{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T06:54:11Z","timestamp":1789541651627,"version":"build-2803163510"},"reference-count":159,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","license":[{"start":{"date-parts":[[2024,3,29]],"date-time":"2024-03-29T00:00:00Z","timestamp":1711670400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2024,3,29]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>Viral cardiac infection represents a significant clinical challenge encompassing several etiological agents, disease stages, complex presentation, and a resulting lack of mechanistic understanding. Myocarditis is a major cause of sudden cardiac death in young adults, where current knowledge in the field is dominated by later disease phases and pathological immune responses. However, little is known regarding how infection can acutely induce an arrhythmogenic substrate before significant immune responses. Adenovirus is a leading cause of myocarditis, but due to species specificity, models of infection are lacking, and it is not understood how adenoviral infection may underlie sudden cardiac arrest. Mouse adenovirus type-3 was previously reported as cardiotropic, yet it has not been utilized to understand the mechanisms of cardiac infection and pathology.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>We have developed mouse adenovirus type-3 infection as a model to investigate acute cardiac infection and molecular alterations to the infected heart before an appreciable immune response or gross cardiomyopathy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      Optical mapping of infected hearts exposes decreases in conduction velocity concomitant with increased Cx43\n                      <jats:sup>Ser368<\/jats:sup>\n                      phosphorylation, a residue known to regulate gap junction function. Hearts from animals harboring a phospho-null mutation at Cx43\n                      <jats:sup>Ser368<\/jats:sup>\n                      are protected against mouse adenovirus type-3\u2013induced conduction velocity slowing. Additional to gap junction alterations, patch clamping of mouse adenovirus type-3\u2013infected adult mouse ventricular cardiomyocytes reveals prolonged action potential duration as a result of decreased\n                      <jats:italic>I<\/jats:italic>\n                      <jats:sub>K1<\/jats:sub>\n                      and\n                      <jats:italic>I<\/jats:italic>\n                      <jats:sub>Ks<\/jats:sub>\n                      current density. Turning to human systems, we find human adenovirus type-5 increases phosphorylation of Cx43\n                      <jats:sup>Ser368<\/jats:sup>\n                      and disrupts synchrony in human induced pluripotent stem cell-derived cardiomyocytes, indicating common mechanisms with our mouse whole heart and adult cardiomyocyte data.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>Together, these findings demonstrate that adenoviral infection creates an arrhythmogenic substrate through direct targeting of gap junction and ion channel function in the heart. Such alterations are known to precipitate arrhythmias and likely contribute to sudden cardiac death in acutely infected patients.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circresaha.122.322437","type":"journal-article","created":{"date-parts":[[2024,2,28]],"date-time":"2024-02-28T05:00:29Z","timestamp":1709096429000},"page":"892-912","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":26,"title":["Acute Adenoviral Infection Elicits an Arrhythmogenic Substrate Prior to Myocarditis"],"prefix":"10.1161","volume":"134","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7426-6272","authenticated-orcid":true,"given":"Rachel L.","family":"Padget","sequence":"first","affiliation":[{"name":"Graduate Program in Translational Biology, Medicine, and Health (R.L.P., G.A.B., K.E.S., D.R.K.), Virginia Tech, Blacksburg."},{"name":"Fralin Biomedical Research Institute at Virginia Tech Carilion, Roanoke (R.L.P., M.J.Z., G.A.B., X.W., K.E.S., C.M.P., D.R.K., S.L., R.G.G., G.S.H., S.A.S., S.P., J.W.S.)."},{"name":"Center for Vascular and Heart Research, FBRI at VTC, Roanoke, VA (R.L.P., M.J.Z., G.A.B., X.W., K.E.S., C.M.P., D.R.K., S.L., R.G.G., G.S.H., S.P., J.W.S.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael J.","family":"Zeitz","sequence":"additional","affiliation":[{"name":"Fralin Biomedical Research Institute at Virginia Tech Carilion, Roanoke (R.L.P., M.J.Z., G.A.B., X.W., K.E.S., C.M.P., D.R.K., S.L., R.G.G., G.S.H., S.A.S., S.P., J.W.S.)."},{"name":"Center for Vascular and Heart Research, FBRI at VTC, Roanoke, VA (R.L.P., M.J.Z., G.A.B., X.W., K.E.S., C.M.P., D.R.K., S.L., R.G.G., G.S.H., S.P., J.W.S.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5633-5497","authenticated-orcid":true,"given":"Grace A.","family":"Blair","sequence":"additional","affiliation":[{"name":"Graduate Program in Translational Biology, Medicine, and 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