{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T13:11:47Z","timestamp":1789391507233,"version":"build-2803163510"},"reference-count":51,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2009,9,1]],"date-time":"2009-09-01T00:00:00Z","timestamp":1251763200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Clin Vaccine Immunol"],"published-print":{"date-parts":[[2009,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Human immunodeficiency virus (HIV) type 1 infection perturbs the T-cell receptor (TCR) V\u03b2 repertoire. The TCR CDR3 length diversity of individual V\u03b2 families was examined within CD45RA and CD45RO CD4 T cells to assess the impact of the virus on clonality throughout CD4 T-cell activation and differentiation. A cross-sectional and longitudinal cohort study of 13 HIV-infected and 8 age-matched healthy children and adolescents examined the V\u03b2 CDR3 length profiles within CD4 T-cell subsets by the use of spectratyping. HIV-infected subjects demonstrated higher numbers of perturbations in CD4 CD45RA T cells (5.8 \u00b1 4.9 V\u03b2 families) than healthy individuals (1.6 \u00b1 1.8 V\u03b2 families) (<jats:italic>P<\/jats:italic>= 0.04). Surprisingly, CD4 CD45RO central memory T cells from infected subjects showed no increased perturbations compared to the perturbations for the same cells from healthy subjects (2.9 \u00b1 3.1 and 1.1 \u00b1 1.8 V\u03b2 families, respectively;<jats:italic>P<\/jats:italic>= 0.11). CD4 CD45RA TCR perturbations were higher among infected subjects with &gt;25% CD4 cells than healthy subjects (mean number of perturbed V<jats:italic>\u03b2<\/jats:italic>families, 6.6 \u00b1 5.4;<jats:italic>P<\/jats:italic>= 0.04). No correlations between perturbations in CD4 subsets and pretherapy age or viral load were evident. In contrast to CD8 T cells, HIV induces TCR disruptions within CD45RA but not CD45RO CD4 T cells. Therapy-induced viral suppression resulted in increases in thymic output and the normalization of the diversity of TCR within CD45RA CD4 T cells after 2 months of treatment. Perturbations occur prior to CD4 T-cell attrition and normalize with effective antiretroviral therapy. The impact of HIV on the diversity of TCR within nai\u0308ve, central memory, and effector memory CD4 T cells is distinctly different from that in CD8 T cells.<\/jats:p>","DOI":"10.1128\/cvi.00074-09","type":"journal-article","created":{"date-parts":[[2009,7,16]],"date-time":"2009-07-16T01:44:51Z","timestamp":1247708691000},"page":"1293-1301","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":20,"title":["Antiretroviral Therapy Restores Diversity in the T-Cell Receptor V\u03b2 Repertoire of CD4 T-Cell Subpopulations among Human Immunodeficiency Virus Type 1-Infected Children and Adolescents"],"prefix":"10.1128","volume":"16","author":[{"given":"Li","family":"Yin","sequence":"first","affiliation":[{"name":"Departments of Pathology, Immunology and Laboratory Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhong Chen","family":"Kou","sequence":"additional","affiliation":[{"name":"Departments of Pathology, Immunology and Laboratory Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carina","family":"Rodriguez","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Hou","sequence":"additional","affiliation":[{"name":"Department of Epidemiology and Health Policy Research, Shands Cancer Center, University of Florida, College of Medicine, Gainesville, Florida"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maureen M.","family":"Goodenow","sequence":"additional","affiliation":[{"name":"Departments of Pathology, Immunology and Laboratory Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John W.","family":"Sleasman","sequence":"additional","affiliation":[{"name":"Division of Allergy, Immunology, and Rheumatology, University of South Florida, College of Medicine, St. Petersburg, Florida"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","first-page":"205","DOI":"10.1016\/j.smim.2004.02.007","volume":"16","year":"2004","unstructured":"Appay, V., and S. 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