Initial infection experiments using a knockin mouse model (in which the human ACE2 gene is under the endogenous mouse ACE2 promoter on a B6 background) in combination with pretreatment with an anti-IFNAR antibody to increase susceptibility, showed detectable virus in the oropharynx but no clinical effect after intranasal (i.n.)or i.v. inoculation of lab-cultivated B1.1.7 virus at doses up to 1.1 × 104 PFU (data not shown). The gene discussed is IFNAR1; the disease is infection.