期刊
VIROLOGY
卷 539, 期 -, 页码 92-103出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2019.10.009
关键词
HBV; HBx; Genotype; PRR signaling; Interferon
类别
资金
- National Natural Science Foundation of China [81772189, 91542207]
- National Science and Technology Major Project of China [2017ZX10202202, 2018ZX10301208]
- Shanghai Municipal Health Commission [20174Y0180]
- Shanghai Municipal Education Commission [2017-01-07-00-07-E00057]
- Chinese Academy of Medical Sciences [2018PT31044, 2019-I2M-5-040]
Hepatitis B virus (HBV) X protein (HBx) has been reported to counteract the innate immune responses through interfering with the pattern recognition receptors signaling activated by retinoic acid-inducible gene-I (RIG-I)-mitochondrial antiviral signaling protein (MAVS). Here, we showed that, compared to the HBx derived from genotype (gt) A, C and D, HBx of gtB exhibited more potent inhibitory activity on the RIG-I-MAVS-mediated interferon-beta promoter activation. Functional analysis of the genotype-associated differences in amino acid sequence and the reciprocal mutation experiments in transient-transfection and infection cell models revealed that HBx with asparagine (N) and glutamic acid (E) at 118-119 positions inhibited RIG-I signaling and interacted with MAVS more efficiently than that with lysine (K) and aspartic acid (D). An impaired RIG-I-induced MAVS aggregation was observed in the presence of HBx-118N119E while MAVS-TRAF3 interaction was not affected. These results implicated that HBx gene heterogeneity may affect the innate immune responses to HBV infection.
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