Occult HBV infection among Egyptian hepatocellular carcinoma patients (original) (raw)
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Hepatitis B virus genotype in Iranian patients with hepatocellular carcinoma
International Journal of Infectious Diseases, 2009
Objective: Chronic hepatitis B virus (HBV) infection is a major risk factor for the development of hepatocellular carcinoma (HCC). HBV appears to be the most common cause of HCC in Iran. To date, no study has been carried out on the HBV genotype in Iranian HCC patients. This study was undertaken to determine the HBV genotype in Iranian patients with HCC. Methods: Paraffin-embedded tissue samples from 40 patients (31 males and nine females) with HBV-associated HCC were collected from different pathology centers during 2000-2007. Genotyping of HBV was performed by nested PCR-mediated amplification of the target sequence. PCR products were sequenced, and the genotype of each HBV sequence was determined by comparison with sequences of known genotypes in the GenBank. A phylogenetic tree was constructed. Results: Phylogenetic analysis revealed that all of the HBV isolates were clustered in genotype D. Conclusions: Our results concur with other reports from Iran, all showing that genotype D is the only detectable genotype in the different clinical forms of HBV infection in this country. #
Carcinogenesis, 2008
The role of genotype mixture and subgenotypes remains controversial in determining the clinical outcome of chronic hepatitis B virus (HBV) infection. We aimed to determine their role on the development and the recurrence of hepatocellular carcinoma (HCC). HBV genotypes, serum viral load and hepatitis B e antigen (HBeAg) seroconversion were determined in 462 HCC patients, 234 chronic hepatitis patients and 425 asymptomatic carriers born in Eastern China. In the 462 HCC patients, 62 (13.4%), 337 (72.9%) and 49 (10.6%) had HBV subgenotype B2, C2 and genotype mixture, respectively. Genotype mixture in HCC patients and hepatitis patients was associated with higher viral load than HBV C2 (P 5 0.012, P 5 0.000) and more frequent than asymptomatic carriers (P 5 0.005, P 5 0.000). HBV C2 was more prevalent in HCC patients compared with controls. Proportion of HBV B2 in HCC patients decreased consecutively from <30 to 50-59 years group (P 5 0.024). Age-related changes of HBeAg seroconversion were not consistent with serum viral load in HCC patients with HBV B2 and genotype mixture, quite in contrast to hepatitis patients. By multivariate regression analysis, age ‡40 years and serum viral load (‡10 000 copies/ml) were independently associated with hepatocarcinogenesis, whereas age £50 years and HBV B2 were independently associated with HCC recurrence after surgical resection. In conclusion, HBV coinfections with two or three genotypes were associated with higher viral load and more severe course of the disease. HBV B2 infection was related to HCC recurrence. HBV C2 predominance in HCC patients was related to the high prevalence in Eastern China.
Journal of Clinical Microbiology, 2009
We aimed to investigate the impact of hepatitis B virus (HBV) DNA on the development of hepatocellular carcinoma (HCC). We conducted a case/control study based on 506 chronic HBV patients followed up since 1997. Forty-one patients developed HCC, and each of them was age and gender matched with two simultaneously recruited controls without HCC. HBV DNA was measured at the initial visit, at yearly intervals, and at the last visit. Patient age at the time of HCC development was 55 ؎ 9 years. Forty-nine (40%) patients experienced antiviral treatment. The median time from diagnosis to the development of HCC was 17 months, and the control patients were followed for 92 months. At the trough level (defined as lowest level among all studied visits), more (27 patients; 66%) HCC patients had HBV DNA levels of >10,000 copies/ml than the controls (17 patients; 21%). The area under the receiver operating characteristic curve of the trough log HBV DNA level for HCC was 0.79 (95% confidence interval [CI], 0.69 to 0.89). Trough log HBV DNA (odds ratio, 11.4; 95% CI, 3.6 to 37.6; P < 0.0001) and liver cirrhosis (odds ratio, 11.4; 95% CI, 3.6 to 36.2; P < 0.0001) levels were independently associated with HCC after an adjustment for age, gender, antiviral treatment, and HBV genotype. The difference in the trough HBV DNA level was more obvious among untreated patients (5.7 ؎ 1.4 log copies/ml in HCC patients versus 3.2 ؎ 1.3 log copies/ml in control patients; P < 0.0001) than among those who had received antiviral treatment (3.0 ؎ 1.4 log copies/ml in HCC patients versus 2.5 ؎ 0.9 log copies/ml in control patients; P ؍ 0.38). A high trough HBV DNA level was associated with a higher risk of HCC. Whether antiviral treatment could prevent HCC was uncertain.
2000
Background: Although chronic infection with hepatitis B virus (HBV) has been established as a cause of hepatocellular carcinoma (HCC), the roles of viral load and HBV genotype remain unclear. Methods: From 1988 through 1992, baseline blood samples were collected from 4841 Taiwanese men who were HBV carriers but had not been diagnosed with HCC. We used real-time polymerase chain reaction assays of plasma DNA samples to quantify HBV DNA levels (a measure of viral load) and determine HBV genotypes for 154 case patients who were diagnosed with HCC during 14 years of follow-up and 316 control subjects. Unconditional logistic regression was used to assess odds ratios (ORs) of HCC for HBV-related factors. All statistical tests were two-sided. Results: The risk of HCC increased with increasing HBV viral load (adjusted OR for the highest versus the lowest quintile of HBV DNA copies/mL = 7.26, 95% confi dence interval [CI] = 3.54 to 14.89; P trend <.001). Genotype C HBV was associated with an increased risk of HCC compared with other HBV genotypes (adjusted OR = 5.11, 95% CI = 3.20 to 8.18). Both viral load and genotype were positively associated with HCC within 10-year age categories among subjects aged 30 years old to older than 60 years. Genotype C HBV was associated with increased viral load, and associations of HBV genotype and viral load with HCC risk were additive. The adjusted OR of HCC for those carrying genotype C HBV and with viral load in the highest quintile was 26.49 (95% CI = 10.41 to 67.42) compared with HBV carriers with other HBV genotypes and viral load in the lowest two quintiles. Conclusions: Measurements of HBV viral load and genotype may help to defi ne which male HBV carriers aged 30 years or older are at high risk for HCC. [J Natl Cancer Inst 2005;97:265-72]
Current Science, 2016
The present study was designed to analyse the whole genome and mutational profile of hepatitis B virus (HBV) isolates in hepatocellular carcinoma (HCC) and asymptomatic carriers from three regions of India. Seventy-five HBV-related HCC and 15 HBV-related asymptomatic carriers were included in the study. HBV DNA was amplified by six sets of walking primers. Amplicons were sequenced commercially, submitted to GenBank translated into amino acid and aligned using BioEdit v7.0.9. Mutations membering 60, 15, 23 and 1 were observed in PC/C, X, P and S genes respectively. Mutations like 10I L were significantly associated with HCC cases from North East India (NEI) [(P = 0.01; OR = 5.63) versus South India (SI)] and [(P < 0.01; OR=16.63) versus North India (NI)]. Mutations like 41S T (P < 0.001; OR = 19.01), 92V G (P < 0.001; OR = 19.01), 96N T (P < 0.001; OR = 19.01) and 164Q P (P = 0.0279; OR = 3.085) were significantly associated with HCC cases from NI [vs SI]. Widely reported 28 W stop mutation was found in a few HCC cases. Also, 132 stop [(P = 0.004486; OR = 5.479 versus SI) and [(P = 0.004486; OR = 5.479) versus NEI] was interesting. 267I N and 268D T were exclusive to HCC from NEI, while 270S F was exclusive to HCC from NI. Reported drug mutants (80L I, 236N T, 169I T and 181A V) were observed. The PC/C region was most prone to mutation followed by P, X and S regions. Maximum variation in HBV genome was observed in HCC cases from NI and least in asymptomatic HBV carriers. Novel mutations in surface (132 stop), polymerase (frameshift mutation at 178), core (10I L, 41S T, 92V G, 96N T and 164Q P) and X (33P S) genes need further studies.
A weak association between occult HBV infection and non-B non-C hepatocellular carcinoma in Japan
Background. In Japan, approximately 10% of hepatocellular carcinoma (HCC) patients are negative for both hepatitis B surface antigen (HBsAg) and antibodies to hepatitis C virus (anti-HCV), i.e., they constitute the so-called category of non-B non-C (NBNC) HCC. Little is known about the characteristics of NBNC-HCC. Methods. Potential risk factors for carcinogenesis (including occult HBV infection [HBsAg is negative but HBV DNA is positive by polymerase chain reaction (PCR)], obesity, and diabetes) were assessed in 233 HCC patients grouped according to hepatitis virus serological status (152 with HCV-HCC, 36 with HBV-HCC, and 45 with NBNC-HCC). Results. The prevalence of patients with obesity or diabetes was signifi cantly higher in the NBNC-HCC group than in the HBV-HCC group. The same trend was observed even when patients with massive alcohol intake were excluded from the analysis. Only 8 patients (18%) in the NBNC-HCC group had detectable serum HBV DNA, and this was at very low levels (HBV/Ce/C2 and HBV/D were determined in 7 and 1 patients, respectively). In the NBNC-HCC group, the determined nucleotide sequences of the enhancer II/core promoter/precore/core region did not contain any HCC-associated mutations, whereas 25 of 30 patients in the HBV-HCC group carried strains with C1653T, T1753V, and/or A1762T/ G1764A mutations. Conclusions. A weak association between occult HBV infection and HCC development was observed in the NBNC patients. This study indicates that nonalcoholic steato-hepatitis should be further investigated to assess its contribution to HCC development in this category of patients.
Association of Hepatocellular Carcinoma with Hepatitis B Virus Genotypes in Sana'a city – Yemen
2020
Hepatitis B remains a potentially Life-threatening infection in the liver caused by extremely infectious blood-born known as the Hepatitis B virus (HBV). HBV increases the risk of developing hepatocellular carcinoma (HCC). The virus can be divided into various HBV genotypes and sub-genotypes due to HBV's high genetic diversity. In order to properly control HBV infection by medical staff and improve public health, an understanding of the distribution of HBV genotype has been of great importance. First our cross-sectional analysis was performed using a multiplex PCR technique to determine the association of HBV genotypes with HCC in Yemeni patients. Secondly, to determine the potential risk factors, including patient information, clinical data, and their association with HBV infection among these HCC patients in Sana'a city, Yemen. Eighty HCC patients clinically diagnosed with HCC were included in this study. They attended the National Oncology Center in Sana'a city during...
Phylogenetic analysis of HBV based on PreS region in Iranian hepatocellular carcinoma patients
Hep Mon, 2007
Results: Phylogenetic analysis based on PreS region sequences disclosed that all isolated strains belonged to genotype D. Analysis of sequences revealed that all the sequences contained amino acid substitutions. In the PreS2 region of two samples, a point mutation in the start codon was found. There were some deletions with 3, 6 and 8 amino acids in PreS2 region of three samples. Conclusions: Despite the low number of samples, these data revealed that the HBV genotype D is dominant in Iranian HCC patients. Most of the mutations are located at immunodominant epitopes involved in B or/and T cell recognition.
Hepatitis monthly, 2011
Chronic infection with hepatitis B virus (HBV) is the major risk factor for hepatocellular carcinoma (HCC) worldwide. Ten HBV genotypes (A-J) have been discovered so far. Genotypes B and C are endemic in East and Southeast Asia. Genotype C HBV is associated with increased risks of cirrhosis and HCC. Genotype B (B2) is associated with the development of HCC in non-cirrhotic patients younger than 50 years and with relapse of HCC after surgical treatment. It is also associated with earlier hepatitis B e antigen seroconversion than genotype C. High HBV load is independently associated with the occurrence and post-treatment recurrence of HCC. Different genotypes have distinct patterns of mutations. Viral mutations in the core promoter region and in the preS region are frequently found to be significantly associated with an increased risk of HCC. These mutations often occur before the onset of HCC and accumulate during the progression of chronic HBV infection. Multiple such mutations are ...