{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,29]],"date-time":"2026-08-29T05:22:05Z","timestamp":1787980925279,"version":"build-2784847793"},"reference-count":42,"publisher":"American Society for Microbiology","issue":"22","license":[{"start":{"date-parts":[[2015,11,15]],"date-time":"2015-11-15T00:00:00Z","timestamp":1447545600000},"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":["J Virol"],"published-print":{"date-parts":[[2015,11,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            There is no licensed vaccine against respiratory syncytial virus (RSV) since the failure of formalin-inactivated RSV (FI-RSV) due to its vaccine-enhanced disease. We investigated immune correlates conferring protection without causing disease after intranasal immunization with virus-like particle vaccine containing the RSV fusion protein (F VLP) in comparison to FI-RSV and live RSV. Upon RSV challenge, FI-RSV immune mice showed severe weight loss, eosinophilia, and histopathology, and RSV reinfection also caused substantial RSV disease despite their viral clearance. In contrast, F VLP immune mice showed least weight loss and no sign of histopathology and eosinophilia. High levels of interleukin-4-positive (IL-4\n            <jats:sup>+<\/jats:sup>\n            ) and tumor necrosis factor alpha-positive (TNF-\u03b1\n            <jats:sup>+<\/jats:sup>\n            ) CD4\n            <jats:sup>+<\/jats:sup>\n            T cells were found in FI-RSV immune mice, whereas gamma interferon-positive (IFN-\u03b3\n            <jats:sup>+<\/jats:sup>\n            ) and TNF-\u03b1\n            <jats:sup>+<\/jats:sup>\n            CD4\n            <jats:sup>+<\/jats:sup>\n            T cells were predominantly detected in live RSV-infected mice. More importantly, in contrast to FI-RSV and live RSV that induced higher levels of CD11b\n            <jats:sup>+<\/jats:sup>\n            dendritic cells, F VLP immunization induced CD8\u03b1\n            <jats:sup>+<\/jats:sup>\n            and CD103\n            <jats:sup>+<\/jats:sup>\n            dendritic cells, as well as F-specific IFN-\u03b3\n            <jats:sup>+<\/jats:sup>\n            and TNF-\u03b1\n            <jats:sup>+<\/jats:sup>\n            CD8\n            <jats:sup>+<\/jats:sup>\n            T cells. These results suggest that F VLP can induce protection without causing pulmonary RSV disease by inducing RSV neutralizing antibodies, as well as modulating specific subsets of dendritic cells and CD8 T cell immunity.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>IMPORTANCE<\/jats:bold>\n            It has been a difficult challenge to develop an effective and safe vaccine against respiratory syncytial virus (RSV), a leading cause of respiratory disease. Immune correlates conferring protection but preventing vaccine-enhanced disease remain poorly understood. RSV F virus-like particle (VLP) would be an efficient vaccine platform conferring protection. Here, we investigated the protective immune correlates without causing disease after intranasal immunization with RSV F VLP in comparison to FI-RSV and live RSV. In addition to inducing RSV neutralizing antibodies responsible for clearing lung viral loads, we show that modulation of specific subsets of dendritic cells and CD8 T cells producing T helper type 1 cytokines are important immune correlates conferring protection but not causing vaccine-enhanced disease.\n          <\/jats:p>","DOI":"10.1128\/jvi.02018-15","type":"journal-article","created":{"date-parts":[[2015,9,10]],"date-time":"2015-09-10T13:48:50Z","timestamp":1441892930000},"page":"11692-11705","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":48,"title":["Virus-Like Particle Vaccine Containing the F Protein of Respiratory Syncytial Virus Confers Protection without Pulmonary Disease by Modulating Specific Subsets of Dendritic Cells and Effector T Cells"],"prefix":"10.1128","volume":"89","author":[{"given":"Ki-Hye","family":"Kim","sequence":"first","affiliation":[{"name":"Center for Inflammation, Immunity, and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, Georgia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Young-Tae","family":"Lee","sequence":"additional","affiliation":[{"name":"Center for Inflammation, Immunity, and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, Georgia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hye Suk","family":"Hwang","sequence":"additional","affiliation":[{"name":"Center for Inflammation, Immunity, and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, Georgia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Young-Man","family":"Kwon","sequence":"additional","affiliation":[{"name":"Center for Inflammation, Immunity, and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, Georgia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Min-Chul","family":"Kim","sequence":"additional","affiliation":[{"name":"Center for Inflammation, Immunity, and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, Georgia, USA"},{"name":"Animal and Plant Quarantine Agency, Anyang City, Gyeonggi-do, South Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eun-Ju","family":"Ko","sequence":"additional","affiliation":[{"name":"Center for Inflammation, Immunity, and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, Georgia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jong Seok","family":"Lee","sequence":"additional","affiliation":[{"name":"Center for Inflammation, Immunity, and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, Georgia, USA"},{"name":"National Institute of Biological Resources, Incheon, Gyeonggi-do, South Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Youri","family":"Lee","sequence":"additional","affiliation":[{"name":"Center for Inflammation, Immunity, and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, Georgia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sang-Moo","family":"Kang","sequence":"additional","affiliation":[{"name":"Center for Inflammation, Immunity, and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, Georgia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(10)60206-1"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.aje.a120955"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1007\/s12026-007-0071-6"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.68.8.5321-5325.1994"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.70.5.2852-2860.1996"},{"key":"e_1_3_2_7_2","first-page":"530","article-title":"Respiratory-syncytial-virus infections, reinfections and immunity","volume":"300","author":"Henderson FW","year":"1979","unstructured":"Henderson FW, Collier AM, Clyde WA Jr., Denny FW. 1979. 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