{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,5]],"date-time":"2026-02-05T22:22:02Z","timestamp":1770330122449,"version":"3.49.0"},"reference-count":48,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2013,10,31]],"date-time":"2013-10-31T00:00:00Z","timestamp":1383177600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["HIV Medicine"],"published-print":{"date-parts":[[2014,3]]},"abstract":"<jats:sec><jats:title>Objectives<\/jats:title><jats:p>Although combination antiretroviral therapy (<jats:styled-content style=\"fixed-case\">cART<\/jats:styled-content>) can restore <jats:styled-content style=\"fixed-case\">CD4 T<\/jats:styled-content>\u2010cell numbers in <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content> infection, alterations in <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010cell regulation and homeostasis persist. We assessed the incidence and predictors of reversing these alterations with <jats:styled-content style=\"fixed-case\">cART<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">ART<\/jats:styled-content>\u2010na\u00efve adults (n\u2009=\u20094459) followed within the <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>anadian <jats:styled-content style=\"fixed-case\">O<\/jats:styled-content>bservational <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>ohort and exhibiting an abnormal <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010cell phenotype (<jats:styled-content style=\"fixed-case\">TCP<\/jats:styled-content>) prior to <jats:styled-content style=\"fixed-case\">cART<\/jats:styled-content> initiation were studied. Abnormal <jats:styled-content style=\"fixed-case\">TCP<\/jats:styled-content> was defined as having (1) a low <jats:styled-content style=\"fixed-case\">CD4 T<\/jats:styled-content>\u2010cell count (&lt;\u2009532 cells\/\u03bc<jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>), (2) lost <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010cell homeostasis (<jats:styled-content style=\"fixed-case\">CD3<\/jats:styled-content>\u2009&lt;\u200965% or &gt;\u200985%) or (3) <jats:styled-content style=\"fixed-case\">CD4<\/jats:styled-content>:<jats:styled-content style=\"fixed-case\">CD8<\/jats:styled-content> ratio dysregulation (ratio\u2009&lt;\u20091.2). To thoroughly evaluate the <jats:styled-content style=\"fixed-case\">TCP<\/jats:styled-content>, <jats:styled-content style=\"fixed-case\">CD4<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">CD8 T<\/jats:styled-content>\u2010cell percentages and absolute counts were also analysed for a median duration of 3.14 years [interquartile range (<jats:styled-content style=\"fixed-case\">IQR<\/jats:styled-content>) 1.48\u20135.47 years]. Predictors of <jats:styled-content style=\"fixed-case\">TCP<\/jats:styled-content> normalization were assessed using adjusted Cox proportional hazards models.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>t baseline, 96% of pateints had <jats:styled-content style=\"fixed-case\">CD4<\/jats:styled-content> depletion, 32% had lost homeostasis and 99% exhibited ratio dysregulation. With treatment, a third of patients had normalized <jats:styled-content style=\"fixed-case\">CD4 T<\/jats:styled-content>\u2010cell counts, but only 85 individuals (2%) had normalized their <jats:styled-content style=\"fixed-case\">TCP<\/jats:styled-content>. In a multivariable model adjusted for age, measurement frequency and baseline regimen, higher baseline <jats:styled-content style=\"fixed-case\">CD4 T<\/jats:styled-content>\u2010cell counts and time\u2010dependent viral suppression independently predicted <jats:styled-content style=\"fixed-case\">TCP<\/jats:styled-content> normalization [hazard ratio (<jats:styled-content style=\"fixed-case\">HR<\/jats:styled-content>) for baseline <jats:styled-content style=\"fixed-case\">CD4<\/jats:styled-content> T\u2010cell count\u2009=\u20091.42 (1.31\u20131.54) per 100\u2009cells\/\u03bc<jats:styled-content style=\"fixed-case\">L<\/jats:styled-content> increase; <jats:italic>P<\/jats:italic>\u2009\u2264\u20090.0001; <jats:styled-content style=\"fixed-case\">HR<\/jats:styled-content> for time\u2010dependent suppressed viral load\u2009=\u20093.69 (1.58\u20138.61); <jats:italic>P<\/jats:italic>\u2010value\u2009\u2264\u20090.01].<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Despite effective <jats:styled-content style=\"fixed-case\">cART<\/jats:styled-content>, complete <jats:styled-content style=\"fixed-case\">TCP<\/jats:styled-content> recovery occurred in very few individuals and was associated with baseline <jats:styled-content style=\"fixed-case\">CD4 T<\/jats:styled-content>\u2010cell count and viral load suppression. <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>\u2010induced alterations of the <jats:styled-content style=\"fixed-case\">TCP<\/jats:styled-content> are incompletely reversed by long\u2010term <jats:styled-content style=\"fixed-case\">ART<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/hiv.12096","type":"journal-article","created":{"date-parts":[[2013,10,31]],"date-time":"2013-10-31T10:27:17Z","timestamp":1383215237000},"page":"153-164","source":"Crossref","is-referenced-by-count":10,"title":["Characteristics and determinants of <scp>T<\/scp>\u2010cell phenotype normalization in <scp>HIV<\/scp>\u20101\u2010infected individuals receiving long\u2010term antiretroviral therapy"],"prefix":"10.1111","volume":"15","author":[{"given":"P","family":"Ndumbi","sequence":"first","affiliation":[{"name":"McGill University Health Centre  Montreal Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J","family":"Gillis","sequence":"additional","affiliation":[{"name":"Toronto General Research Institute University Health Network  Toronto 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