<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Kuanhui Xiang</style></author><author><style face="normal" font="default" size="100%">Yiwei Xiao</style></author><author><style face="normal" font="default" size="100%">Li, Yao</style></author><author><style face="normal" font="default" size="100%">Lingyuan He</style></author><author><style face="normal" font="default" size="100%">Luwei Wang</style></author><author><style face="normal" font="default" size="100%">Hui Zhuang</style></author><author><style face="normal" font="default" size="100%">Li, Tong</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">The Effect of the Hepatitis B Virus Surface Protein Truncated sC69∗Mutation on Viral Infectivity and the Host Innate Immune Response</style></title><secondary-title><style face="normal" font="default" size="100%">Front Microbiol </style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2019</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">https://pubmed.ncbi.nlm.nih.gov/31249567/</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">10</style></volume><pages><style face="normal" font="default" size="100%">1341</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">
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∗&amp;nbsp;in small hepatitis B surface protein (SHBs) that resulted in premature stop was investigated and the frequency of sC69∗&amp;nbsp;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∗&amp;nbsp;mutant was associated with lower viral spread, but could be rescued by coexisting with the WT. The sC69∗&amp;nbsp;mutant showed to attenuate host innate immune response during infection and poly (I:C) treatment such as IL29, ISG15, and RIG-I (&lt;em&gt;p&lt;/em&gt;&amp;nbsp;&amp;lt; 0.05). The lower immune response was not caused by the lower replication of sC69∗&amp;nbsp;mutant. Our data provide information that sC69∗&amp;nbsp;coexisting with the WT might facilitate the fitness and persistence of the viral quasispecies in the host.

&lt;strong class=&quot;sub-title&quot;&gt;Keywords:&amp;nbsp;&lt;/strong&gt;HBV; innate immune response; sC69∗; truncated mutant; viral infectivity.</style></abstract></record></records></xml>