{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,12]],"date-time":"2026-06-12T14:05:01Z","timestamp":1781273101300,"version":"3.54.1"},"reference-count":93,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"10","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2025,10]]},"abstract":"<jats:sec>\n            <jats:title>BACKGROUND:<\/jats:title>\n            <jats:p>People with HIV are at higher risk of atherosclerotic cardiovascular disease than uninfected individuals; however, the molecular mechanisms behind this association remain elusive due to the lack of suitable animal models.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>METHODS:<\/jats:title>\n            <jats:p>\n              To study the impact of HIV on atherosclerotic cardiovascular disease, we infected the atheroprone\n              <jats:italic toggle=\"yes\">Ldlr<\/jats:italic>\n              <jats:sup>\n                <jats:italic toggle=\"yes\">\u2212\/\u2212<\/jats:italic>\n              <\/jats:sup>\n              mice with the chimeric virus EcoHIV.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>RESULTS:<\/jats:title>\n            <jats:p>\n              In comparison to uninfected controls, EcoHIV infection increased the ratio of circulating inflammatory monocytes, monocyte recruitment, and CD68\n              <jats:sup>+<\/jats:sup>\n              content in the atherosclerotic lesion. These changes occurred independently of alterations in plasma lipid profile or lesion size between groups. Lesions of EcoHIV-infected mice displayed greater vulnerability to rupture, as determined by increased necrotic core area and CD38\n              <jats:sup>+<\/jats:sup>\n              content, and reduced presence of collagen compared with uninfected mice. Last, we report the presence of active viral replication of EcoHIV in the atherosclerotic lesion.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS:<\/jats:title>\n            <jats:p>\n              Our data suggest that EcoHIV infection in\n              <jats:italic toggle=\"yes\">Ldlr<\/jats:italic>\n              <jats:sup>\n                <jats:italic toggle=\"yes\">\u2212\/\u2212<\/jats:italic>\n              <\/jats:sup>\n              mice resembles the pathogenesis of atherosclerotic cardiovascular disease in people with HIV. Our findings have therapeutic implications for people with HIV, a vulnerable population with an elevated risk of cardiovascular disease.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/atvbaha.125.323004","type":"journal-article","created":{"date-parts":[[2025,9,4]],"date-time":"2025-09-04T09:00:17Z","timestamp":1756976417000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":1,"title":["EcoHIV Infection Promotes Atherosclerosis Progression in LDLR-Deficient Mice"],"prefix":"10.1161","volume":"45","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2236-8936","authenticated-orcid":true,"given":"Ivan","family":"Pinos","sequence":"first","affiliation":[{"name":"Division of Nutritional Sciences (I.P., A.B., J.A.), University of Illinois 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