Abstract
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.
Highlights
Despite the availability of an effective vaccine and the improvement of antiviral treatment, chronic hepatitis B virus (HBV) infection remains a severe public health problem
Among 435 chronic hepatitis B (CHB) patients, we identified 19 samples carrying HBV sC69∗ mutant by analyzing entire small hepatitis B surface protein (SHBs) amino acid (AA)
In order to know the distribution of sC69∗ mutant in different patient groups, we stratified patients by hepatitis B e antigen (HBeAg) status and LMV exposure and analyzed the SHBs sequences
Summary
Despite the availability of an effective vaccine and the improvement of antiviral treatment, chronic HBV infection remains a severe public health problem. Hepatitis B surface antigen (HBsAg) is a major viral protein of hepatitis B virus (HBV) circulating in patient serum and serves as an important virological marker for the evaluation of chronic HBV infection and antiviral response. We found that 4.37% (19/435) of the studied patients with genotype C HBV chronic infection carried the small hepatitis B surface (SHBs) sC69∗ mutant resulting in the truncated SHBs [about 1/3 length of wild-type (WT) SHBs]. This mutant usually existed in older people with lower HBV DNA levels. These results indicate that HBV sC69∗ coexisting with WT might facilitate the viral fitness and surviving from the host surveillance
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