Abstract:Host antiviral innate immunity is the first line of defense against viral infections. Studies have reported that almost all kinds of cells can induce type I interferon (IFN-I) and its downstream interferon-stimulated genes (ISG)， both of which exert a crucial effect in antiviral innate immunity. Latest researches found that cellular components， especially lipid metabolism， can facilitate almost all stages of the viral replication cycle， including initial interactions of the virion with the host cell， envelope fusion， assembly and budding. All the stages are not only the potential targets of the antiviral innate responses， but also effective approaches to prevent and treat viral infections. Thus， cell metabolism， especially lipid metabolism， must play a pivotal role in virus-induced innate immunity. Researches on roles of metabolism in antiviral innate responses would provide more effective therapeutics for prevention and treatment of viral infections. This review will focus on the role of metabolism in host antiviral innate immunity where the mitochondria， peroxisome， and several ISGs are involved.