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1.
Background:
Mutations in basal core promoter (BCP) and precore regions of hepatitis B virus (HBV) are associated with course and treatment outcomes of chronic HBV infection. While BCP and precore mutation analysis have been carried out in adult patients between different genotypes, this analysis has rarely been performed for chronically infected children.Objectives:
The aim of this study was to assess the mutation profiles of BCP and precore regions in different HBV genotypes in chronically infected children.Patients and Methods:
A cohort of 245 children and 92 adults with chronic HBV infection was included in this study. BCP and precore regions were analyzed by PCR amplification and sequenced.Results:
Ten nucleotide positions, including nt1679, nt1721, nt1753, nt1757, nt1758, nt1762, nt1764, nt1775, nt1856 and nt1858 in BCP/precore regions of HBV genome, showed obviously higher frequencies of mutation in genotype C subjects than in genotype B subjects among children, while there were only three positions, including nt1679, nt1758 and nt1775 showing higher mutation frequencies in genotype C subjects than in genotype B subjects in adults. Several combined mutations were obviously highly distributed in children with chronic HBV genotype C infection, such as G1721A/A1775G/T1858C triple mutation; a novel combined mutation type, exclusively detected in children with chronic HBV genotype C infection. In addition, G1721A/A1775G/T1858C combined mutation was associated with higher viral load and lower age distribution.Conclusions:
The mutation ratio difference between genotypes B and C in children was higher than that of adults and several combined mutations were exclusively detected in children with chronic HBV genotype C infection associated with higher viral load. 相似文献2.
Sima Besharat Hossein Poustchi Ashraf Mohamadkhani Aezam Katoonizadeh Abdolvahab Moradi Gholamreza Roshandel Neal David Freedman Reza Malekzadeh 《Hepatitis monthly》2015,15(2)
Background:
Although certain HBV mutations are known to affect the expression of Hepatitis e antigen, their association with HBV viral level or clinical outcomes is less clear.Objectives:
We evaluated associations between different mutations in the Basal Core promoter (BCP) and Pre-core (PC) regions of HBV genome and subsequent changes in HBV viral DNA level over seven years in a population of untreated HBeAg negative chronic hepatitis B (CHB) participants in Northeast of Iran.Materials and Methods:
Participants in the current study were drawn from the Golestan Hepatitis B Cohort Study (GHBCS), a cohort of approximately 2590 HBsAg positive subjects (living in Gonbad city) embedded in the Golestan Cohort Study (GCS). At baseline, HBsAg was measured in all participants and revealed 2590 HBsAg positive cases. We randomly selected 304 participants who their blood sample were taken at both baseline and seven years later in follow-up and had not been treated for HBV during this time. HBV viral load were assessed at baseline and at year 7. The BCP and PC regions of the HBV DNA, at baseline, were amplified via hemi-nested PCR and sequenced by cycle sequencing. At year 7, liver stiffness was assessed by fibroscan; also, other parameters of liver disease were assessed following standard clinical protocols. Associations were assessed via tabulation, chi-square, t-tests and logistic regression. P values < 0.05 were considered statistically significant and all tests were two-sided.Results:
Among 304 HBsAg positive participants, 99 had detectable HBV DNA at study baseline. Of these, 61.6% had PC mutations (48.5% A1896 and 25.2% G1899). In contrast to other mutations, A1896 was associated with a higher proportion of detectable HBV DNA at year 7 (39.6%) compared to patients with the wild type (13.7%) (OR: 4.36, CI95% = 1.63-11.70; P Value = 0.002). Although participants with the A1896 mutation had higher year-7 HBV viral load than participants with G1896 (2.30 ± 1.66 IU/mL vs. 1.76 ± 1 IU/mL among patients with detectable HBV; P value = 0.052), no association was observed with either serum level ALT or liver stiffness. Interestingly, mutations in the basal core promoter (BCP) region had no significant effect on virus DNA detection.Conclusions:
In this population with chronic HBeAg negative hepatitis B, an association was observed between the G1896A mutation in the Pre-core region of HBV and subsequent level of HBV DNA seven years later, which indicated that mutations in this region of HBV genome may contribute to disease progression in these patients and play an important role in HBV natural course of disease. 相似文献3.
Jeyanthi Suppiah Rozainanee Mohd Zain Norazlah Bahari Salbiah Haji Nawi Zainah Saat 《Hepatitis monthly》2015,15(10)
Background:
Precore stop codon (G1896A) mutation is one of the commonest mutations found in patients with chronic hepatitis B. However, over the years, this mutation was not reported much in Malaysia.Objectives:
We therefore investigated the presence of G1896A mutation in Malaysian population and its association with HBeAg status, clinical stage, hepatitis B virus (HBV) genotype and e-seroconversion rate.Patients and Methods:
Serum samples from 93 patients confirmed as hepatitis B carriers were collected for molecular assay. The whole genome of HBV was amplified by polymerase chain reaction and directly sequenced. The precore and basal core promoter regions were analyzed for presence of mutations.Results:
The most commonly observed mutation in the precore region was C1858T with 64.5% prevalence. The precore mutation of interest (G1896A) was identified in 25.8% of isolates. The basal core promoter mutations detected were A1762T-G1764A (26.9%), C1653T (8.6%), A1752G (10.8%) and C1766T (2.2%). No significant association was observed between G1896A mutation and HBeAg-negativity. Nonetheless, G1896A was highly prevalent among HBV genotype B. Clinical association revealed that subjects with G1896A mutations were mainly detected in asymptomatic chronic hepatitis B (58.3%) and liver cirrhosis (41.7%). One subject was diagnosed with fulminant hepatitis (4.2%) and 8.3% had hepatocellular carcinoma (HCC).Conclusions:
Our data suggested an intermediate prevalence of G1896A mutation among Malaysian hepatitis B carriers. The stop codon mutation has a significant association with genotype B and patients with chronic hepatitis B and liver cirrhosis. 相似文献4.
Aimin Zhang Zhihong Wan Shaoli You Hongling Liu Bing Zhu Jing Chen Yihui Rong Hong Zang Chen Li Huifen Wang Shaojie Xin 《Hepatitis monthly》2013,13(9)
Background
As most HBV-related acute-on-chronic liver failure (ACLF) have concurrent cirrhosis, it is important to clarify the association of viral factors with ACLF with or without cirrhosis.Objectives
The aim of this study was to analyze the association of HBV genotypes and mutations with ACLF development underlying different chronic liver diseases.Patients and Methods
Eighty-seven ACLF patients including 29 patients with chronic hepatitis (ACLF-CHB) and 58 patients with liver cirrhosis (ACLF-LC) were enrolled. Age and sex matched patients with chronic hepatitis (CHB) and liver cirrhosis (LC) were enrolled as controls. The genotypes and mutations at HBV basic core promoter (BCP), precore (PC), and partial C regions were determined by nested PCR and direct sequencing.Results
Our results revealed significantly higher incidences (P < 0.05) of genotype B with C1913A/G or A1846T in patients with ACLF-CHB than those with CHB; genotype C with C1913A/G or A1846T in patients with ACLF-CHB and ACLF-LC than those with CHB and LC, respectively. Multivariable analysis indicated that A1846T and C1913A/G mutations were independent factors for ACLF (OR = 2.86 and 5.93, respectively), suggesting an association between the mutations and development of ACLF. In addition, there were no significant differences in mutations at T1753V, A1762T, G1764A, G1896A, and G1899A which were found between either CHB and ACLF-CHB or LC and ACLF-LC patients， suggesting no associations of these mutations with ACLF development.Conclusions
Our findings suggest that CHB or LC patients infected with HBV A1846T and C1913A/G mutants are more susceptible to develop ACLF. 相似文献5.
Farah Bokharaei-Salim Hossein Keyvani Seyed Hamidreza Monavari Maryam Esghaei Shahin Fakhim Angila Ataei Pirkooh Bita Behnava 《Hepatitis monthly》2014,14(12)
Background:
Hepatitis B virus (HBV) has been classified into ten genotypes (A-J) based on genome sequence divergence, which is very important for etiological and clinical investigations. HBV genotypes have distinct geographical distributions worldwide.Objectives:
The aim of this study was to investigate the distribution of HBV genotypes among Azerbaijani patients with chronic hepatitis B, came from the Republic of Azerbaijan country to Iran to receive medical care.Patients and Methods:
One hundred and three patients with chronic HBV infection, referred to hospitals related to Iran University of Medical Sciences and Tehran Hepatitis Center from August 2011 to July 2014, were enrolled in this cross sectional study. About 3-milliliter of peripheral blood was taken from each patient. After viral DNA extraction, HBV genotypes were tested using the INNO-LiPA™ HBV kit (Innogenetics, Ghent, Belgium). HBV genotyping was confirmed using sequencing of hepatitis B surface antigen (HBsAg) and polymerase (pol) regions of HBV.Results:
The mean age of patients was 35.9 ± 11.7 years (19-66). Of 103 patients, 72 (69.9%) were male. In the present study, the predominant HBV genotype was D (93.2%) followed by genotype A (5.8%) and concurrent infection with A and D genotypes (0.97%).Conclusions:
The main and frequent HBV genotype among Azerbaijani patients with chronic hepatitis B virus infection was genotype D followed by genotype A. 相似文献6.
Background
Genotype G is the least common of all the hepatitis B virus (HBV) genotypes. The existence of the genotype G strain of HBV was first noted in 2000 and little information is available on its global geographical distribution. Previous studies have demonstrated the dominance of genotype D in patients with HBV infections in Turkey.Objectives
To report for the first time in Turkey, the case of a 61 year old male patient who developed the HBV genotype G infection.Case report
According to HBV genotyping using phylogenetic analysis and an INNO-LiPA assay, the patient was infected with genotype G and G+A, respectively.Conclusions
The present clinical study suggests that the transmission of an HBV genotype other than genotype D, namely HBV genotype G, is possible in Turkey. Epidemiological and clinical information on genotype G infection is currently limited, and this is most likely due to its low prevalence throughout the world. Therefore, it may be important to determine the epidemiologic and molecular characteristics of the HBV genotype G as it relates to chronic hepatitis, to enable better understanding of its circulation and progression around the world. 相似文献7.
Rim Ouneissa Olfa Bahri Ahlem Ben Yahia Henda Touzi Mohamed Msaddak Azouz Nabyl Ben Mami Henda Triki 《Hepatitis monthly》2013,13(10)
Background
Hepatitis B virus (HBV) infection is a public health problem in developing countries. HBV genotypes play major role in the evolution of infection since they were involved in different clinical presentations and response to treatment.Objectives
This study was conducted to evaluate the efficiency of restriction fragment length polymorphism (RFLP) analysis for HBV genotyping.Patients and Methods
We investigated 98 samples collected from patients chronically infected with HBV. HBV genotypes were determined by analysis of patterns obtained after amplification in Pre-S region and digestion of the amplicon by two endonucleases AvaII and DpnII. Obtained results were confirmed by partial sequencing in the same region.Results
Two different HBV genotypes were detected in this study, Genotype D (in 95. 9%) and Genotype A (in 4.1%). Seventy-four samples (75.5%) were successfully genotyped with RFLP analysis and all classified as genotype D. The remaining 24 samples (24.5%) which were un-genotyped by RFLP analysis, were classified by partial sequencing of the pre-S region as HBV genotype D (20 samples, 20.4%) and genotype A (4 samples, 4.1%). Atypical profiles were significantly associated with advanced liver disease (P = 0.001) as well as older age (P < 0.05).Conclusions
Several previous studies used PCR-RFLP to genotype HBV; however, we showed the high risk to obtain atypical profiles, especially in advanced stages of chronic infection, with as results difficulties to genotype the virus. These profiles resulted from the accumulation of mutations during natural course of infection resulting in a modification in restriction sites for enzymes. So, we recommended completing the investigation by partial sequencing to confirm obtained results. 相似文献8.
Meaghan O’Brien Adara Casselman Gerry Smart Ainsley Gretchen Kelly Kaita Kamran Kadkhoda 《Journal canadien de gastroenterologie》2015,29(8):e1-e6
BACKGROUND:
Hepatitis B virus (HBV) precore (PC) and basal core promoter (BCP) variants are well known; however, their prevalence in North America is unclear, especially among hepatitis B e antigen-negative patients.OBJECTIVE:
To investigate the prevalence of PC/BCP mutations and their clinical significance.METHODS:
One hundred twenty-eight patients positive for both hepatitis B surface antigen and hepatitis B e antibody were selected, and PC/BCP mutations were identified using a line probe assay. The subjects’ charts were reviewed for race/ethnicity, HBV genotype, HBV viral load, sex, liver enzyme levels, imaging and biopsy results up to 10 years before the study.RESULTS:
The prevalence of PC and BCP variants were 47.6% and 62.5%, respectively. Older age was associated with aspartate aminotransferase-to-platelet index ratio (APRI) ≥0.7 (P=0.011) and abnormal imaging/biopsy results (P=0.0008). Although the presence of BCP variant(s) was associated with APRI ≥0.7 (P=0.029), it was not associated with abnormal imaging/biopsy results. The combination of age ≥50 years and the presence of BCP variant(s) was associated with abnormal imaging/biopsy results, suggestive of either cirrhosis or hepatocellular carcinoma (not observed with PC mutation). Neither sex or genotype, or median HBV viral load showed significant influence on any of these outcomes.CONCLUSIONS:
The present study suggests that the prevalence of PC and BCP mutations are higher than what has been previously reported. One potential explanation would be increased immigration in the past decade. Considering the potential public health and clinical implications of these variants, long-term multicentre and prospective studies could further unravel the uncertainty around these variants. 相似文献9.
Guifeng Yang Meifang Han Feng Chen Ying Xu Enqiang Chen Xiaojing Wang Yu Liu Jian Sun Jinlin Hou Qin Ning Zhanhui Wang 《Hepatology International》2014,8(4):508-516
Background and aim
In China, acute-on-chronic liver failure (ACLF) is mostly caused by hepatitis B virus (HBV). However, the mechanism remains unclear. This study aims to investigate the association between both HBV genotype and mutations in basal core promoter (BCP) and pre-core/core (pre-C/C) regions with the development of HB-ACLF.Methods
A multicenter cross-sectional study was performed in China. Serum samples from 522 patients were analyzed, including 231 patients with mild-chronic hepatitis B (CHB-M), 84 with severe-chronic hepatitis B (CHB-S) and 207 with HB-ACLF. HBV genotype and related mutations in the BCP and pre-C/C regions were determined by direct sequencing.Results
A significantly higher ratio of HBV genotype B to C was detected in HB-ACLF patients than in CHB-M or CHB-S patients. The A1762T/G1764A, A1846T and G1896A mutations were significantly more common in HB-ACLF patients infected with either genotype B or C as compared with CHB-M, whereas the C1913A/G and A2159G mutations were more associated with HB-ACLF in genotype C patients. Comparing with CHB-S, the A1762T/G1764A mutation in genotype B and the A2159G mutation in genotype C were significantly more common in HB-ACLF patients. A multivariate analysis showed that factors such as HBV genotype B, age ≥40 years and A1762T/G1764A, A1846T and G1896A mutations were independently associated with the development of HB-ACLF.Conclusion
Chronic HBV infection with genotype B, A1762T/G1764A, A1846T and G1896A mutations has a higher possibility to develop HB-ACLF. These virological factors could serve as possible molecular markers for prediction of the clinical outcomes of chronic HBV infection. 相似文献10.
Background
The relationship between hepatitis B virus (HBV) mutations in basal core promoter (BCP) and precore (PC) regions and the risk of hepatitis B-related acute-on-chronic liver failure (HB-ACLF) remains uncertain.Methods
Databases were searched for papers that were published in English or Chinese until April 31, 2015. The odds ratios (ORs) of HBV mutation were pooled by using a fixed or random-effects model according to heterogeneity.Results
Data for 13 studies with a total of 1,149 HB-ACLF and 1,867 chronic hepatitis B (CHB) cases were retrieved. Statistically significant summary ORs for HB-ACLF were obtained for T1753V (1.99; 95 % confidence interval 1.30–3.02) and A1762T/G1764A (2.11; 95 %, 1.75–2.54) in the BCP region and for A1846T (3.33; 95 %, 2.23–4.97), G1896A (2.78; 95 %, 2.07–3.74), and G1899A (3.09; 95 %, 1.82–5.25) in the PC region. In subgroup analysis, BCP mutations were found to have higher ORs in age-matched studies, but PC mutations were found to have higher ORs in age-unmatched studies; patients with the mutations in HBV genotype C were more susceptible to HB-ACLF; patients with pre-existing liver cirrhosis had a higher risk of HB-ACLF occurrence. In sensitivity, specificity, and accuracy analysis, A1762T/G1764A had the highest sensitivity (67.43 %); A1762T/G1764A + G1896A triple mutations had the highest specificity (93.70 %); and T1753V + A1762T + G1764A mutation had the highest accuracy (65.42 %).Conclusions
HBV T1753V, A1762T/G1764A, A1846T, G1896A, and G1899A mutations are correlated with an increase in the risk of HB-ACLF. These mutations alone and in combination may be predictive of the susceptibility of patients with CHB to developing HB-ACLF.11.
Asadollah Mohammadi Nader Tajik Alireza Shah-Hosseini Seyed Moayed Alavian Zohreh Sharifi Lida Jarahi 《Hepatitis monthly》2015,15(10)
Background:
The FAS and FAS-Ligand (FASL) system is an important apoptosis pathway in the liver. The FAS-mediated pathway functions by binding the FASL on the activated cytotoxic T lymphocytes and Natural Killer (NK) cells to the FAS receptor on infected hepatocytes. FAS and FASL polymorphisms, which are related to apoptosis, might influence the outcome of Hepatitis B Virus (HBV) infection.Objectives:
Thus, the present study aimed to determine if FAS and FASL promoter polymorphisms are associated with the clinical outcome of HBV infection.Patients and Methods:
DNA samples were obtained from the infected individuals including chronic carrier (n = 50), chronic hepatitis (n = 50), cirrhosis (n = 25), naturally recovered (n = 26) and compared with those of their matched healthy controls (n = 100). Genotyping for polymorphisms of FAS-670 A/G and -1377 G/A, and FASL -844 C/T was performed using polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) assays.Results:
Multiple analyses for genetic association of FAS and FASL polymorphisms were not statistically different between HBV patients (n = 125) and healthy controls (n = 100). However, genotype and allele frequencies of FASL-844 C/T were significantly different between recovered individuals and patients with cirrhosis (P = 0.02 and P=0.01, respectively). Whereas, FAS-670A/G and -1377G/A polymorphisms were similarly distributed in these two groups (P = 0.8 and P = 0.47, respectively).Conclusions:
The current study results showed that bearing -844T allele in FASL promoter region has a protective effect on cirrhosis and is involved in recovery from infection. In conclusion, it is proposed that HBV infection outcome might be influenced by FASL-844C/T polymorphism through alteration in apoptosis of hepatocytes. 相似文献12.
Context:
The variation in clinical outcome of hepatitis B virus (HBV) infection is determined by virological, immunological and host genetic factors. Genes encoding cytokines are one of the candidates among host genetic factors. Polymorphisms in gene promoter can lead to different levels of cytokine expression and unique immune response. Being involved in the inflammatory cytokine network, interleukin-18 (IL-18) plays an important role in pathogenesis of HBV infection. The aim of this review is considering available literature on the association between IL-18 gene promoter single nucleotide polymorphisms (-137 C/G and -607 A/C) and susceptibility to chronic HBV infection.Evidence Acquisition:
Published literature from PubMed, EMBASE, and other databases were retrieved. All studies investigating the association of IL-18 gene promoter SNPs, -137 C/G and -607 A/C, with susceptibility to chronic HBV infection were included.Results:
Findings showed that the genotype -607A/A is associated with the susceptibility to chronic hepatitis B. Furthermore, allele C at position -137 is suggested to play a protective role against development of chronic HBV infection.Conclusions:
Host genetic factors play an important role in determining the outcome of HBV infection. It is suggested that IL-18 genotype -607 A/A is associated with susceptibility to chronic hepatitis B. Furthermore, the carriage of allele C at position -137 may play a protective role in the development of chronic HBV infection. 相似文献13.
Mumtaz K Hamid S Ahmed S Moatter T Mushtaq S Khan A Mizokami M Jafri W 《Hepatitis monthly》2011,11(1):14-18
Background
Hepatitis B virus (HBV) genotypes and mutations are gaining importance in determining the clinical course of chronic liver disease.Objectives
To determine and compare the distribution of HBV genotypes and genomic variations in Pakistan to other parts of the world.Patients and Methods
We conducted a prospective study at Aga Khan University Hospital from December 2006 to December 2008. HBV genotype was determined in 257 HBV DNA-positive patients. Patients were divided into two groups according to HBeAg positivity. Mutations in the pre-core and core promoter regions of HBV were determined in HBeAg-negative patients by line probe INNOLIPA assay.Results
The mean±SD age of patients was 28±5 years; there were 201 (78%) men. HBeAg was positive in 219 (85%) patients and negative in 38 (15%). HBeAg-positive patients were younger than HBeAg-negative patients (95% vs 21% in ≤30 years, p<0.001). HBV genotype D found in 247 (96.2 %) patients followed by a combined infection with HBV genotype B+D in 9 (3.3%) and 1 (0.5%) with genotype A. The mutations identified in 38 HBeAg-negative patients were T1762/A1764 in 21 (55.2%), PC mutant in 7 (18.4%), T1762/A1764/PC mutant in 2 (5%) and T1762/A1764/PC wild mutation in 1 (2%); no mutation identified in 7 (18.4%). Phylogenetic analysis did not show any significant differences between HBV genotype D isolated from Pakistan and those isolated from other parts of the world.Conclusions
HBV genotype D is predominant in Pakistan, irrespective of HBeAg status. PC and BCP mutations were found in significant numbers of patients infected with genotype D. The HBV genotype D isolates from Pakistan are identical to the sequences isolated from other parts of the world. 相似文献14.
Masoomeh Sofian Ebrahim Kalantar Arezoo Aghakhani Soudabeh Hosseini Mohammad Banifazl Ali Eslamifar Ali jourabchi Ali Asghar Farazi Amitis Ramezani 《Hepatitis monthly》2013,13(5)
Background
Single nucleotide polymorphisms (SNP) in the promoter region of the interleukin (IL)-10 genes have a role in determining hepatitis B virus (HBV) outcome.Objectives
This study evaluates the correlation between HBV infection and SNP in IL-10 gene promoter.Patients and Methods
Ninety-six HBV-infected patients (32 chronic hepatitis B infection patients, 34 healthy carriers, 30 spontaneously recovered cases) and 31 healthy controls were enrolled. Three biallelic (-819,-592,-1082) regions in the IL-10 gene promoter were sequenced for all patients.Results
Genotypes and haplotypes of IL-10 gene promoter region at position -1082, -819 and -592 were not significantly different among controls, HBV recovered cases, carriers and chronic HBV patients. Nevertheless, A/A genotype at position -592 and T/T genotype at position -819 were more frequently seen in the HBV clearance group, while frequency of G/G genotype at position -1082 was more prevalent in the persistence group. GCC/GCC and GCC/ACC haplotypes were significantly observed in anti-HBe positive individuals.Conclusions
Our findings showed that IL-10 promoter polymorphisms were not correlated with HBV infection prognosis. Nevertheless, individuals carrying high and intermediate producer of IL-10 haplotypes had a better ability to develop anti-HBe than low producer carriers. 相似文献15.
Jeyanthi Suppiah Rozainanee Mohd Zain Salbiah Haji Nawi Norazlah Bahari Zainah Saat 《Hepatitis monthly》2014,14(1)
Background:
Mutations in the polymerase (P) gene of hepatitis B virus are often associated with drug resistance. The pattern of mutations varies geographically, thus giving rise to genotypes diversity.Objectives:
This study was carried out to detect mutations in P gene of hepatitis B virus isolated from Malaysian HBV carriers.Materials and Methods:
A total of 58 sera samples were analyzed by PCR and sequencing, of which the P gene of isolated HBV was successfully amplified and sequenced from 40 samples.Results:
Genotyping of these samples revealed that the predominant genotype was genotype C (22/40, 55.0%), followed by genotype B (17/40, 42.5%), and only 1 sample showed genotype D (2.5%). A number of significant drug resistant mutations were found in five patients including S202I, N236T, M250L, L180M/V, M204I, A181T, T184G, M250V, and V173L. Of these, L180M/V and M204I were most frequently detected (80%) and associated with lamivudine in combination with emtricitabine and telbivudine drug resistance. Association with age, sex, and clinical symptoms revealed that these patients were all male, mid to elderly age and almost all hadcirrhotic liver disease.Conclusions:
Detection and surveillance of the significant sites of mutations in HBV is crucial for clinicians to decide on the choice of antiviral treatment and further management of hepatitis B carriers. 相似文献16.
X. Ren Z. Xu Y. Liu X. Li S. Bai N. Ding Y. Zhong L. Wang P. Mao F Zoulim D Xu 《Journal of viral hepatitis》2010,17(12):887-895
Summary. The study was undertaken to investigate the features and clinical implications of hepatitis B virus (HBV) genotypes, basal core promoter (BCP) and precore (PC) mutations in hepatitis B‐related acute‐on‐chronic liver failure (HB‐ACLF). Samples from 75 patients with HB‐ACLF and without pre‐existing liver cirrhosis and 328 age‐matched patients with chronic hepatitis B (CHB) were analyzed. HBV genotype and BCP/PC mutations were determined by direct sequencing. Mutations at 8 sites of the BCP/PC region were compared between the two groups of patients. A significantly higher ratio of genotype B to C was found in patients with HB‐ACLF than in patients with CHB (30.7–69.3%vs16.5–82.6%, P < 0.01). Single mutations including T1753V (C/A/G), A1762T, G1764A, G1896A and G1899A and triple mutations T1753V/A1762T/G1764A and A1762T/G1764A/C1766T (or T1768A) were more frequently detected in patients with HB‐ACLF than in patients with CHB. Correspondingly, BCP/PC wild‐type sequences were absent in patients with HB‐ACLF in contrast to 27.1% in patients with CHB. The BCP/PC mutations were found to be associated with increased HBeAg negativity, higher alanine aminotransferase level and lower viral load. Patients with HB‐ACLF infected with the PC mutant virus had a higher mortality. The findings suggest that patients with CHB infected with genotype B with BCP/PC mutations were more likely to develop HB‐ACLF than those with genotype C with wild‐type BCP/PC regions, and patients with HB‐ACLF with the PC mutation had increased risk of a fatal outcome. 相似文献
17.
Qin-Yan Chen Tim J Harrison Caroline A Sabin Guo-Jian Li Gao-Ming Huang Jin-Ye Yang Xue-Yan Wang Hai Li Mo-Han Liu Zhong-Liao Fang 《Hepatitis monthly》2014,14(2)
Background:
Association of hepatitis B virus (HBV) genotype C with hepatocellular carcinoma (HCC) development remains controversial. HBV basal core promoter (BCP) double mutations (T1762A1764) are very strong confounding factors of genotypes B and C in HCC development.Objectives:
To investigate the association of HBV genotype C with HCC development after controlling for BCP double mutations.Materials and methods:
Four hundred and two serum samples from patients with HCC, liver cirrhosis (LC) and chronic hepatitis (CH) and also from asymptomatic HBsAg carriers were analyzed.Results:
Genotypes B (31.1%), C (62.8%), and I (6.1%) were detected. With the severity of liver disease the prevalence of genotype B decreased, but genotype C increased. No trend was found for genotype I. The prevalence of BCP double mutations in genotypes C and I viruses was significantly higher than genotype B. BCP double mutations are risk factors for CH, LC and HCC. Genotype C was not identified as a particular risk factor for HCC prior to the stratification analysis but after that genotype C viruses with BCP double mutations were found to be a particular risk factor for HCC (P = 0.008, OR = 17.19 [95% CI: 2.10 - 140.41]), but those with the wild-type BCP were not. In the interaction analysis, genotype C and BCP double mutations were found to have a synergistic effect on HCC development (P < 0.0001, OR = 52.56 [95% CI: 11.49-240.52]).Conclusions:
The effect of HBV genotype C on the development of HCC differs between wild-type viruses and those with BCP double mutations, suggesting that not all individuals infected with genotype C HBV are at increased risk of HCC. 相似文献18.
Hiva Saffar Abolghasem Ajami Mohammed Jafar Saffar Jalil Shojaei Maryam Sotudeh-Anvari Kiarash Shams-Esfandabad Ali Reza Khalilian 《Hepatitis monthly》2014,14(5)
Background:
The epidemiological impact and the duration of protection provided by infant hepatitis B (HB) vaccination are unknown.Objectives:
This study was designed to determine the hepatitis B virus (HBV) infection seromarkers in young adults who have been vaccinated against HBV as the first group of Iranian neonates during 1993 and 1994.Patients and Methods:
We recruited 510 young adults with a history of complete HB vaccination at birth. HBV seromarkers (HB surface antigen (HBs Ag), antibody against HBs Ag (Anti-HBs), and antibody against HB core antigen (Anti-HBc) were measured using ELISA method. Anti-HBs titers ≥ 10 IU/L were considered protective and titers more than 300 IU/L were indicative of a natural boosting. Positive results for Anti-HBc and HBs Ag were considered as breakthrough infection and possible vaccine failure, respectively. The history of acute symptomatic clinical hepatitis was also investigated.Results:
Anti-HBs seropositivity rate was detected in 224 of 510 [95% CI: 39-47] young adults. Breakthrough infection (positive sera for Anti-HBc without chronic infection) was observed in 18 [95% CI: 2.5-3.5] subjects. There were neither HBs Ag positive results nor symptomatic hepatitis cases.Conclusions:
The study results indicated that the neonatal HBV immunization induced a long-term protection against HBV and was very efficacious in reducing chronic HBV infection rate in vaccinated young adults in Iran. 相似文献19.
Shiva Ghamari Seyed Moayed Alavian Mario Rizzetto Antonella Olivero Antonina Smedile Abulfazl Khedive Seyed Ehsan Alavian Mohammad Reza Zolfaghari Seyed Mohammad Jazayeri 《Hepatitis monthly》2013,13(8)
Background
Probably 5% of the HBV carriers have HDV super infection. The risk of fulminant hepatitis, cirrhosis and hepatocellular carcinoma is higher in superinfection than the settings when HBV is alone.Objectives
The aim of this study was to evaluate the prevalence of HDV in Iranian HBV isolates and to compare their clinical and virological pictures as well as their HDV genetic variations with other worldwide isolates.Patients and Methods
81 carriers with positive results for HBsAg with upper limit ranges of ALT and low or undetectable levels of HBV viral load who did not respond to HBV therapy were selected. After RT amplification of HDV Delta antigen, direct sequencing and phylogenetic study were performed to explore the genotype(s) and nucleotide/amino acid variations.Results
12 (14.8%) patients had positive results for both HDV RNA and anti-HDV. The mean ALT level was higher in HDV positive patients (75.9 U/ML) than HBV-mono-infected individuals; however, the mean HBV viral load was lower in coinfected patients than HBV-mono-infected patients. Phylogenetically, genotype I was the only detected genotype, and the most closely related isolates were of Turkish, Italian and Mongolian origin. Within the delta Ag, there were 326 nucleotide mutations, of which 111 and 215 were silent and missense, respectively. The total number of amino acid substitution was 148; most were located in known functional/epitopic domains. There was no correlation between the numbers of amino acid mutations, with clinical, virological status of the patients.Conclusions
HDV should be suspected in HBV carriers with unusual clinical and virological pictures. Relatedness of Iranian HDV isolates to Italian and Turkish sequences proposed a common Caucasian origin for the distribution of HDV genotype I in this ethnic group. 相似文献20.
Thomas Mina Samad Amini-Bavil-Olyaee Frank Tacke Piet Maes Marc Van Ranst Mahmoud Reza Pourkarim 《Hepatitis monthly》2015,15(6)