Abstract: Influenza, also known as the flu, is an acute respiratory infectious disease causedby the influenza virus. It has a high incidence rate and can lead to patient mortality. To create a suitable environment for replication and proliferation, the influenza virus engages in complex interactions with the host, including the regulation of host cell gene expression and various signaling pathways by the virus. The type I interferon signaling pathway, as the first line of defense against viral infections, is an important component of the host’s antiviral innate immunity. Meanwhile, type Ⅱ and type Ⅲ interferon systems also influence viral replication through different mechanisms. Literature reports that influenza virus can induce degradation of related cellular proteins to evade the host’s antiviral immune response. This article focuses on the regulation of the interferon system by influenza virus, discussing the molecular mechanisms and biological significance of how the virus promotes ubiquitination and degradation of proteins related to typeⅠ , Ⅱ , and Ⅲ interferon pathways. Understanding how influenza virus antagonizes interferon-mediated antiviral responses is conducive to the development of new anti-influenza therapies by targeting host factors.

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