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ERVEBO is a replication-competent recombinant vesicular stomatitis virus-vectored vaccine encoding the EBOV glycoprotein (recombinant vesicular stomatitis virus [rVSV]\/EBOV), which is licensed to control EVD outbreaks. EVD outbreaks occur in regions endemic for\n                      <jats:italic toggle=\"yes\">Plasmodium<\/jats:italic>\n                      -caused malaria.\n                      <jats:italic toggle=\"yes\">Plasmodium<\/jats:italic>\n                      infections persist due in part to the parasite\u2019s ability to evade sterilizing immunity, which also dampens immune responses to heterologous vaccines. Acute murine\n                      <jats:italic toggle=\"yes\">Plasmodium<\/jats:italic>\n                      infection at the time of rVSV\/EBOV vaccination reduced vaccine-mediated protection against mouse-adapted EBOV (ma-EBOV) challenge. Decreased protection was associated with a\n                      <jats:italic toggle=\"yes\">Plasmodium-<\/jats:italic>\n                      induced interferon gamma-mediated decrease of rVSV\/EBOV replication in lymph node macrophages, resulting in reduced primary anti-EBOV glycoprotein antibody responses. Higher doses of rVSV\/EBOV partially overcame the antibody deficits and elicited protective responses. Evidence of the negative impact of\n                      <jats:italic toggle=\"yes\">Plasmodium<\/jats:italic>\n                      on the efficacy of low-dose rVSV\/EBOV vaccine protocols supports the use of high antigen loads in the effective management of EVD outbreaks.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>IMPORTANCE<\/jats:title>\n                    <jats:p>\n                      We show that a blood-stage murine\n                      <jats:italic toggle=\"yes\">Plasmodium<\/jats:italic>\n                      infection negatively impacts the primary antibody response elicited by low-dose recombinant vesicular stomatitis virus (rVSV)\/Ebola virus (EBOV) vaccination and results in reduced protection against a lethal dose of mouse-adapted EBOV. This defect occurs within the draining lymph node due to the elevation of interferon gamma elicited in\n                      <jats:italic toggle=\"yes\">Plasmodium yoelii<\/jats:italic>\n                      (\n                      <jats:italic toggle=\"yes\">Py)<\/jats:italic>\n                      -infected mice. The\n                      <jats:italic toggle=\"yes\">Py<\/jats:italic>\n                      -imposed decrease in vaccine-mediated protection can be overcome with higher doses of rVSV\/EBOV. While the strong protection conferred by rVSV\/EBOV and significant side effects known to be associated with this vaccine have led to the suggestion that the vaccine dosage be reduced, our studies provide a rationale for maintaining the current higher dose.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.02796-25","type":"journal-article","created":{"date-parts":[[2025,12,30]],"date-time":"2025-12-30T14:54:17Z","timestamp":1767106457000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":1,"title":["Acute malaria dysregulates specialized lymph node macrophages to suppress vaccine-elicited protection against the Ebola 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