Fig. 2

The potential immunopathogenesis of Mpox infection is depicted in this diagram, including humoral immunity, innate immunity, adaptive immunity, and immune evasion. (a) The expression of chemokines (CCR5, CXCR3, and CCR6) is inhibited by the Mpox virus, which depletes NK cell function and reduces IFN-γ and TNF-α secretion. (b) Abnormalities of granulocytes and monocytes, such as basophil, eosinophil, neutrophil, and monocyte, are induced by the Mpox virus. b) Mpox may stop natural killer cells from releasing inflammatory cytokines and eliminating virus-infected cells. Mpox may also impede T cell receptor trans-signaling, disrupting the adaptive immune response. (c) By inhibiting the antiviral type 1 IFN responses, Mpox avoids the innate immune response. By decreasing mRNA production and inhibiting type-I interferon, which mediates protein kinase R phosphorylation, Mpox may evade the protein kinase R pathway. By interfering with the phosphorylation of the MAPK/ERK1/2 pathways, Mpox may also lower the generation of inflammatory mediators. By making the ATK pathway more phosphorylated, it inhibits cell apoptosis. e) Patients with Mpox are likelier to have a worse prognosis because a monoclonal AB that neutralizes the virus may enhance viral entrance into cells via the Fc region of the AB attached to the Fc receptor (FcR) on cells. A substantial T helper 2 (Th2) immune response is linked to the cytokine storm that Mpox infection causes. This response is marked by increased serum levels of IL-4, IL-6, IL-5, IL-8, and IL-10, and a decrease in Th1-associated cytokines such (IFN-α, IFN-γ, TNF-α, IL-2, and IL-12). A greater total AB titer is seen, along with increased levels of IgG and IgM [55, 56]