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Viruses could rapidly diversify into variants, which has long been known to facilitate viral adaption in the host. Recent studies showed that cooperation among variants and wild-type (WT) also increased viral fitness. Here, a mutant of sC69 ∗  in small hepatitis B surface protein (SHBs) that resulted in premature stop was investigated and the frequency of sC69 ∗  was 4.37% (19/435), most of which coexisted with the WT (78.95%, 15/19), indicating mixed viral populations. Functional studies showed that sC69 ∗  mutant was associated with lower viral spread, but could be rescued by coexisting with the WT. The sC69 ∗  mutant showed to attenuate host innate immune response during infection and poly (I:C) treatment such as IL29, ISG15, and RIG-I ( p  < 0.05). The lower immune response was not caused by the lower replication of sC69 ∗  mutant. Our data provide information that sC69 ∗  coexisting with the WT might facilitate the fitness and persistence of the viral quasispecies in the host.

The Effect of the Hepatitis B Virus Surface Protein Truncated sC69∗ Mutation on Viral Infectivity and the Host Innate Immune Response