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Gammaherpesviruses reprogram long-term myelopoiesis through CD8⁺ T cell–monocyte dialogue within the bone marrow niche [bulk ATAC-Seq]

ABSTRACT: The immune system is continuously shaped by microorganisms, with viruses emerging as key drivers of immune variability. Gammaherpesviruses (γHVs), including Epstein–Barr virus, have coevolved with their hosts to establish lifelong infections, and may imprint durable innate immune memory. Using Murid herpesvirus 4 in wild-type mice and EBV in humanized models, we show that γHVs remodel monocytes and hematopoietic stem cells at phenotypic, transcriptomic, and epigenetic levels, resulting in altered responses to heterologous challenge. Viral persistence is required for immune priming, and IFN-γ signaling directly reprograms myelopoiesis. During latency, virus-specific resident CD8⁺ T cells accumulate in the bone marrow, and remain poised for rapid IFN-γ release. Upon low-dose LPS stimulation, monocyte-derived IL-27, IL-18, and IL-12 promote bystander IFN-γ secretion from these CD8+ T cells, amplifying myelopoietic rewiring. Thus, γHV latency establishes a cytokine circuit that shapes innate immune training and defines a new equilibrium between host and persistent viruses.

ORGANISM(S): Mus musculus

PROVIDER: GSE324548 | GEO | 2026/03/17

REPOSITORIES: GEO

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Gammaherpesviruses reprogram long-term myelopoiesis through CD8⁺ T cell–monocyte dialogue within the bone marrow niche [scMultiome]

Project description:The immune system is continuously shaped by microorganisms, with viruses emerging as key drivers of immune variability. Gammaherpesviruses (γHVs), including Epstein–Barr virus, have coevolved with their hosts to establish lifelong infections, and may imprint durable innate immune memory. Using Murid herpesvirus 4 in wild-type mice and EBV in humanized models, we show that γHVs remodel monocytes and hematopoietic stem cells at phenotypic, transcriptomic, and epigenetic levels, resulting in altered responses to heterologous challenge. Viral persistence is required for immune priming, and IFN-γ signaling directly reprograms myelopoiesis. During latency, virus-specific resident CD8⁺ T cells accumulate in the bone marrow, and remain poised for rapid IFN-γ release. Upon low-dose LPS stimulation, monocyte-derived IL-27, IL-18, and IL-12 promote bystander IFN-γ secretion from these CD8+ T cells, amplifying myelopoietic rewiring. Thus, γHV latency establishes a cytokine circuit that shapes innate immune training and defines a new equilibrium between host and persistent viruses.

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