Hepatitis B virus evades immune recognition via RNA adenosine deaminase ADAR1-mediated viral RNA editing in hepatocytes

Wang, Liyuan; Sun, Yang; Song, Xiaojia; Wang, Zehua; Zhang, Yankun; Zhao, Ying; Peng, Xueqi; Zhang, Xiaodong; Li, Chunyang; Gao, Chengjiang; N, Li; Gao, Lifen; Liang, Xiaohong; Wu, Zhuanchang; Ma, Chao

doi:10.1038/s41423-021-00729-1

Cited by 31 publications

(35 citation statements)

References 53 publications

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“…Among them, 4205 genes had one RDD, followed by 1794, 1068 and 588 genes with 2, 3 and 4 RDDs, and 1020 genes with more than 5 RDDs, respectively. Overall, 15,623,11,216,12,809 RDDs corresponding to 6618, 4959 and 5331 genes were found in crown, leaves and root respectively, of which 6645 RDDs in 3151 genes were commonly found in all of the three tissues (Figure 1C). For RNA/DNA difference type, all of the 12 conversion types were found, of which the conversion between C and T accounted for 24.19% of all sites, and conversion between A and G accounted for 24.31% respectively, which were the two canonical RNA/DNA difference types [31].…”

Section: Identification Of Rna/dna Differences Based On Rna-seq Data ...mentioning

confidence: 99%

“…Together with alternative splicing, RDD provides a crucial way to enrich genetic information and diversify transcripts, playing an important role in regulating growth, development and stress response in eukaryotes [12]. 'Substitution' by simple base modification is the most common type of RDD, and is widely identified in plant organelle and higher eukaryotic nuclei genomes [13,14] as well as some viral sequences [15]. In mammals, the common type of RDD is A-to-I (G) (adenosine to inosine, guanosine), which is mainly catalyzed by double-stranded RNAspecific ADAR family proteins [16].…”

Section: Introductionmentioning

confidence: 99%

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Genome-Wide Identification and Characterization of RNA/DNA Differences Associated with Drought Response in Wheat

Pan

Huang

et al. 2022

IJMS

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RNA/DNA difference (RDD) is a post-transcriptional RNA modification to enrich genetic information, widely involved in regulating diverse biological processes in eukaryotes. RDDs in the wheat nuclear genome, especially those associated with drought response or tolerance, were not well studied up to now. In this study, we investigated the RDDs related to drought response based on the RNA-seq data of drought-stressed and control samples in wheat. In total, 21,782 unique RDDs were identified, of which 265 were found to be drought-induced, representing the first drought-responsive RDD landscape in the wheat nuclear genome. The drought-responsive RDDs were located in 69 genes, of which 35 were differentially expressed under drought stress. Furthermore, the effects of RNA/DNA differences were investigated, showing that they could result in changes of RNA secondary structure, miRNA-target binding as well as protein conserved domains in the RDD-containing genes. In particular, the A to C mutation in TraesCS2A02G053100 (orthology to OsRLCK) led to the loss of tae-miR9657b-5p targeting, indicating that RNA/DNA difference might mediate miRNA to regulate the drought-response process. This study reported the first drought-responsive RDDs in the wheat nuclear genome. It sheds light on the roles of RDD in drought tolerance, and may also contribute to wheat genetic improvement based on epi-transcriptome methods.

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Section: Identification Of Rna/dna Differences Based On Rna-seq Data ...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Genome-Wide Identification and Characterization of RNA/DNA Differences Associated with Drought Response in Wheat

Pan

Huang

et al. 2022

IJMS

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“…HBx can suppress the transcription of TRIM22 through a single CpG methylation in its 5’-UTR, reducing the binding affinity of IRF-1 and inhibiting IFN-mediated anti-HBV response [ 94 ]. Recently, a key mechanism of innate immune evasion by HBx in hepatocytes has been reported, where HBx-induced adenosine deaminases acting on RNA 1 (ADAR1) deaminates adenosine to generate inosine by interacting with HBV RNAs and avoiding host immune recognition [ 19 ]. Immune evasion by attenuating RIG-I signaling via N 6 methyladenosine (m 6 A) modification of HBV RNAs has been reported previously [ 95 ].…”

Section: Inhibition Of Innate Immune Response By Hbv Infectionmentioning

confidence: 99%

“…For example, the lack of innate immune response, including induction of interferons (IFNs) and IFN-stimulated genes (ISGs), in acute HBV-infected chimpanzees [ 14 ] the woodchuck model of HBV infection [ 15 ] and patients with HBV infection [ 16 ] highlights HBV as a stealth virus. A recent study demonstrated that HBV remains invisible to pattern recognition receptors (PRRs) [ 17 ], which could be due to the ability of HBV proteins to inhibit or evade the host innate immune system [ 18 , 19 , 20 , 21 , 22 ]. Notably, in our previous study, we observed a significant suppression of interferon regulatory factor 7 (IRF-7) and ISG15, as well as no increase in IFN-β production at 1- or 3-days post-infection in the tree shrew model [ 23 ], which was suggestive of the inhibition of innate immune response at early stage of infection in this model.…”

Section: Introductionmentioning

confidence: 99%

Toll-Like Receptor Response to Hepatitis B Virus Infection and Potential of TLR Agonists as Immunomodulators for Treating Chronic Hepatitis B: An Overview

Kayesh

Kohara

Tsukiyama-Kohara

2021

IJMS

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Chronic hepatitis B virus (HBV) infection remains a major global health problem. The immunopathology of the disease, especially the interplay between HBV and host innate immunity, is poorly understood. Moreover, inconsistent literature on HBV and host innate immunity has led to controversies. However, recently, there has been an increase in the number of studies that have highlighted the link between innate immune responses, including Toll-like receptors (TLRs), and chronic HBV infection. TLRs are the key sensing molecules that detect pathogen-associated molecular patterns and regulate the induction of pro- and anti-inflammatory cytokines, thereby shaping the adaptive immunity. The suppression of TLR response has been reported in patients with chronic hepatitis B (CHB), as well as in other models, including tree shrews, suggesting an association of TLR response in HBV chronicity. Additionally, TLR agonists have been reported to improve the host innate immune response against HBV infection, highlighting the potential of these agonists as immunomodulators for enhancing CHB treatment. In this study, we discuss the current understanding of host innate immune responses during HBV infection, particularly focusing on the TLR response and TLR agonists as immunomodulators.

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“…Alzheimer's disease [61,62] Lewy body dementia [62] Frontotemporal dementia [ Yersinia pestis infection [63] Table 1 The corresponding diseases caused by the similar signaling of autoinflammatory diseases (Continued) SLE and other autoimmune diseases [75,76] Cervical cancer via human papilloma virus [77] SAMHD1 dNTPase activity against viral RNA/DNA Epstein-Barr virus infection [78] Human immunodeficiency virus infection [79] ADAR1 Viral RNA processing Hepatitis B virus infection [80] Marburg and Ebola virus [81] MDA5/IFIH1 PRR for viral RNA detection Paramyxovirus infection [82] Picornavirus infection [83] SAVI STING/TMEM173 PRR for viral DNA/RNA detection Infections and aberrant inflammatory responses:…”

Section: Nlrp12 Autoinflammatory Syndromementioning

confidence: 99%

Molecular biology of autoinflammatory diseases

et al. 2021

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The long battle between humans and various physical, chemical, and biological insults that cause cell injury (e.g., products of tissue damage, metabolites, and/or infections) have led to the evolution of various adaptive responses. These responses are triggered by recognition of damage-associated molecular patterns (DAMPs) and/or pathogen-associated molecular patterns (PAMPs), usually by cells of the innate immune system. DAMPs and PAMPs are recognized by pattern recognition receptors (PRRs) expressed by innate immune cells; this recognition triggers inflammation. Autoinflammatory diseases are strongly associated with dysregulation of PRR interactomes, which include inflammasomes, NF-κB-activating signalosomes, type I interferon-inducing signalosomes, and immuno-proteasome; disruptions of regulation of these interactomes leads to inflammasomopathies, relopathies, interferonopathies, and proteasome-associated autoinflammatory syndromes, respectively. In this review, we discuss the currently accepted molecular mechanisms underlying several autoinflammatory diseases.

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Hepatitis B virus evades immune recognition via RNA adenosine deaminase ADAR1-mediated viral RNA editing in hepatocytes

Cited by 31 publications

References 53 publications

Genome-Wide Identification and Characterization of RNA/DNA Differences Associated with Drought Response in Wheat

Genome-Wide Identification and Characterization of RNA/DNA Differences Associated with Drought Response in Wheat

Toll-Like Receptor Response to Hepatitis B Virus Infection and Potential of TLR Agonists as Immunomodulators for Treating Chronic Hepatitis B: An Overview

Molecular biology of autoinflammatory diseases

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