{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T01:28:39Z","timestamp":1786411719300,"version":"build-2736575974"},"posted":{"date-parts":[[2026,8,9]]},"group-title":"Immunology","reference-count":81,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,8,9]],"date-time":"2026-08-09T00:00:00Z","timestamp":1786233600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.biorxiv.org\/about\/FAQ#license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,8,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:p>\n                  Chikungunya virus (CHIKV) infection is increasingly linked to cardiovascular complications, but the mechanisms underlying CHIKV-induced cardiovascular disease (CVD) remain unclear, and targeted therapies are lacking. Although elevated interleukin-17A (IL-17A) levels have been reported in CHIKV patients and associated with cardiovascular pathology, its role in CHIKV-induced cardiac disease is poorly defined. To address this question, we employed our newly developed heterozygous interferon \u03b1\/\u03b2\/\u03b3 receptor-deficient (\n                  <jats:italic>Ifnag<\/jats:italic>\n                  <jats:sup>+\/\u2212<\/jats:sup>\n                  ) mice and primary human cardiac fibroblasts to investigate the contribution of IL-17A signaling to CHIKV-associated cardiac pathology. We found that CHIKV infection induced IL-17A production in the heart, and that mice deficient in\n                  <jats:italic>Il17a<\/jats:italic>\n                  (\n                  <jats:italic>\n                    Il17a\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                  <\/jats:italic>\n                  ) and in its receptor gene,\n                  <jats:italic>Il-17ra<\/jats:italic>\n                  (\n                  <jats:italic>\n                    Il17ra\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                  <\/jats:italic>\n                  ), exhibited marked resistance to CHIKV infection in both cardiac tissue and primary cardiac fibroblasts. Genetic deletion of IL-17A signaling significantly enhanced type I interferon responses and decreased viral burden in mouse hearts. Interestingly, blockade of IL-17RA with an FDA-approved monoclonal antibody for plaque psoriasis, Brodalumab, drastically increased type I interferon production and reduced viral replication in both human cardiac fibroblasts and human embryonic kidney 293 (HEK 293) cells. In addition, inhibition of IL-17A signaling suppressed the expression of pro-inflammatory mediators, including\n                  <jats:italic>Il-1\u03b2<\/jats:italic>\n                  ,\n                  <jats:italic>Tnf-\u03b1<\/jats:italic>\n                  , and\n                  <jats:italic>Cxcl2<\/jats:italic>\n                  , reduced immune cell infiltration into cardiac tissue, and mitigated cardiac injury. Importantly, therapeutic blockade of IL-17A signaling after CHIKV infection reduced viral replication in both the heart and circulation. Collectively, these findings identify IL-17A signaling as a critical regulator of CHIKV replication and cardiac inflammation and highlight the IL-17A\/IL-17RA axis as a promising therapeutic target for CHIKV-associated cardiovascular disease.\n                <\/jats:p>\n                <jats:sec>\n                  <jats:title>Importance<\/jats:title>\n                  <jats:p>Chikungunya virus (CHIKV) infection has been frequently associated with cardiovascular complications, yet the host pathways that promote viral infection and cardiac injury remain poorly understood. Here, we identify IL-17A signaling as a previously unrecognized regulator of CHIKV pathogenesis in the heart. Using a novel heterozygous interferon receptor-deficient mouse model and primary human cardiac fibroblasts, we demonstrate that IL-17A signaling facilitates CHIKV replication via suppressing antiviral type I interferon responses. Genetic deletion or pharmacological blockade with an FDA-approved monoclonal antibody of IL-17A signaling reduced viral burden, attenuated inflammatory cytokine production, limited immune cell infiltration, and protected against cardiac injury. Importantly, therapeutic inhibition of IL-17A signaling after infection remained effective in reducing viral replication in both cardiac tissue and circulation and mitigating cardiac damage. These findings reveal a critical role for the IL-17A\/IL-17RA axis in linking antiviral immunity to CHIKV-induced cardiovascular disease and identify a potential translatable therapeutic target for CHIKV-caused cardiac complications.<\/jats:p>\n                <\/jats:sec>","DOI":"10.64898\/2026.08.07.743518","type":"posted-content","created":{"date-parts":[[2026,8,9]],"date-time":"2026-08-09T13:20:13Z","timestamp":1786281613000},"source":"Crossref","is-referenced-by-count":0,"title":["IL-17A Restrains Antiviral Immunity to Promote Chikungunya Virus Infection and Pathogenesis in the Heart"],"prefix":"10.64898","author":[{"given":"Shazeed-Ul","family":"Karim","sequence":"first","affiliation":[{"name":"Cell and Molecular Biology Program, School of Biological, Environmental, and Earth Sciences, The University of Southern Mississippi, Hattiesburg, MS 39406, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Prince M.D.","family":"Denyoh","sequence":"additional","affiliation":[{"name":"Cell and Molecular Biology Program, School of Biological, Environmental, and Earth Sciences, The University of Southern Mississippi, Hattiesburg, MS 39406, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sabin","family":"Shrestha","sequence":"additional","affiliation":[{"name":"Cell and Molecular Biology Program, School of Biological, Environmental, and Earth Sciences, The University of Southern Mississippi, Hattiesburg, MS 39406, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ayokanmi","family":"Osobukola","sequence":"additional","affiliation":[{"name":"Cell and Molecular Biology Program, School of Biological, Environmental, and Earth Sciences, The University of Southern Mississippi, Hattiesburg, MS 39406, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nathan S.","family":"Bai","sequence":"additional","affiliation":[{"name":"Oak Grove High School, Hattiesburg, MS 39402, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fengwei","family":"Bai","sequence":"additional","affiliation":[{"name":"Cell and Molecular Biology Program, School of Biological, Environmental, and Earth Sciences, The University of Southern Mississippi, Hattiesburg, MS 39406, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"54368","reference":[{"key":"2026081017450734000_2026.08.07.743518v1.1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMp1407698"},{"key":"2026081017450734000_2026.08.07.743518v1.2","doi-asserted-by":"publisher","DOI":"10.1038\/nrrheum.2012.64"},{"key":"2026081017450734000_2026.08.07.743518v1.3","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.0030201"},{"key":"2026081017450734000_2026.08.07.743518v1.4","doi-asserted-by":"crossref","first-page":"390","DOI":"10.12688\/f1000research.11078.2","article-title":"Cardiovascular involvement and manifestations of systemic Chikungunya virus infection: A systematic review","volume":"6","year":"2017","journal-title":"F1000Res"},{"key":"2026081017450734000_2026.08.07.743518v1.5","doi-asserted-by":"crossref","unstructured":"Traverse EM , Hopkins HK , Vaidhyanathan V , Barr KL . 2021. 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