTS: The Hemophilia Growth and Development Study enrolled 207 HIV-1-infected hemophiliacs between 6 and 19 years of age in 1989 and 1990. Subjects were followed every 6 months through 1997 with pol replication capacity measurements available from 128 of the subjects. MAIN OUTCOME MEASURES: A univariate model defined the relationship between pol replication capacity and HIV-1 RNA and CD4 T-cell number. A random effects model assessed the ability of this measure to predict CD4 T-cell decline over time and a Cox proportional hazards model and Kaplan-Meier analyses defined how it predicts clinical progression. RESULTS: Pol replication capacity measures correlated with baseline HIV-1 RNA, R = 0.189 (P = 0.03) and CD4 T-cell number, -0.197 (P = 0.03). It also independently predicted CD4 T-cell decline over time and progression to AIDS. CONCLUSIONS: This study demonstrates that pol replication capacity independently influences the natural history of HIV-1 infection.
OBJECTIVE: To determine the influence of pol replication capacity on the natural history of HIV-1 infection. DESIGN: Pol replication capacity was measured using a recombinant virus single cycle assay on baseline plasma specimens from subjects enrolled in the Hemophilia Growth and Development Study. SETTING:Children and adolescents with hemophilia and HIV-1 infection were enrolled at multiple sites across the USA into a natural history study. PARTICIPANTS: The Hemophilia Growth and Development Study enrolled 207 HIV-1-infected hemophiliacs between 6 and 19 years of age in 1989 and 1990. Subjects were followed every 6 months through 1997 with pol replication capacity measurements available from 128 of the subjects. MAIN OUTCOME MEASURES: A univariate model defined the relationship between pol replication capacity and HIV-1 RNA and CD4 T-cell number. A random effects model assessed the ability of this measure to predict CD4 T-cell decline over time and a Cox proportional hazards model and Kaplan-Meier analyses defined how it predicts clinical progression. RESULTS: Pol replication capacity measures correlated with baseline HIV-1 RNA, R = 0.189 (P = 0.03) and CD4 T-cell number, -0.197 (P = 0.03). It also independently predicted CD4 T-cell decline over time and progression to AIDS. CONCLUSIONS: This study demonstrates that pol replication capacity independently influences the natural history of HIV-1 infection.
Authors: Gail Skowron; John G Spritzler; Jodi Weidler; Gregory K Robbins; Victoria A Johnson; Ellen S Chan; David M Asmuth; Rajesh T Gandhi; Yolanda Lie; Michael Bates; Richard B Pollard Journal: J Acquir Immune Defic Syndr Date: 2009-03-01 Impact factor: 3.731
Authors: Matthew Bidwell Goetz; Robert Leduc; Nicole Wyman; Jay R Kostman; Ann M Labriola; Yolanda Lie; Jodi Weidler; Eoin Coakley; Michael Bates; Roberta Luskin-Hawk Journal: J Acquir Immune Defic Syndr Date: 2010-04-01 Impact factor: 3.731
Authors: Thierry Buclin; Amalio Telenti; Rafael Perera; Chantal Csajka; Hansjakob Furrer; Jeffrey K Aronson; Paul P Glasziou Journal: PLoS One Date: 2011-04-08 Impact factor: 3.240
Authors: Roger D Kouyos; Viktor von Wyl; Trevor Hinkley; Christos J Petropoulos; Mojgan Haddad; Jeannette M Whitcomb; Jürg Böni; Sabine Yerly; Cristina Cellerai; Thomas Klimkait; Huldrych F Günthard; Sebastian Bonhoeffer Journal: PLoS Pathog Date: 2011-11-03 Impact factor: 6.823