{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T23:27:40Z","timestamp":1780529260715,"version":"3.54.1"},"reference-count":43,"publisher":"American Society for Clinical Investigation","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2017,4,6]]},"abstract":"<jats:p>\n                    <jats:bold>BACKGROUND.<\/jats:bold>\n                    Bacillus Calmette-Gu\u00e9rin (BCG) vaccine is administered at birth to protect infants against tuberculosis throughout Africa, where most perinatal HIV-1 transmission occurs. We examined whether BCG vaccination alters the levels of activated HIV target T cells in HIV-exposed South African infants.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>METHODS.<\/jats:bold>\n                    HIV-exposed infants were randomized to receive routine (at birth) or delayed (at 8 weeks) BCG vaccination. Activated and CCR5-expressing peripheral blood CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cell, monocyte, and NK cell frequencies were evaluated by flow cytometry and immune gene expression via PCR using Biomark (Fluidigm).\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>RESULTS.<\/jats:bold>\n                    Of 149 infants randomized, 92% (\n                    <jats:italic>n<\/jats:italic>\n                    = 137) were retained at 6 weeks: 71 in the routine BCG arm and 66 in the delayed arm. Routine BCG vaccination led to a 3-fold increase in systemic activation of HIV target CD4\n                    <jats:sup>+<\/jats:sup>\n                    CCR5\n                    <jats:sup>+<\/jats:sup>\n                    T cells (HLA-DR\n                    <jats:sup>+<\/jats:sup>\n                    CD38\n                    <jats:sup>+<\/jats:sup>\n                    ) at 6 weeks (0.25% at birth versus 0.08% in delayed vaccination groups;\n                    <jats:italic>P<\/jats:italic>\n                    = 0.029), which persisted until 8 weeks of age when the delayed arm was vaccinated. Vaccination of the infants in the delayed arm at 8 weeks resulted in a similar increase in activated CD4\n                    <jats:sup>+<\/jats:sup>\n                    CCR5\n                    <jats:sup>+<\/jats:sup>\n                    T cells. The increase in activated T cells was associated with increased levels of MHC class II transactivator (CIITA), IL12RB1, and IFN-\u03b11 transcripts within peripheral blood mononuclear cells but minimal changes in innate cells.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>CONCLUSION.<\/jats:bold>\n                    BCG vaccination induces immune changes in HIV-exposed infants, including an increase in the proportion of activated CCR5\n                    <jats:sup>+<\/jats:sup>\n                    CD4\n                    <jats:sup>+<\/jats:sup>\n                    HIV target cells. These findings provide insight into optimal BCG vaccine timing to minimize the risks of HIV transmissions to exposed infants while preserving potential benefits conferred by BCG vaccination.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>TRIAL REGISTRATION.<\/jats:bold>\n                    ClinicalTrials.gov NCT02062580.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>FUNDING.<\/jats:bold>\n                    This trial was sponsored by the Elizabeth Glaser Pediatric AIDS Foundation (MV-00-9-900-01871-0-00) and the Thrasher Foundation (NR-0095); for details, see Acknowledgments.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.91963","type":"journal-article","created":{"date-parts":[[2017,4,6]],"date-time":"2017-04-06T22:24:53Z","timestamp":1491517493000},"source":"Crossref","is-referenced-by-count":13,"title":["BCG vaccination induces HIV target cell activation in HIV-exposed infants in a randomized trial"],"prefix":"10.1172","volume":"2","author":[{"given":"Melanie A.","family":"Gasper","sequence":"first","affiliation":[{"name":"University of Washington, Seattle, Washington, USA."},{"name":"Center for Infectious Disease Research, Seattle, Washington, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anneke C.","family":"Hesseling","sequence":"additional","affiliation":[{"name":"Department of Paediatrics and Child Health, Faculty of Medicine and Health Sciences, Stellenbosch University, Tygerberg, South Africa."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Isaac","family":"Mohar","sequence":"additional","affiliation":[{"name":"Center for Infectious Disease Research, Seattle, Washington, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Landon","family":"Myer","sequence":"additional","affiliation":[{"name":"Division of Epidemiology and Biostatistics, School of Public Health and Family Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tali","family":"Azenkot","sequence":"additional","affiliation":[{"name":"Center for Infectious Disease Research, Seattle, Washington, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jo-Ann S.","family":"Passmore","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Cape Town, Cape Town, South Africa."},{"name":"National Health Laboratory Service, Cape Town, South Africa."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Willem","family":"Hanekom","sequence":"additional","affiliation":[{"name":"South African Tuberculosis Vaccine Initiative, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Cape Town, South Africa."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark F.","family":"Cotton","sequence":"additional","affiliation":[{"name":"Department of Paediatrics and Child Health, Faculty of Medicine and Health Sciences, Stellenbosch University, Tygerberg, South Africa."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"I. Nicholas","family":"Crispe","sequence":"additional","affiliation":[{"name":"University of Washington, Seattle, Washington, USA."},{"name":"Center for Infectious Disease Research, Seattle, Washington, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Donald L.","family":"Sodora","sequence":"additional","affiliation":[{"name":"University of Washington, Seattle, Washington, USA."},{"name":"Center for Infectious Disease Research, Seattle, Washington, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Heather B.","family":"Jaspan","sequence":"additional","affiliation":[{"name":"University of Washington, Seattle, Washington, USA."},{"name":"Center for Infectious Disease Research, Seattle, Washington, USA."},{"name":"Department of Pathology, University of Cape Town, Cape Town, South Africa."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"232","published-online":{"date-parts":[[2017,4,6]]},"reference":[{"key":"B1","unstructured":"UNAIDS report on the global AIDS epidemic 2013. 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