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The best-characterized mechanism employed by HCMV to suppress host immunity is the production of a viral interleukin-10 homolog (\n                      <jats:sub>CMV<\/jats:sub>\n                      IL-10). While\n                      <jats:sub>CMV<\/jats:sub>\n                      IL-10 is known to suppress immune responses and promote viral persistence, its capacity to promote increased susceptibility to co-infecting pathogens like\n                      <jats:italic toggle=\"yes\">Aspergillus fumigatus<\/jats:italic>\n                      remains unknown. Therefore, we studied the impact of wild-type (WT) HCMV (strain TB40), a\n                      <jats:sub>CMV<\/jats:sub>\n                      IL-10-deficient HCMV mutant (\u0394\n                      <jats:italic toggle=\"yes\">UL111A<\/jats:italic>\n                      ), and recombinant\n                      <jats:sub>CMV<\/jats:sub>\n                      IL-10 on the immune activity of monocyte-derived dendritic cells (moDCs) during co-infection with\n                      <jats:italic toggle=\"yes\">A. fumigatus<\/jats:italic>\n                      . Using a combination of transcriptomic and phenotypic readouts, our data revealed a strong and time-dependent immuno-paralytic effect of HCMV by suppressing pathogen recognition pathways, cytokine production, DC maturation, and expression of genes that are essential for host defense and tissue repair. Although infection with \u0394\n                      <jats:italic toggle=\"yes\">UL111A<\/jats:italic>\n                      lacking\n                      <jats:sub>CMV<\/jats:sub>\n                      IL-10 led to stronger expression of type I interferons, IFN-\u03b3-inducible chemokines, and proinflammatory cytokines than WT infection, interference with antifungal immune defense and fungal clearance during co-infection was largely similar between both strains. The limited effect of\n                      <jats:sub>CMV<\/jats:sub>\n                      IL-10 on antifungal immune defense persisted even after prolonged pre-exposure of DCs to the recombinant virokine. In summary, although\n                      <jats:sub>CMV<\/jats:sub>\n                      IL-10 contributes to shaping an anti-inflammatory environment, HCMV\u2019s suppression of antifungal immunity appears to be multifactorial, with\n                      <jats:sub>CMV<\/jats:sub>\n                      IL-10 alone playing a rather subtle role in altering DC responses to\n                      <jats:italic toggle=\"yes\">A. fumigatus<\/jats:italic>\n                      during viral-fungal co-infection.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        Human cytomegalovirus (HCMV) is a highly prevalent herpesvirus that establishes lifelong latency and frequently reactivates in immunocompromised individuals, including hematopoietic stem cell transplant recipients. Reactivation not only causes direct disease but also increases the risk of secondary infections, such as invasive pulmonary aspergillosis caused by\n                        <jats:italic toggle=\"yes\">Aspergillus fumigatus<\/jats:italic>\n                        . Specifically, studies estimated that about 6%\u201325% of critically ill HCMV-positive patients develop HCMV-associated pulmonary aspergillosis. However, the mechanisms by which HCMV creates a permissive environment for fungal superinfection remain poorly understood. HCMV encodes a viral homolog of interleukin-10 (\n                        <jats:sub>CMV<\/jats:sub>\n                        IL-10), which mimics host IL-10 and elicits potent immunomodulatory activity. Here, we show that\n                        <jats:sub>CMV<\/jats:sub>\n                        IL-10 dampens specific anti-viral responses, DC activation, and cytokine signaling. However, HCMV-mediated impairment of fungal control in co-infection settings occurred largely independent of\n                        <jats:sub>CMV<\/jats:sub>\n                        IL-10 expression. These findings suggest that HCMV undermines antifungal defenses through multifactorial mechanisms beyond\n                        <jats:sub>CMV<\/jats:sub>\n                        IL-10, highlighting the need for targeted strategies to restore immune function in high-risk patients.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.01541-25","type":"journal-article","created":{"date-parts":[[2025,9,22]],"date-time":"2025-09-22T12:00:32Z","timestamp":1758542432000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":4,"title":["Unveiling immune interference: how the dendritic cell response to co-infection with\n                    <i>Aspergillus fumigatus<\/i>\n                    is modulated by human cytomegalovirus and its virokine\n                    <sub>CMV<\/sub>\n                    IL-10"],"prefix":"10.1128","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0009-0004-2255-5178","authenticated-orcid":false,"given":"Linda","family":"Heilig","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/03pvr2g57","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Internal Medicine II, University Hospital Wuerzburg","place":["Wuerzburg, Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lydia","family":"Bussemer","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/03pvr2g57","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Internal Medicine II, University Hospital Wuerzburg","place":["Wuerzburg, Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lea","family":"Strobel","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/03pvr2g57","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Internal Medicine II, University Hospital 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