Cellular DNA repair cofactors affecting hepatitis B virus infection and replication

Zhao, Fan; Hou, Ning-Bo; Song, Ting; He, Xiang; Zheng, Zhu-Jun; Ma, Qingjun; Li, Li; Zhang, Yanhong; Zhong, Hui

doi:10.3748/wjg.14.5059

Cited by 25 publications

(25 citation statements)

References 28 publications

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“…Therefore, it will be interesting to evaluate, whether efficient repair system in crustaceans can protect these organisms from infections. Previous studies indicate that, DNA repair proteins may suppress viral infections, in higher organisms 49 . Studies suggest that DNA repair proteins may inhibit and can have an effect on retrotransposons and viral infections in yeast and mammals 50 – 52 .…”

Section: Discussionmentioning

confidence: 99%

DNA double-strand break repair inPenaeus monodonis predominantly dependent on homologous recombination

Srivastava

Dahal

Naidu

et al. 2017

DNA Res

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DNA double-strand breaks (DSBs) are mostly repaired by nonhomologous end joining (NHEJ) and homologous recombination (HR) in higher eukaryotes. In contrast, HR-mediated DSB repair is the major double-strand break repair pathway in lower order organisms such as bacteria and yeast. Penaeus monodon, commonly known as black tiger shrimp, is one of the economically important crustaceans facing large-scale mortality due to exposure to infectious diseases. The animals can also get exposed to chemical mutagens under the culture conditions as well as in wild. Although DSB repair mechanisms have been described in mammals and some invertebrates, its mechanism is unknown in the shrimp species. In the present study, we show that HR-mediated DSB repair is the predominant mode of repair in P. monodon. Robust repair was observed at a temperature of 30 °C, when 2 µg of cell-free extract derived from hepatopancreas was used for the study. Although HR occurred through both reciprocal recombination and gene conversion, the latter was predominant when the bacterial colonies containing recombinants were evaluated. Unlike mammals, NHEJ-mediated DSB repair was undetectable in P. monodon. However, we could detect evidence for an alternative mode of NHEJ that uses microhomology, termed as microhomology-mediated end joining (MMEJ). Interestingly, unlike HR, MMEJ was predominant at lower temperatures. Therefore, the results suggest that, while HR is major DSB repair pathway in shrimp, MMEJ also plays a role in ensuring the continuity and stability of the genome.

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Section: Discussionmentioning

confidence: 99%

DNA double-strand break repair inPenaeus monodonis predominantly dependent on homologous recombination

Srivastava

Dahal

Naidu

et al. 2017

DNA Res

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“…DNA repair protein in higher organisms suppresses the viral infection instead of leading to establishment is partially observed. It has been demonstrated that DNA repair molecules inhibit and down‐regulate hepatitis B virus replication in mammals (Zhao et al. 2008).…”

Section: Discussionmentioning

confidence: 99%

Deciphering the DNA repair protein, Rad23 from kuruma shrimp Marsupenaeus japonicus: full-length cDNA cloning and characterization

Sudhakaran

Okugawa

Mekata

et al. 2011

Letters in Applied Microbiology

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Aims: Lesions of DNA are removed by nucleotide excision repair (NER) process in the living systems. NER process‐related host factors are believed to aid recovery steps during viral integration. Here, we report identification and characterization of a DNA repair molecule Rad23 from kuruma shrimp Marsupenaeus japonicus. Methods and Results: The full‐length cDNA of M. japonicus Rad23 gene (MjRad23) has 1149 bp coding for a putative protein of 382 amino acids with a 5′ untranslated region (UTR) of 92 bp and 3′ UTR region of 1116 bp. Quantitative expression analysis revealed MjRad23 is constitutively expressed in all the organs of healthy shrimp, whereas with high level in muscle tissue. Although MjRad23 expression is observed in every haemolymph samplings to post‐white spot syndrome virus infection, high expression is recorded at 2 h post infection (h.p.i.). MjRad23 consists of putative functional domains including one ubiquitin domain (UBQ), two ubiquitin‐associated domains (UBA) and one heat‐shock chaperonin‐binding motif (STI1). Multiple alignment of MjRad23 with Rad23 of other species showed highly significant identity ranging from 37 to 53%; however, high homology is observed with Rad23 of Bombyx mori (BmRad23). UBQ domain region alignment revealed maximum of 66% homology with Rad23 of Apis melifera (AmRad23). MjRad23 clustered with invertebrate sector along with insect species in evolution analysis. Three‐dimensional structural analyses demonstrated the highest identity between MjRad23 and human Rad23A (hHR23A). Conclusions: The present work revealed the presence of MjRad23 gene, which is essential in DNA repair process. Further studies are required to clarify the involvement of MjRad23 in NER process. Significance and Impact of the Study: This is the first report on identification and characterization of DNA repair protein in crustaceans, which will lead to further investigation to explore the molecular mechanisms behind the NER process.

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“…Mechanically, p53 can directly suppress HBV replication by binding and repressing the HBV enhancer 45 . Recently, Ying Yan et al 42 proposed a new mechanism that p53 controls HBV infection; they found that p53 can inhibit the entry of HBV into hepatocytes by binding to sodium taurocholate cotransporting polypeptide (NTCP) promoter region (which is the key receptor to recognize HBV hepatocytes) and thereby inhibiting NTCP synthesis.…”

Section: Hbv-induced Hepatoma Cell Transformationmentioning

confidence: 99%

The role of MDM2–p53 axis dysfunction in the hepatocellular carcinoma transformation

et al. 2020

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Liver cancer is the second most frequent cause of cancer-related death globally. The main histological subtype is hepatocellular carcinoma (HCC), which is derived from hepatocytes. According to the epidemiologic studies, the most important risk factors of HCC are chronic viral infections (HBV, HCV, and HIV) and metabolic disease (metabolic syndrome). Interestingly, these carcinogenic factors that contributed to HCC are associated with MDM2-p53 axis dysfunction, which presented with inactivation of p53 and overactivation of MDM2 (a transcriptional target and negative regulator of p53). Mechanically, the homeostasis of MDM2-p53 feedback loop plays an important role in controlling the initiation and progression of HCC, which has been found to be dysregulated in HCC tissues. To maintain long-term survival in hepatocytes, hepatitis viruses have lots of ways to destroy the defense strategies of hepatocytes by inducing TP53 mutation and silencing, promoting MDM2 overexpression, accelerating p53 degradation, and stabilizing MDM2. As a result, genetic instability, chronic ER stress, oxidative stress, energy metabolism switch, and abnormalities in antitumor genes can be induced, all of which might promote hepatocytes' transformation into hepatoma cells. In addition, abnormal proliferative hepatocytes and precancerous cells cannot be killed, because of hepatitis viruses-mediated exhaustion of Kupffer cells and hepatic stellate cells (HSCs) and CD4 + T cells by disrupting their MDM2-p53 axis. Moreover, inefficiency of hepatic immune response can be further aggravated when hepatitis viruses co-infected with HIV. Unlike with chronic viral infections, MDM2-p53 axis might play a dual role in glucolipid metabolism of hepatocytes, which presented with enhancing glucolipid catabolism, but promoting hepatocyte injury at the early and late stages of glucolipid metabolism disorder. Oxidative stress, fatty degeneration, and abnormal cell growth can be detected in hepatocytes that were suffering from glucolipid metabolism disorder, and all of which could contribute to HCC initiation. In this review, we focus on the current studies of the MDM2-p53 axis in HCC, and specifically discuss the impact of MDM2-p53 axis dysfunction by viral infection and metabolic disease in the transformation of normal hepatocytes into hepatoma cells. We also discuss the therapeutic avenues and potential targets that are being developed to normalize the MDM2-p53 axis in HCC.

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Cellular DNA repair cofactors affecting hepatitis B virus infection and replication

Cited by 25 publications

References 28 publications

DNA double-strand break repair inPenaeus monodonis predominantly dependent on homologous recombination

DNA double-strand break repair inPenaeus monodonis predominantly dependent on homologous recombination

Deciphering the DNA repair protein, Rad23 from kuruma shrimp Marsupenaeus japonicus: full-length cDNA cloning and characterization

The role of MDM2–p53 axis dysfunction in the hepatocellular carcinoma transformation

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