The genotoxic effects of hepatitis B virus to host DNA

Ozkal, P.; Ilgin-Ruhi, Hatice; Akdoğan, Meral; Elhan, Atilla Halil; Kaçar, Sabite; Şaşmaz, Nurgül

doi:10.1093/mutage/gei021

Cited by 15 publications

(9 citation statements)

References 21 publications

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“…In the present study, we demonstrated that the lymphocytes of HBV-infected patients and HCV-infected patients exhibited an increased frequency of MN compared with lymphocytes from healthy, non-infected individuals. This result is in contrast to findings previously reported by Ozkal et al (2005) . However, these authors reported a higher frequency of chromosome breaks, leading to the formation of acentric chromosome/chromatid fragments that ultimately contributed to the formation of MN.…”

Section: Discussioncontrasting

confidence: 99%

Increased frequency of micronuclei in the lymphocytes of patients chronically infected with hepatitis B or hepatitis C virus

Leite

Silva

Pepato

et al. 2014

Mem. Inst. Oswaldo Cruz

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In this study, we analysed the frequency of micronuclei (MN), nucleoplasmic bridges (NPBs) and nuclear buds (NBUDs) and evaluated mutagen-induced sensitivity in the lymphocytes of patients chronically infected with hepatitis B virus (HBV) or hepatitis C virus (HCV). In total, 49 patients with chronic viral hepatitis (28 HBV-infected and 21 HCV-infected patients) and 33 healthy, non-infected blood donor controls were investigated. The frequencies (‰) of MN, NPBs and NBUDs in the controls were 4.41 ± 2.15, 1.15 ± 0.97 and 2.98 ± 1.31, respectively. The frequencies of MN and NPBs were significantly increased (p < 0.0001) in the patient group (7.01 ± 3.23 and 2.76 ± 2.08, respectively) compared with the control group. When considered separately, the HBV-infected patients (7.18 ± 3.57) and HCV-infected patients (3.27 ± 2.40) each had greater numbers of MN than did the controls (p < 0.0001). The HCV-infected patients displayed high numbers of NPBs (2.09 ± 1.33) and NBUDs (4.38 ± 3.28), but only the HBV-infected patients exhibited a significant difference (NPBs = 3.27 ± 2.40, p < 0.0001 and NBUDs = 4.71 ± 2.79, p = 0.03) in comparison with the controls. Similar results were obtained for males, but not for females, when all patients or the HBV-infected group was compared with the controls. The lymphocytes of the infected patients did not exhibit sensitivity to mutagen in comparison with the lymphocytes of the controls (p = 0.06). These results showed that the lymphocytes of patients who were chronically infected with HBV or HCV presented greater chromosomal instability.

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Section: Discussioncontrasting

confidence: 99%

Increased frequency of micronuclei in the lymphocytes of patients chronically infected with hepatitis B or hepatitis C virus

Leite

Silva

Pepato

et al. 2014

Mem. Inst. Oswaldo Cruz

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“…The presence of ALS in the genome appears to be a structural feature of chromatin. The induction of chromatin changes is an emerging topic in the study of viral tumorigenesis in humans, not only in relation to high-risk HPV types 20 but also to hepatitis B virus, 21 Kaposi's sarcoma herpesvirus, 22 and human T-cell leukemia virus type 1 (HTLV-1). 23 …”

Section: Results and Dicussionmentioning

confidence: 99%

Koilocytes are enriched for alkaline-labile sites

et al. 2010

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This study investigated possible variations in the chromatin structure of koilocytes resulting from human papillomavirus (HPV) infection. Alkaline-labile sites (ALS) were detected with the DNA breakage detection–fluorescence in situ hybridization (DBD-FISH) technique using a whole human genome DNA probe obtained from individuals without koilocytosis. The variable levels of ALS present were measured quantitatively using image analysis after whole-genome DNA hybridization. A significant increase in the number of ALS was observed in koilocytes compared with normal cells. We demonstrated that the presence of ALS could be an indicator of chromatin change in koilocytes caused by HPV infection.

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“…There is increasing evidence that HBV infection can cause genetic changes within somatic cells, including hepatocytes and blood cells, as demonstrated by increased chromosomal breakage, sister chromatid exchange and decreased mitotic index (22,23). The HBV genome can integrate into the host genome; these non-specific integrations exist within different regions, leading to chromosomal instability (23).…”

Section: Discussionmentioning

confidence: 99%

Role of p53 codon 72 polymorphism in chromosomal aberrations and mitotic index in patients with chronic hepatitis B

Akbas

Yalçın

Isi

et al. 2012

Braz J Med Biol Res

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Polymorphisms of the p53 gene, which participates in DNA repair, can affect the functioning of the p53 protein. The Arg and Pro variants in p53 codon 72 were shown to have different regulation properties of p53-dependent DNA repair target genes that can affect various levels of cytogenetic aberrations in chronic hepatitis B patients. The present study aimed to examine the frequency of chromosomal aberrations and the mitotic index in patients with chronic hepatitis B and their possible association with p53 gene exon 4 codon 72 Arg72Pro (Ex4+119 G>C; rs1042522) polymorphism. Fifty-eight patients with chronic hepatitis B and 30 healthy individuals were genotyped in terms of the p53 gene codon 72 Arg72Pro polymorphism by PCR-RFLP. A 72-h cell culture was performed on the same individuals and evaluated in terms of chromosomal aberrations and mitotic index. A high frequency of chromosomal aberrations and low mitotic index were detected in the patient group compared to the control group. A higher frequency of chromosomal aberrations was detected in both the patient and the control groups with a homozygous proline genotype (13 patients, 3 control subjects) compared to patients and controls with other genotypes [Arg/Pro (38 patients, 20 control subjects) and Arg/Arg (7 patients, 7 control subjects)]. We observed an increased frequency of cytogenetic aberrations in patients with chronic hepatitis B. In addition, a higher frequency of cytogenetic aberrations was observed in p53 variants having the homozygous proline genotype compared to variants having other genotypes both in patients and healthy individuals.

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The genotoxic effects of hepatitis B virus to host DNA

Cited by 15 publications

References 21 publications

Increased frequency of micronuclei in the lymphocytes of patients chronically infected with hepatitis B or hepatitis C virus

Increased frequency of micronuclei in the lymphocytes of patients chronically infected with hepatitis B or hepatitis C virus

Koilocytes are enriched for alkaline-labile sites

Role of p53 codon 72 polymorphism in chromosomal aberrations and mitotic index in patients with chronic hepatitis B

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