Furthermore, compared with wild-type ASFV, infection of ASFVΔI267L increased RIG-I ubiquitination (Fig 6E), enhanced RIG-I-VISA interaction (Fig 6F), and induced higher levels of IRF3 phosphorylation (Fig 6G), suggesting that deletion of I267L attenuates the ability of ASFV to antagonize RIG-I-mediated signaling. The gene discussed is IRF3; the disease is infection.