@article {31227,
	title = {The Effect of the Hepatitis B Virus Surface Protein Truncated sC69*Mutation on Viral Infectivity and the Host Innate Immune Response},
	journal = {Front Microbiol },
	volume = {10},
	year = {2019},
	pages = {1341},
	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*\&nbsp;in small hepatitis B surface protein (SHBs) that resulted in premature stop was investigated and the frequency of sC69*\&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*\&nbsp;mutant was associated with lower viral spread, but could be rescued by coexisting with the WT. The sC69*\&nbsp;mutant showed to attenuate host innate immune response during infection and poly (I:C) treatment such as IL29, ISG15, and RIG-I (p\&nbsp;\&lt; 0.05). The lower immune response was not caused by the lower replication of sC69*\&nbsp;mutant. Our data provide information that sC69*\&nbsp;coexisting with the WT might facilitate the fitness and persistence of the viral quasispecies in the host.

Keywords:\&nbsp;HBV; innate immune response; sC69*; truncated mutant; viral infectivity.},
	url = {https://pubmed.ncbi.nlm.nih.gov/31249567/},
	author = {Kuanhui Xiang and Yiwei Xiao and Li, Yao and Lingyuan He and Luwei Wang and Hui Zhuang and Li, Tong}
}
