{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,19]],"date-time":"2026-09-19T20:28:28Z","timestamp":1789849708931,"version":"4.0.1"},"reference-count":31,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2014,3,24]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Diastolic dysfunction is a highly prevalent cardiac abnormality in asymptomatic as well as\n              <jats:styled-content style=\"fixed-case\">ART<\/jats:styled-content>\n              \u2010treated human immunodeficiency virus (\n              <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>\n              ) patients. Although the mechanisms underlying depressed cardiac function remain obscure, diastolic dysfunction in\n              <jats:styled-content style=\"fixed-case\">SIV<\/jats:styled-content>\n              \u2010infected rhesus macaques is highly correlated with myocardial viral load. As cardiomyocytes are not productively infected, damage may be an indirect process attributable to a combination of pro\u2010inflammatory mediators and viral proteins.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Given the diverse roles of CCR5 in mediating recruitment of leukocytes to inflammatory sites and serving as a receptor for HIV entry into cells, we investigated the role of CCR5 in the SIV\/macaque model of diastolic dysfunction. We found that in SIV\u2010infected macaques, CCR5 inhibition dramatically impacted myocardial viral load measured by\n              <jats:styled-content style=\"fixed-case\">qRT<\/jats:styled-content>\n              \u2010PCR and prevented diastolic dysfunction measured by echocardiography. Complementary in vitro experiments using fluorescence microscopy showed that CCR5 ligands impaired contractile function of isolated cardiomyocytes, thus identifying CCR5 signaling as a novel mediator of impaired cardiac mechanical function.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Together, these findings incriminate\n              <jats:styled-content style=\"fixed-case\">SIV<\/jats:styled-content>\n              \/\n              <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>\n              gp120\u2010\n              <jats:styled-content style=\"fixed-case\">CCR<\/jats:styled-content>\n              5 as well as chemokine\u2010\n              <jats:styled-content style=\"fixed-case\">CCR<\/jats:styled-content>\n              5 interactions in\n              <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>\n              \u2010associated cardiac dysfunction. These findings also have important implications for the treatment of\n              <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>\n              \u2010infected individuals: in addition to antiviral properties and reduced chemokine\u2010mediated recruitment and activation of inflammatory cells,\n              <jats:styled-content style=\"fixed-case\">CCR<\/jats:styled-content>\n              5 inhibition may provide a cardioprotective benefit by preventing cardiomyocyte\n              <jats:styled-content style=\"fixed-case\">CCR<\/jats:styled-content>\n              5 signaling.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.114.000874","type":"journal-article","created":{"date-parts":[[2014,4,3]],"date-time":"2014-04-03T06:34:37Z","timestamp":1396506877000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":38,"title":["CCR5 Inhibition Prevents Cardiac Dysfunction in the SIV\/Macaque Model of HIV"],"prefix":"10.1161","volume":"3","author":[{"given":"Kathleen M.","family":"Kelly","sequence":"first","affiliation":[{"name":"Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, MD"},{"name":"Department of Biomedical Sciences, Cornell University College of Veterinary Medicine, Ithaca, NY"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carlo G.","family":"Tocchetti","sequence":"additional","affiliation":[{"name":"Clinica Montevergine, Mercogliano (AV), Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexey","family":"Lyashkov","sequence":"additional","affiliation":[{"name":"Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, MD"},{"name":"Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrick M.","family":"Tarwater","sequence":"additional","affiliation":[{"name":"Division of Biostatistics and Epidemiology, Paul L. 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