{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T21:31:16Z","timestamp":1789421476587,"version":"build-2803163510"},"reference-count":58,"publisher":"American Society for Microbiology","issue":"7","license":[{"start":{"date-parts":[[2025,7,29]],"date-time":"2025-07-29T00:00:00Z","timestamp":1753747200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,7,29]],"date-time":"2025-07-29T00:00:00Z","timestamp":1753747200000},"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":["R21AI166168"],"award-info":[{"award-number":["R21AI166168"]}],"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":["R01DE029471,R21AI178143"],"award-info":[{"award-number":["R01DE029471,R21AI178143"]}],"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":["K01CA285946"],"award-info":[{"award-number":["K01CA285946"]}],"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":["R25GM102795"],"award-info":[{"award-number":["R25GM102795"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100001368","name":"V Foundation for Cancer Research","doi-asserted-by":"publisher","award":["V2023-005"],"award-info":[{"award-number":["V2023-005"]}],"id":[{"id":"10.13039\/100001368","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100009238","name":"Virginia Commonwealth University","doi-asserted-by":"publisher","award":["Breakthrough Award"],"award-info":[{"award-number":["Breakthrough Award"]}],"id":[{"id":"10.13039\/100009238","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mSphere"],"published-print":{"date-parts":[[2025,7,29]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">Sneathia vaginalis<\/jats:italic>\n                      is a bacterial component of the vaginal microbiome that is of clinical interest because of its association with preterm birth and other obstetric complications. It produces a cytotoxin, but little is known about the mechanism through which it kills epithelial cells or the role that cytotoxicity plays in bacterial survival. Recent microbiome studies demonstrate an association between\n                      <jats:italic toggle=\"yes\">S. vaginalis<\/jats:italic>\n                      and human papillomavirus (HPV) within the female reproductive tract, suggesting that HPV and\n                      <jats:italic toggle=\"yes\">S. vaginalis<\/jats:italic>\n                      could interact in some way within this shared niche. We analyzed 16S rRNA survey and HPV typing data from our Vaginal Human Microbiome Project and found, in agreement with other reports, that\n                      <jats:italic toggle=\"yes\">S. vaginalis<\/jats:italic>\n                      was associated with HPV infection. To test the hypothesis that HPV promotes the growth of\n                      <jats:italic toggle=\"yes\">S. vaginalis<\/jats:italic>\n                      , growth and cytotoxicity of\n                      <jats:italic toggle=\"yes\">S. vaginalis<\/jats:italic>\n                      in co-culture with HPV16-positive and HPV-negative human cervical keratinocytes (HCK) were quantitatively assessed. Organotypic HCK rafts expressing HPV16 were more resistant to\n                      <jats:italic toggle=\"yes\">S. vaginalis<\/jats:italic>\n                      -induced damage, as assessed by histology, and supported increased bacterial growth relative to HPV-negative HCK rafts. When\n                      <jats:italic toggle=\"yes\">S. vaginalis<\/jats:italic>\n                      was co-cultured with HPV16-positive and HPV-negative HCK monolayers, cytotoxicity was observed in both HPV16-positive and HPV-negative cells, but HPV16-positive cells were more resistant to the toxic effects of the bacteria and supported bacterial growth for an extended period of time. In conclusion, HPV16 may protect cervical keratinocytes from the cytotoxic effects of\n                      <jats:italic toggle=\"yes\">S. vaginalis<\/jats:italic>\n                      , preventing the eradication of colonized cells and supporting bacterial growth, and this could underlie the association between\n                      <jats:italic toggle=\"yes\">S. vaginalis<\/jats:italic>\n                      and HPV\n                      <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                      .\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        <jats:italic toggle=\"yes\">Sneathia vaginalis<\/jats:italic>\n                        (\n                        <jats:italic toggle=\"yes\">S. vaginalis<\/jats:italic>\n                        ) is a bacterial species that lives in the human vagina and can cause complications during pregnancy if it invades the uterus. It is capable of killing cervical epithelial cells. Human papillomaviruses (HPV) are sexually transmitted viruses that can cause genital lesions and cervical cancer. Recently, multiple reports describe an association between\n                        <jats:italic toggle=\"yes\">S. vaginalis<\/jats:italic>\n                        and HPV. This study used cultured cervical epithelial cells expressing the high-risk HPV type, HPV16, and HPV-negative cells to determine whether HPV promotes the growth of\n                        <jats:italic toggle=\"yes\">S. vaginalis<\/jats:italic>\n                        . We found that HPV16 promotes the survival of cervical epithelial cells that are exposed to\n                        <jats:italic toggle=\"yes\">S. vaginalis<\/jats:italic>\n                        . Survival of cervical epithelial cells may benefit the growth of\n                        <jats:italic toggle=\"yes\">S. vaginalis<\/jats:italic>\n                        , which adhere to and feed off of these cells to survive in the female reproductive tract.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/msphere.00152-25","type":"journal-article","created":{"date-parts":[[2025,7,1]],"date-time":"2025-07-01T09:00:41Z","timestamp":1751360441000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":7,"title":["Human papillomavirus 16 mitigates\n                    <i>Sneathia vaginalis<\/i>\n                    -induced damage to cervical keratinocytes"],"prefix":"10.1128","volume":"10","author":[{"given":"Phoebe 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