Cytokine-Driven Hematologic Changes in Mpox: Linking Inflammation to Blood Dyscrasias

Mpox (previously referred to as monkeypox) has evolved from a rare zoonotic disease to a worldwide public health issue, with outbreaks exhibiting unusual manifestations and systemic effects. Aside from the typical skin-related symptoms, blood-related irregularities have arisen as important but overlooked aspects of the condition. Growing evidence indicates that these blood disorders—spanning anemia and changes in leukocytes to thrombocytopenia and coagulopathies—are significantly associated with imbalanced cytokine responses. Cytokines, although essential for antiviral immunity, can trigger harmful cascades that disrupt hematopoiesis, modify iron metabolism, and encourage the peripheral destruction of blood cells. The Mpox cytokine profile often shows increased levels of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), and interleukin-1 beta (IL-1β), which together promote inflammation while potentially interrupting hematologic balance. IL-6–driven excess hepcidin limits iron availability, playing a role in anemia linked to inflammation. TNF-α and IFN-γ inhibit bone marrow progenitors, whereas IL-1β and TNF-α hinder platelet production and stimulate endothelium, increasing the risk of thrombosis and coagulopathy in patients. These hematologic alterations might be associated with viral load, disease severity, and prognosis, making them possible diagnostic and prognostic indicators