%0 Generic %A Xiang, Kuanhui %A Xiao, Yiwei %A Li, Yao %A He, Lingyuan %A Wang, Luwei %A Zhuang, Hui %A Li, Tong %D 2019 %T Table_1_The Effect of the Hepatitis B Virus Surface Protein Truncated sC69∗ Mutation on Viral Infectivity and the Host Innate Immune Response.docx %U 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 %R 10.3389/fmicb.2019.01341.s002 %2 https://frontiersin.figshare.com/ndownloader/files/15458534 %K HBV %K truncated mutant %K sC69∗ %K viral infectivity %K innate immune response %X
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.
%I Frontiers