Xiang, Kuanhui Xiao, Yiwei Li, Yao He, Lingyuan Wang, Luwei Zhuang, Hui Li, Tong Table_1_The Effect of the Hepatitis B Virus Surface Protein Truncated sC69∗ Mutation on Viral Infectivity and the Host Innate Immune Response.docx <p>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<sup>∗</sup> in small hepatitis B surface protein (SHBs) that resulted in premature stop was investigated and the frequency of sC69<sup>∗</sup> 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<sup>∗</sup> mutant was associated with lower viral spread, but could be rescued by coexisting with the WT. The sC69<sup>∗</sup> 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<sup>∗</sup> mutant. Our data provide information that sC69<sup>∗</sup> coexisting with the WT might facilitate the fitness and persistence of the viral quasispecies in the host.</p> HBV;truncated mutant;sC69∗;viral infectivity;innate immune response 2019-06-13
    https://frontiersin.figshare.com/articles/dataset/Table_1_The_Effect_of_the_Hepatitis_B_Virus_Surface_Protein_Truncated_sC69_Mutation_on_Viral_Infectivity_and_the_Host_Innate_Immune_Response_docx/8267456
10.3389/fmicb.2019.01341.s002