{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,4]],"date-time":"2026-11-04T03:43:34Z","timestamp":1793763814670,"version":"4.6.1"},"reference-count":65,"publisher":"American Society for Microbiology","issue":"10","license":[{"start":{"date-parts":[[2025,10,23]],"date-time":"2025-10-23T00:00:00Z","timestamp":1761177600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,10,23]],"date-time":"2025-10-23T00:00:00Z","timestamp":1761177600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 AI134733"],"award-info":[{"award-number":["R01 AI134733"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R21 139902"],"award-info":[{"award-number":["R21 139902"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["T32 AI007533"],"award-info":[{"award-number":["T32 AI007533"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["UH2AI186375-01S1"],"award-info":[{"award-number":["UH2AI186375-01S1"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"name":"University of Iowa College of Medicine"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2025,10,23]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      Ebola virus (EBOV), the causative agent of Ebola virus disease, remains one\n                        of the World Health Organization\u2019s top 10 threats to global health.\n                        Infectious EBOV virions can be found on the surface of skin late in\n                        infection and may be transmitted to others through skin-to-skin contact. We\n                        investigate\n                      <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                      EBOV tropism and the kinetics of virus\n                        movement to and from the skin. Increasing viral loads were detected over\n                        time in the skin of EBOV-infected non-human primates and mice, with antigen\n                        detected in dermal stromal and immune cells. Epidermal cells within and\n                        surrounding hair follicles also harbored viral antigen, suggesting a novel\n                        mechanism of virus egress to the epidermal surface. During late infection,\n                        proinflammatory responses were elevated in infected visceral organs but\n                        minimal in the skin despite significant viral loads. We observed similar\n                        viral trafficking and cell tropism in the skin of mice intraperitoneally\n                        infected with a low containment EBOV model virus, rVSV\/EBOV GP, allowing\n                        more detailed mechanistic studies. Sites of virus infection in the skin were\n                        patchy, with intense focal areas of infection surrounded by uninfected\n                        areas. To investigate virus entry into the body through skin, rVSV\/EBOV GP\n                        was applied to the surface of gently abraded skin to remove the stratum\n                        corneum; epidermal keratinocytes were robustly infected with subsequent\n                        systemic viral dissemination observed in some mice. Optimal levels of\n                        infection within the skin required expression of the phosphatidylserine\n                        receptor, AXL. Collectively, our data demonstrate that skin serves as an\n                        important organ targeted by EBOV, facilitating virus entry into and egress\n                        from the body.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        Ebola virus (EBOV) remains one of the World Health Organization\u2019s\n                            top 10 threats to global health, despite the availability of a U.S. Food\n                            and Drug Administration-approved vaccine. EBOV spreads through\n                            human-to-human contact, yet the role of skin in viral transmission\n                            remains unclear. Here, we identify skin as a site of EBOV infection,\n                            serving as a potential portal for entry into and egress from the body.\n                        <jats:italic toggle=\"yes\">In vivo<\/jats:italic>\n                        , infectious virions and viral RNA increased\n                            in the skin over time, localizing to dermal myeloid and stromal cells\n                            and to cells within and surrounding hair follicles, suggesting a novel\n                            mechanism for viral shedding. Skin infection was patchy and associated\n                            with minimal inflammation, despite significant viral loads. Using a\n                            surrogate EBOV model, we demonstrate that systemic infection can occur\n                            following topical administration through abraded skin and requires\n                            phosphatidylserine receptor, AXL, for optimal infection of skin. These\n                            findings redefine the role of skin in EBOV pathogenesis, with\n                            implications for barrier-targeted interventions.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/jvi.01300-25","type":"journal-article","created":{"date-parts":[[2025,9,12]],"date-time":"2025-09-12T13:01:22Z","timestamp":1757682082000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":5,"title":["Ebola virus\u2019 hidden target: virus transmission to and                    infection of skin"],"prefix":"10.1128","volume":"99","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9488-3101","authenticated-orcid":false,"given":"Paige T.","family":"Richards","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/036jqmy94","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, 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