Fig. 6

Illustrates the signaling pathways associated with the targeted actions of certain drugs following Mpox virus infection. Upon infection, Mpox inhibits pyroptosis, impeding the formation of inflammasomes and activation of caspase-1. This blockade prevents pyroptosis and hampers the adequate activation of the immune response against Mpox infection. However, nigericin, an activator of NLRP3 can induce pyroptosis in host cells, making it a promising candidate for an anti-Mpox drug. Moreover, tBID, a protein involved in apoptosis, is suppressed upon Mpox virus infection, thereby inhibiting both intrinsic and extrinsic apoptotic pathways and ensuring the survival of Mpox virus within host cells. This mechanism can be exploited by employing apoptosis inducers as a strategy to combat Mpox virus. Furthermore, Mpox virus infection triggers the binding of EGF and EGFR, activation downstream MAPK and MEK signaling pathways, leading to the release of inflammatory and chemotactic factors, and modulation of immune cells. That is, EGFR inhibitors like gefitinib may exhibit significant anti-Mpox activity