However, when interferons are induced in the host cell following viral infection, ISGs (interferon stimulated genes) such as ISG15, a dimer homologue of ubiquitin, may be activated.57 ISG15 may then conjugate to CHMP5 and promote its accumulation in the membrane, effectively blocking the interaction of VTA with VPS4 and preventing viral budding.57 The novel interaction of CHMP5 with NUP98 may serve as the critical juncture at which the IFN-stimulated anti-viral mechanism interferes with viral budding. The gene discussed is IFNA1; the disease is viral infectious disease.