CpG和polyG比例的不平衡导致IFN-α表达受损。

StephenW

J Med Virol. 2019 Jan 31. doi: 10.1002/jmv.25419. [Epub ahead of print]
Imbalance in the ratio of CpG and polyG contributes to impaired IFN-α expression.
Lv S1, Li S2, Wang Z1, Xia J1.
Author information

1
    Department of Microbiology, School of Basic Medical Sciences, Anhui Medical University, Hefei, China.
2
    Blood Transfusion Institute, Anhui Blood Center, Hefei, China.

Abstract

The secretion of IFN-α is impaired during hepatitis B virus (HBV) infection. DNA sequences purified from distinct viruses, e.g., HBV versus members of Herpesviridae, have been shown to differ in their interferon alpha (IFN-α) signaling properties. The present study found that DNA from HBV inhibited, while DNA from members of Herpesviridae induced, the expression of IFN-α. Furthermore, stimulatory CpG sequences derived from these DNA viruses could induce the secretion of IFN-α, while inhibitory polyG oligonucleotide sequences derived from these DNA viruses could inhibit CpG-induced IFN-α secretion. Using a computational analysis of genomic DNA sequences, the discrimination between the genomes of HBV and those of other DNA viruses that can also cause inflammation of the liver is based on different frequencies of the CpG and polyG motifs. The underrepresentation of stimulatory CpG motifs and overrepresentation of inhibitory polyG motifs were documented in HBV genomes, whereas the DNA from other viral genomes displayed the opposite trend. Moreover, it was demonstrated that HBV could suppress the activation of IFN-α via its own DNA through the high proportion of polyG motifs. To our knowledge, this is the first demonstration of a specific role for polyG motifs in the inhibition of the IFN-α response following DNA virus infection. This article is protected by copyright. All rights reserved.

This article is protected by copyright. All rights reserved.
KEYWORDS:

CpG; Hepatitis B virus; Interferon-α; ODN; Toll-like receptor 9

PMID:
    30701565
DOI:
    10.1002/jmv.25419

StephenW

J Med Virol。 2019年1月31日。土井：10.1002 / jmv.25419。 [印刷前的电子版]
CpG和polyG比例的不平衡导致IFN-α表达受损。
Lv S1，李S2，王Z1，夏J1。
作者信息

1
    安徽医科大学基础医学院微生物学系，合肥
2
    安徽省血液中心输血研究所，合肥，中国。

抽象

在乙型肝炎病毒（HBV）感染期间，IFN-α的分泌受损。从不同病毒（例如HBV）与疱疹病毒科成员纯化的DNA序列已显示出其干扰素α（IFN-α）信号传导特性不同。本研究发现，来自HBV的DNA抑制了疱疹病毒科成员的DNA诱导IFN-α的表达。此外，源自这些DNA病毒的刺激性CpG序列可诱导IFN-α的分泌，而源自这些DNA病毒的抑制性polyG寡核苷酸序列可抑制CpG诱导的IFN-α分泌。使用基因组DNA序列的计算分析，HBV的基因组与也可引起肝脏炎症的其他DNA病毒的基因组之间的区别是基于CpG和polyG基序的不同频率。在HBV基因组中记录了刺激性CpG基序的代表性不足和抑制性polyG基序的过度表现，而来自其他病毒基因组的DNA显示出相反的趋势。此外，证明HBV可通过高比例的polyG基序通过其自身的DNA抑制IFN-α的活化。据我们所知，这是polyG基序在DNA病毒感染后抑制IFN-α反应的特定作用的首次证明。本文受版权保护。版权所有。

本文受版权保护。版权所有。
关键词：

CpG的;乙型肝炎病毒;干扰素α; ODN; Toll样受体9

结论：
    30701565
DOI：
    10.1002 / jmv.25419