Japanese case of hepatitis B virus genotypes C/D hybrid

Hepatitis B virus (HBV) is classified into eight genotypes based on complete genome sequence. Each genotype is related to geographic distribution and race. In Japan, most of the genotypes are B and C. In the present study, we report the first Japanese strain of HBV having a recombination between genotypes C and D. A 30-year-old woman was admitted to Kobe Medical Center because of liver dysfunction. She was diagnosed with spontaneous reactivation of chronic hepatitis B. She had no history of blood transfusion and her parents were negative for HBV. The phylogenetic analysis based on the complete genome sequences revealed that this strain was classified into genotype C, whereas the analysis based on Sgene sequence showed that this strain was genotype D. By using a SimPlot program, this strain was confirmed as a recombinant strain between genotypes C and D. Compared with previous recombinant strains in China, the breakpoint was the same and the difference was only 0.8% of the complete genome sequence. It was unclear whether or not this strain was transmitted from China, but the recombinant strains and intergenotypes of HBV have already existed in Japan.     

Virological and clinical implication of core promoter C1752/V1753 and T1764/G1766 mutations in hepatitis B virus genotype D infection in Mongolia

Background and Aim: The aim of the present study was to reveal virological and clinical features of hepatitis B virus (HBV) genotype D infection. Methods: One hundred and twenty‐two Mongolian chronic liver disease (CLD) patients infected with HBV were subjected for serological HBV‐markers screening and HBV‐enzyme immunoassay (EIA) genotyping. Nucleotide sequences were analyzed for 48 HBV/D strains (23 isolated from hepatocellular carcinoma (HCC) and 25 from CLD patients). Results: Prevalence of hepatitis B e antigen (HBeAg) positivity was low (25.9%) in young patients (≤30 years old) indicating early HBeAg seroclearance in HBV/D carriers. The T1764/G1766 double mutation was the most common basal core promoter (BCP) mutation (29.2%) and was frequent in HBeAg‐negative patients (39.3%). Patients harboring T1764/G1766 mutants exhibited lower HBV‐DNA and HBV core antigen (HBcAg) levels than those with wild‐type BCP strains (P = 0.024, 0.049, respectively). C1752 and/or V (not T) 1753 mutation was significantly prevalent in HCC patients (HCC vs CLD; 52.2% vs 20%, P = 0.033). T1762/A1764 mutation was detected in 75.0% of HCC patients with high viral load (≥5 log copies/mL). Precore stop codon mutation A1896 was detected in (70.8%) of HBV/D‐infected patients. Conclusions: In Mongolians infected with HBV/D, C1752 and/or V1753 mutation was associated with HCC.     

北京和非北京基因型结核分枝杆菌生长曲线及mazEF系统的研究

目的 研究北京与非北京基因型结核分枝杆菌的生长曲线、mazEF3,6,9系统表达有无差异方法 测绘上述菌株及其mazEF3,6,9基因缺失和过表达菌株在标准、低氧和营养饥饿培养条件下的生长曲线。使用qRT-PCR技术检测各菌株的mazEF3, 6, 9、mazF3, 6,9和mazE3, 6,9基因mRNA表达水平;利用Western Blot技术检测MazF9 蛋白表达水平结果 在标准和低氧条件下培养的第4、6、8、10 d,营养饥饿条件下培养的第2、4、6、8 d,北京基因型菌株的OD值(细菌数量)均高于非北京基因型菌株,差异有统计学意义(P<0.05);在上述3种培养条件下,北京和非北京基因型mazEF3,6,9缺失突变株和过表达株菌数均低于其亲本株。在mRNA、蛋白水平上,与非北京基因型菌株相比,北京基因型菌株mazEF3高表达9.55倍、mazF3高表达4.86倍、mazF6高表达2.64倍、mazF9高表达5.27倍和mazE9低表达0.16倍;mazF9蛋白高表达1.62倍,差异均具有统计学意义(P<0.05)结论 北京与非北京基因型结核分枝杆菌的生长曲线、mazEF3,6,9系统表达存在差异,mazEF系统与北京基因型菌株流行相关。     

The value of molecular stratification for CEBPADM and NPM1MUTFLT3WT genotypes in older patients with acute myeloid leukaemia

Older adult patients (≥60 years) with acute myeloid leukaemia (AML) are generally considered to be poor‐risk and there is limited information available regarding risk stratification based on molecular characterization in this age group, particularly for the double‐mutant CEBPA (CEBPA^DM) genotype. To investigate whether a molecular favourable‐risk genotype can be identified, we investigated CEBPA, NPM1 and FLT3 status and prognostic impact in a cohort of 301 patients aged 60 years or more with intermediate‐risk cytogenetics, all treated intensively. Overall survival (OS) at 1 year was highest in the 12 patients (4%) that were CEBPA^DM compared to the 76 (28%) with a mutant NPM1 and wild‐type FLT3 (NPM1^MUTFLT3^WT) genotype or all other patients (75%, 54%, 33% respectively), with median survival 15·2, 13·6 and 6·6 months, although the benefit was short‐term (OS at 3 years 17%, 29%, 12% respectively). Combination of the CEBPA^DM and NPM1^MUTFLT3^WT genotype patients defined a molecular group with favourable prognosis (P < 0·0001 in multivariate analysis), with 57% of patients alive at 1 year compared to 33% for all other patients. Knowledge of genotype in older cytogenetically intermediate‐risk patients might influence therapy decisions.     

不同基因型丙型肝炎病毒感染临床研究

AIM To study the clinical peculiarities of patients infected with different genotypes of hepatitis C virus (HCV).METHODS Genotypes of HCV in 90 HCV-RNA-positive patients in Xuzhou area were examined. Clinical data of the patients were compared.RESULTS HCV Ⅱamounted to 78.9% (71/ 90), predominating over HCV Ⅲand HCV Ⅱ/ Ⅲwhich held 18.9% (17/ 90) and 2.2% (2/ 90) respectively in the area. ALT level and ALT positivity rate were higher in HCV Ⅱthan in HCV Ⅲ(P＜0.05) within a range of ＞200 U/ L. Anti-HCV OD value and anti-HCV positivity rate when its OD value was over 2, were lower in HCV Ⅱthan in HCV Ⅲ(P＜0.05). Most jaundice patients (87%) were infected with HCV Ⅱ. No significant difference was found in age, sex and transfusion experience between HCV Ⅱand HCV Ⅲpatients (P＞0.05).CONCLUSION Distribution of HCV genotypes in Xuzhou area is consistent with that in the whole China, reflecting its distribution in eastern coastal areas. The immunogenicity of HCV Ⅱis lower than that of HCV Ⅲ, but the damage of hepatic function is more serious in HCV Ⅱpatients than in HCV Ⅲpatients, which might be due to different pathogenic mechanisms. Infection with HCV Ⅱ/ Ⅲis related to repeated usage of blood products and repeated hemodialysis. HCV Ⅱand HCV Ⅲ, we believe, might play coordinated roles in pathogenesis.     

The neglected hepatitis C virus genotypes 4, 5 and 6: an international consensus report

Hepatitis C virus (HCV) genotypes 4, 5 and 6 represent >20% of all HCV cases worldwide. HCV‐4 is mainly seen in Egypt, where it represents 90% of all HCV cases. Antischistosomal therapy was the main cause of contamination there, followed by procedures performed by informal providers and traditional healers such as dental care, wound treatment, circumcision, deliveries, excision and scarification. It is also highly prevalent in sub‐Saharan Africa and in the Middle East. In Europe, its prevalence has recently increased particularly among intravenous drug users and in immigrants. HCV‐5 is mainly found in South Africa, where it represents 40% of all HCV genotypes, but four pockets of HCV‐5 were found in France, Spain, Syria and Belgium and sporadic cases were found elsewhere. The mode of transmission is mainly iatrogenic and transfusion. HCV‐6 is found in Hong Kong, Vietnam, Thailand and Myanmar and also in American and Australian from Asian origin. The response to treatment in HCV‐4 is intermediate between HCV‐1 and HCV‐2 and HCV‐3. A sustained viral response is achieved in 43–70% with pegylated interferon and ribavirin. It is higher in Egyptians than Europeans and Africans and is negatively related to insulin resistance and to the severity of fibrosis. It increases to >80% with 24 weeks of therapy only if a rapid virological response is achieved. In HCV‐5, a sustained virological response is achieved in >60% with 48 weeks of therapy. HCV‐6 is also considered an easy‐to‐treat genotype, leading to a response in 60–85% of cases.     

耐甲氧西林金黄色葡萄球菌杀白细胞素基因检测

目的 调查临床分离的耐甲氧西林金黄色葡萄球菌(MRSA)杀白细胞毒素基因携带率。方法 收集非重复MRSA菌株83株,按照美国疾病预防控制中心的CA-MRSA 定义分为HA-MRSA和CA-MRSA两组。采用多重PCR法进行SCCmec分型,普通PCR+测序法进行spa分型,普通PCR检测杀白细胞素(PVL)基因。结果 83株MRSA中HA-MRSA、CA-MRSA分别占47.0%、53.0%,SCCmec分型中SCCmecⅠ、Ⅱ、Ⅲ、Ⅳa型和未分型各占1.2%、3.6%、65.1%、28.9%、1.2%,spa分型中83株MRSA共检出15个型,主要分型为t437,t062,t015分别占39.8%, 21.7%,10.8%;PVL阳性的MRSA中HA-MRSA和CA-MRSA分别10.3%、36.4%,两者差异有显著性(P=0.006);33株spa t437中有18株携带PVL基因,阳性率54.5%,50株其他spa分型中仅2株携带PVL基因,阳性率4.0%,两者差异有显著性(P=0.000)。PVL基因阳性的MRSA特征CA-MRSA-Ⅳa-t437 9株,HA-MRSA-Ⅲ-t437 4株,HA-MRSA-Ⅳa-t437 3株;20株PVL基因阳性的MRSA中10株分离自皮肤软组织感染病例,6株分离于耳鼻喉科感染病例,3株分离于呼吸道感染病例,1株分离于败血症病例。结论 CA-MRSA菌株较HA-MRSA菌株的 PVL基因阳性率更高,同时也发现携带有更高毒力的CA-MRSA的克隆已经播散到医院的环境中,引起医院获得性相关感染。     

Resistance Analyses of Japanese Hepatitis C‐Infected Patients Receiving Sofosbuvir or Ledipasvir/Sofosbuvir Containing Regimens in Phase 3 Studies

High rates of sustained virologic response (SVR) has been achieved in Japanese patients with chronic hepatitis C virus (HCV) genotype (GT)1 and GT2 infection treated with ledipasvir/sofosbuvir (LDV/SOF) ±ribavirin (RBV) and SOF+RBV, respectively. We evaluated the effect of baseline HCV NS5A and NS5B resistance‐associated variants (RAVs) on treatment outcome and characterized variants at virologic failure. Baseline deep sequencing for NS5A and NS5B genes was performed for all GT1 patients. Deep sequencing of NS5A (GT1 only) and NS5B (GT1 and GT2) was performed for patients who failed treatment or discontinued early with detectable HCV RNA (i.e., >25 IU/mL). In patients with HCV GT1 infection, 22.3% (GT1a: 2/11; GT1b: 74/330) had ≥1 baseline NS5A RAV. The most frequent NS5A RAVs in GT1b were Y93H (17.9%, 59/330) and L31M (2.4%, 8/330). Despite the presence of NS5A RAVs at baseline, 100% and 97% of patients achieved SVR12, compared with 100% and 99% for those with no NS5A RAVs with LDV/SOF and LDV/SOF+RBV, respectively. All patients with NS5B RAVs at baseline achieved SVR12. Of the 153 patients with GT2 infection (GT2a 60.1%, GT2b 39.9%), 3.3% (5/153) experienced viral relapse. No S282T or other NS5B RAVs were detected at baseline or relapse; no change in susceptibility to SOF or RBV was observed at relapse. In conclusion, LDV/SOF and SOF+RBV demonstrate a high barrier to resistance in Japanese patients with HCV GT1 and GT2 infection. The presence of baseline NS5A RAVs did not impact treatment outcome in GT1 Japanese patients treated with LDV/SOF for 12 weeks.     

Variability of the pancreatic islet beta cell/liver (GLUT 2) glucose transporter gene in NIDDM patients

Summary The purpose of these experiments was to test the hypothesis that impaired glucose-stimulated insulin secretion in NIDDM is due to mutations in the islet beta cell/liver glucose transporter (GLUT 2) gene. Using oligonucleotide primers flanking each of the 11 exons, the structural portion of the gene was studied by PCR-SSCP analysis. DNA from African-American females (n=48), who had gestational diabetes but developed overt NIDDM after delivery, was studied. Each SSCP variant was sequenced directly from genomic DNA. Two amino acid substitutions from the previously reported sequence were found, one in exon 3 and the other in exon 4 B. Four additional silent mutations in the coding region, and six intron mutations outside the splice junction consensus sequences, were also identified. The mutation GTC x ATC in exon 4B substituted Val¹⁹⁷ to Ile¹⁹⁷. This amino acid substitution was found in only one NIDDM patient in a single allele, and was not found in 52 control subjects. This residue exists in the fifth membrane spanning domain, and Val at this position is conserved in mouse and rat GLUT 2, and human GLUT 1 to GLUT 4. The other codon change in exon 3, ACT x ATT, substituted Thr¹¹⁰ to Ile¹¹⁰ in the second membrane spanning domain. To determine the frequency of this non-conservative amino acid substitution, a PCR-LCR assay was developed. This assay was simple and highly specific for detection of this single nucleotide substitution. The allelic frequency of the ATT (Ile¹¹⁰) in NIDDM patients (39.6%, n=48) and that in controls (47.1%, n=52) did not differ (p=0.32, Fisher's exact test). In conclusion, we identified two variant GLUT 2 glucose transporters in a subset of NIDDM patients. The rare variant in exon 4 B may contribute to the diabetic susceptibility and awaits further investigation. However, structural abnormalities of the GLUT 2 transporter associated with NIDDM appeared to be rare and were not likely to be a major determinant of genetic susceptibility to this type of diabetes in the population studied.Abbreviations NIDDM Non-insulin-dependent diabetes mellitus - GLUT 2 islet beta cell/liver glucose transporter - PCR polymerase chain reaction - SSCP single strand conformation polymorphism - LCR ligase chain reaction - bp base pair     

Hepatitis B virus infection and genotype in asymptomatic people from 10 ethnic groups in Yunnan,China

AIM: To evaluate the infection and genotype distribution of hepatitis B virus(HBV) in ethnic groups in Yunnan, China.METHODS: Two thousand five hundred and eightyfour asymptomatic local people from 10 ethnic groups were investigated in Yunnan, China. Infection and genotype distribution were evaluated by serological and genetic methods. Genotyping was verified by sequencing. Ethnic genotype distribution was compared by proportion test. RESULTS: Four types of infection model based on HBV serum markers were identified, and the average HBV infection rate was 5.7% in those asymptomatic local people. The genotype prevalence was 59.6% for B, 21.1% for C and 19.3% BC; subgenotypes Ba, Cs and Ce were identified in this study. Hepatitis B surface antigen-positive rate and the proportion of genotype B were significantly lower in ethnic groups with a northern origin compared to those with a southern origin(50% vs 73.9%, P = 0.037; 4.2% vs 10.5%, P = 0.000).CONCLUSION: Genotype B is dominant and genotype BC has high occurrence in asymptomatic local ethnic groups in Yunnan. HBV infection status and genotype distribution may associate with ethnic origin.     

Genotype/phenotype correlations of childhood-onset congenital sideroblastic anaemia in a European cohort

Congenital sideroblastic anaemia (CSA) is a rare disease caused by germline mutations of genes involved in haem and iron-sulphur cluster formation, and mitochondrial protein biosynthesis. We performed a retrospective multicentre European study of a cohort of childhood-onset CSA patients to explore genotype/phenotype correlations. We studied 23 females and 20 males with symptoms of CSA. Among the patients, the most frequently mutated genes were ALAS2 (n = 10; 23·3%) and SLC25A38 (n = 8; 18·6%), causing isolated forms of microcytic anaemia of varying severity. Five patients with SLC19A2 mutations suffered from thiamine-responsive megaloblastic anaemia and three exhibited the ‘anaemia, deafness and diabetes’ triad. Three patients with TRNT1 mutations exhibited severe early onset microcytic anaemia associated with thrombocytosis, and two exhibited B-cell immunodeficiency, inflammatory syndrome and psychomotor delay. The prognoses of patients with TRNT1 and SLC2A38 mutations were generally dismal because of comorbidities or severe iron overload. No molecular diagnosis could be established in 14/43 cases. This study emphasizes the frequency of ALAS2 and SLC25A38 mutations and provides the largest comprehensive analysis to date of genotype/phenotype correlations in CSA. Further studies of CSA patients with data recorded in an international registry would be helpful to improve patient management and establish standardized guidelines.     

CD209-336A/G promotor polymorphism and its clinical associations in sickle cell disease Egyptian Pediatric patients

Objectives

To detect the frequency of CD209 A>G polymorphism in sickle cell disease (SCD) Egyptian patients and to evaluate the use of CD209 A>G polymorphism as a genetic predictor of SCD clinical heterogeneity.

The Fyx phenotype is associated with a missense mutation in the Fyb allele predicting Arg89Cys in the Duffy glycoprotein

The molecular basis of the three major alleles ( Fy^a / Fy^b / Fy ) of the Duffy (FY) blood group system has recently been established but the Fy^x phenotype associated with weak expression of the Fy^b and other FY antigens is poorly understood.
In the Fy^x genes of five unrelated British and Swedish donors with the Fy(a+b+^weak) phenotype we found two missense mutations predicting amino acid changes Arg89Cys and Ala100Thr in the FY glycoprotein.
The same mutations were found in two Fy(a−b+^weak) samples from individuals of Swedish and Algerian origin. Their red blood cells showed a marked decrease in Fy^b, Fy3 and Fy6 expression measured by routine serology and flow cytometry. The rare FY genotypes Fy^xFy^x and Fy^xFy were confirmed by family studies and DNA sequencing.
Screening by allele-specific primer PCR (ASP-PCR) for these mutations among 100 Caucasian and 100 Black random blood donors indicated allele frequencies of 2.5% and 0%, respectively. Ala100Thr alone was present in 33% of the Caucasians (but none of the Blacks) with no weakening of FY expression.
A novel allele at the FY locus associated with the Fy^x phenotype was studied. Mistyping of this weak Fy^b antigen in clinical transfusion medicine may lead to delayed haemolytic transfusion reactions in immunized patients. A potential role for genomic typing is proposed.     

The accuracy of baseline viral load for predicting the efficacy of elbasvir/grazoprevir in participants with hepatitis C virus genotype 1a infection: An integrated analysis

European treatment guidelines for hepatitis C virus (HCV) infection recommend that people with genotype (GT) 1a infection and baseline viral load ≤800 000 IU/mL receive elbasvir/grazoprevir (EBR/GZR) for 12 weeks, and those with baseline viral load >800 000 IU/mL receive EBR/GZR plus ribavirin for 16 weeks. This analysis was conducted to clarify whether baseline viral load can serve as an accurate, sensitive or specific stratification factor for defining EBR/GZR regimens. In this post hoc, integrated analysis, participants with GT1a infection who received EBR 50 mg/GZR 100 mg for 12 weeks were stratified according to baseline viral load. Sustained virologic response at 12 weeks post‐treatment was achieved by 95.2% (911/957) of participants and was higher among participants with baseline viral load ≤800 000 IU/mL vs >800 000 IU/mL (98.5% vs 93.9%). The 800 000 IU/mL threshold had a positive predictive value of 98.5%, a negative predictive value of 6.1%, a specificity of 91.3%, a sensitivity of 28.4% and an overall accuracy of 31.5%. A baseline viral load cutpoint of 800 000 IU/mL had high positive predictive value and specificity but poor negative predictive value, sensitivity and accuracy in predicting treatment outcomes in this population. Baseline NS5A resistance‐associated substitutions (RASs) were detected in 25% (1/4) of virologic failures with baseline viral load ≤800 000 IU/mL and 59.5% (25/42) of those with baseline viral load >800 000 IU/mL. Overall, these data suggest that, compared with the use of a baseline viral load cutpoint, baseline testing for NS5A RASs enables more individuals to receive the 12‐week EBR/GZR regimen without compromising the opportunity for SVR.     

Characterization of demographics and NS5A genetic diversity for hepatitis C virus genotype 4‐infected patients with or without cirrhosis treated with ombitasvir/paritaprevir/ritonavir

Hepatitis C virus (HCV) genotype 4 (GT4) is genetically diverse with 17 confirmed and 4 provisional subtypes. In this report, HCV GT4‐infected patient samples from Phase 2/3 clinical studies were analysed to characterize global demographics and genetic diversity of GT4 infection among patients treated with ombitasvir (OBV, NS5A inhibitor) plus paritaprevir/r (NS3/4A inhibitor codosed with ritonavir). Among 17 subtypes isolated from GT4‐infected patients in the PEARL‐I and AGATE‐I studies, subtype prevalence by country of enrolment and country of origin suggested that subtypes 4a and 4d were likely circulating in Europe, while heterogeneous GT4 subtypes and a portion of GT4a detected in European and North American countries were likely due to immigration of HCV‐infected patients from Africa. The distributions of birth cohort and race were also significantly different across GT4 subtypes 4a, 4d, and non‐4a/4d. In addition, phylogenetic analyses of NS5A sequences revealed clustering within subtype 4a which segregated by the patient‐reported country of origin and the presence of the L30R/S polymorphism. HCV NS5A sequences derived from GT4a‐infected patients who originated from Europe and the United States clustered separately from sequences derived from patients who originated from Egypt, suggesting that genetically distinct strains of subtype 4a may be circulating globally. Finally, NS5A baseline polymorphisms were frequently detected at amino acid positions of interest for the inhibitor‐class and OBV retained activity against 37 of 39 NS5A GT4 clinical isolates, with no impact on treatment outcome in the PEARL‐I and AGATE‐I studies.     

Revisiting host/parasite interactions: molecular analysis of parasites collected during longitudinal and cross-sectional surveys in humans

This paper summarizes the first conclusions arising from an analysis of parasite diversity in blood samples collected during longitudinal surveys conducted in Senegal. Parasite typing was carried out using a PCR-based molecular analysis of allelic polymorphism. The parasite populations circulating in the village of Dielmo during periods of intense transmission (when the inoculation rate was 0.5–1 infective bite/night) are characterized by a considerable allelic diversity of the MSP-1, MSP-2 and TRAP loci. A large proportion of blood samples contained several MSP-1 or MSP-2 alleles. In asymptomatic carriers, the complexity of the infections (number of alleles and genetic diversity of these alleles) was age-dependent. In children, the trend was for a reduced complexity during clinical episodes. Molecular typing showed that successive clinical episodes experienced by children were caused by genetically distinct parasites. Longitudinal analysis of asymptomatic carriers indicated that in the absence of transmission, the same parasite types were carried for long periods, while rapidly changing profiles were observed during intense transmission season. The consequences of these findings on our understanding of acquired anti-parasite immunity in humans living in endemic are discussed.     

Clinical features of patients with chronic liver disease associated with hepatitis C virus genotype 1a/I in Okinawa, Japan

The clinical characteristics of chronic hepatitis C virus (HCV) carriers with HCV genotype 1a/I infection were investigated and compared with those of chronic HCV carriers infected with 1b/II, 2a/III, 2b/IV and the mixed type of infection. We found that 16 of 408 (3.9%) carriers had HCV genotype 1a infection, comprising four of 67 (6.0%) blood donors, 11 of 263 (4.2%) patients with chronic hepatitis and one of 39 (2.6%) patients with liver cirrhosis. Three of 408 subjects had a mixed infection of genotypes 1a/I and 1b/II. All carriers with genotype 1a (including those with the mixed infection) were of Japanese origin and all, except one who was born in Brazil, were born in Okinawa Prefecture. Nine of 14 patients infected with genotype 1a for whom medical records were obtained had a history suggestive of infection through blood exposure; six had had blood transfusions, one had tattoos, one is a nurse and one had a history of drug addiction. There were no haemophiliacs or other multitransfused patients in the genotype 1a group. Of 10 patients infected with genotype 1a who received interferon (IFN) therapy, four (40%) showed a complete response. Although the small number of patients infected with genotype 1a in the present study precluded statistical analysis of the response to IFN, the response in patients with genotype 1a was better than the response in those infected with genotype 1b and poorer than the response in those patients infected with genotype 2a/III or 2b/IV.     

不同基因型丙型肝炎病毒Core蛋白HLA-DRBl^＊0311、0401表位预测

目的预测各型丙型肝炎病毒（HCV）Core区的人类白细胞抗原（HLA）-DRB1＊0311及0401抗原表位。方法从NCBI数据库中检索出十条包含六种分型的HCV完整氨基酸序列,使用生物信息学工具剪切Core区氨基酸序列并对其二级结构、可塑性、亲水性和抗原性指数进行预测,选择可能区域预测HLA-DRB1＊0311及0401的抗原表位。结果 HCV Core区二级结构、可塑性、亲水性和抗原性指数预测分析可认为16～28、60～74、98～120区域或为抗原表位区域。HLA-DRB1＊0311预测中,HCV-1a/b、4a、6a预测评分高的区域为28～36,HCV-2a/b为63～71,HCV-3a为29～37,HCV-5a为94～102。HLA-DRB1＊0401中,HCV-1a、2b、4a、6a预测评分高区域为84～92,HCV～5a为120～128,HCV-1b中120～128可以预测到表位但评分低。结论 HCV Core区HLA-Ⅱ类分子抗原表位具有型间差异。