The study assessed the correlation between cortisol (COR) levels and concurrent infection for the patients with hepatitis B cirrhosis for corresponding countermeasure analysis. In total, 86 patients with hepatitis B cirrhosis (non-infection group) and 32 patients with hepatitis B cirrhosis complicated with infection (infection group) who were diagnosed and treated in the Beijing YouAn Hospital from March 2014 to March 2017 were selected. The fasting venous blood of all the patients was drawn to detect COR, cortisol binding globulin (CBG), blood routine indexes, C-reactive protein (CRP), procalcitonin (PCT), endotoxin and other indicators. The relative expression of CBG mRNA was detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR). The differences and correlation of COR levels between the infection and non-infection groups were compared and analyzed. The concentrations of COR and CBG were decreased with the increase of Child-Pugh grade, and the difference was statistically significant (P<0.05). COR, CBG and free cortisol (FC) concentrations with the same Child-Pugh grade in the non-infection group were higher than those in the infection group (P<0.05). COR, CBG and FC concentrations of abdominal infection complicated with sepsis or abdominal infection complicated with pulmonary infection were lower than those of simple abdominal infection (P<0.05). The relative expression of CBG mRNA was detected by RT-qPCR, which also showed that: for Child-Pugh grade, grade A > grade B > grade C (P<0.05), non-infection group > infection group (P<0.05), abdominal infection + sepsis group and abdominal infection + pulmonary infection group were lower than the simple abdominal infection group (P<0.05). The values of white blood cells (WBC), neutrophils, CRP, PCT and endotoxin in the infection group were higher than those in the non-infection group, and the differences were statistically significant (P<0.05). COR, CGB and FC were negatively correlated with inflammatory indexes such as WBC, neutrophils, CRP, PCT and endotoxin. The r value of COR and FC in the non-infection group was 0.678, while that of OR and FC in the infection group was 0.787. COR was positively correlated with FC before and after infection. The results of the study show that the cortisol levels of patients with hepatitis B cirrhosis are significantly correlated with whether infected or not, levels of disease condition and infection types, and can be used as sensitive indicators of hepatitis B cirrhosis infection.

Hepatitis B cirrhosis is caused by liver cell necrosis, residual liver cell nodular regeneration, connective tissue hyperplasia and fiber formation, which frequently leads to adrenal insufficiency. Previous reports have demonstrated that human fibroblast growth factor (hFGF)-21 is a multifunctional protein that exhibits potential therapeutic value for metabolic diseases. The present study investigated the diagnostic value of hFGF-21 and analyzed the potential molecular mechanism in the progression of hepatitis B cirrhosis combined with adrenal insufficiency. Characteristics of cellular immunity and humoral immunity were analyzed in patients with hepatitis B cirrhosis combined with adrenal insufficiency (PhbA). Results demonstrated that expression levels of hFGF-21 were downregulated in plasma and liver cells isolated from clinical specimens. Plasma concentration levels of hFGF-21 were upregulated in prognostic PhbA. In vitro assays indicated that hFGF-21 treatment decreased the continuous deposition of extracellular matrix and reactive oxygen species in liver cells isolated from clinical specimens. Results also demonstrated that hFGF-21 treatment downregulated inflammatory cytokines. It was observed that hFGF-21 treatment downregulated nuclear factor (NF)-κB and Kruppel-like factor 6. Notably, transforming growth factor (TGF)-β, platelet-derived growth factor and epidermal growth factor levels were improved by hFGF-21 treatment. In conclusion, these results indicated that hFGF-21 inhibits inflammation by regulation of the NF-κB-mediated TGF-β signaling pathway, which may serve as a predictor and prognostic factor in PhbA.

Objective To analyze the pathogen spectrum of hand,foot and mouth disease (HMFD)in 2014 in Beijing Youan Hospital for providing scientific basis for the prevention of HFMD.Methods The related data of HFMD in 2014 was analyzed by LIS system,including the characteristics of pathogen spectrum.The other enterovirus(EV) was partially identified by DNA sequencing analysis.Results The number of confirmed HMFD cases in 2014 was 2 031,and the proportion of male and female patients was about 1.5:1.The pathogen spectrum of HMFD was EV-A71 (34.6％),CVA16 (34.6％) and other EV (30.8％).The HMFD peak of incidence was from April to August in 2014.During the period,the composition ratios of EV-A71,CVA16 and other enterovirus were respectively 46.5％/30.8％/22.7％、41.3％/29.6％/29.1％ 、31.8％/38.4％/29.8％ 、32.6％/36.1％/31.3％ 和 30.9％/37.4％/31.7％ in each month.The difference among them was statistically significant (chi-square =x2 =24.866,P =0.002 ＜ 0.05).During the period of high incidence of HFMD,the predominant patients were the children under five years old,the younger the age,the higher the incidence rate.Conclusions The major causative agents of HFMD in 2014 are still EV-a71 and CVA16.The other EV encounters a considerable proportion and the incidence of CVA10 and CVA6 is relatively higher,which could cause severe cases of HFMD.

The aim of this study was to analyze the genetic characteristics of the VP1 gene of coxsackievirus A16(CA16)strains isolated from Jiangsu Province, China, in 2015.The VP1 regions of 20CA16 virus strains from Jiangsu Province in 2015 were amplified, and the amplification products were sequenced. Mega 6.0and DNA Star software were applied to build the phylogenetic tree and analyze the homogeneity of nucleotides and amino acids. The sequence homologies of the nucleotides and amino acids of the VP1 gene were 88.2%~100.0%and 98.0%~100.0%among 20CA16 isolates, respectively. Comparison with the sequence of the prototype strain A-G10 showed 75.3%~77.4% homologies in nucleotide sequence and90.6%~92.3%in amino-acid sequences, respectively. Comparison with the sequence of the representative strain B1 showed 88.3%~98.4% homologies in nucleotide sequence and 96.3%~100.0%in amino-acid sequence, respectively. Comparison with the sequence of the representative strain B2 showed 88.4%~90.8% homologies in nucleotide sequence and 96.6%~100.0%in amino-acid sequence, respectively. Twenty CA16 isolates were subgenotype B1.One isolate was subgenotype B1a, whereas the remainder of isolates was subgenotype B1b among 20 CA16 isolates. A subgenotype B1b transmission chain was also noted. The CA16 strains isolated from Jiangsu Province in 2015 belonged to subgenotype B1.There were two evolutionary branches, whereby B1 a and B1bwere co-circulating and evolving together. The epidemic strain was subgenotype B1b.

Andrographolide sulfonate treatment has been shown to improve clinical severe hand, foot, and mouth disease (HFMD) efficacies when combined with conventional therapy. However, the mechanisms for its therapeutic effects remain elusive. In this study, we aimed to investigate whether andrographolide sulfonate exerts its efficacy by acting on neutrophil activation. We obtained serial plasma samples at two time points (before and after 5 days of therapy) from 28 HFMD patients who received conventional therapy and 18 patients who received combination therapy (andrographolide sulfonate plus conventional therapy). Then, we measured plasma myeloperoxidase (MPO), S100A8/A9, histone, and inflammatory cytokine levels. Furthermore, we examined if andrographolide sulfonate had direct effects on neutrophil activation in vitro. We observed that MPO and S100A8/A9 levels were markedly elevated in the HFMD patients before clinical treatment. At 5 days post‐medication, the MPO, S100A8/A9, histone, and interleukin‐6 levels were markedly lower in the combination therapy group compared with the conventional therapy group. In vitro studies showed that andrographolide sulfonate inhibited lipopolysaccharide‐stimulated neutrophil activation, demonstrated by the decreased production of reactive oxygen species and cytokines. These data indicate that neutrophil activation modulation by andrographolide sulfonate may be a critical determinant for its clinical HFMD treatment efficacy. Copyright © 2015 John Wiley & Sons, Ltd.

BACKGROUND:Hand, foot, and mouth disease (HFMD) is a common infectious disease in children, characterized by acute viral infection accompanying acute inflammatory responses. Circulating histones are leading mediators of the inflammatory processes. This study aimed to elucidate whether circulating histones play a contributory role during HFMD.METHODS:We measured plasma levels of histones, myeloperoxidase (MPO), lactate dehydrogenase (LDH), and cytokines in HFMD patients (n = 126) and compared the results with those of a control group (n = 30).RESULTS:Circulating histone levels were significantly increased in HFMD patients (3.794 ± 0.156 μg/ml) compared with healthy controls (0.238 ± 0.023 μg/ml, p < 0.0001). In addition, their levels were remarkably higher in severe HFMD (n = 38) than in mild HFMD patients (n = 88) (5.232 ± 0.246 vs 3.293 ± 0.161 μg/ml, p < 0.0001). As for other inflammatory markers, MPO, LDH, IL-1β, IL-6, IL-10, MIP-1, and TNF-ɑ were found to be significantly higher in HFMD patients than in healthy subjects. Of these, LDH, IL-6, and TNF-ɑ levels correlated with disease severity (all p < 0.05). In mild HFMD, circulating histones correlated positively with plasma IL-6 and IL-10, whereas in severe HFMD, histones were associated with elevated IL-6 and TNF-ɑ levels.CONCLUSIONS:These data demonstrate that circulating histones are excessively released in patients with HFMD, which may indicate disease severity and contribute to systemic inflammation by promoting cytokine production (e.g. IL-6). We suggest that in mild HFMD, circulating histones may originate largely from neutrophil activation, whereas in severe HFMD, dying tissue cells and neutrophil activation may be synergistically involved in the increased levels of histones.

[目的]探讨单纯性肥胖患者伴发非酒精性脂肪肝病与外周血脂肪细胞因子的关系.[方法]160例研究对象分为正常对照组30例(A组),单纯性肥胖组40例(B组),非酒精性脂肪肝组50例(C组)、单纯性肥胖合非酒精性脂肪肝组40例(D组);检测各组血脂和血清瘦素(Leptin)、脂联素(APN)的水平变化.[结果]与A组比较,B组、C组、D组的总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL)、Leptin水平升高,高密度脂蛋白(HDL)、脂联素(APN)水平下降,差异均有统计学意义(P＜0.05或P＜0.01);上述指标在B组和C组之间比较差异不显著(P＞0.05).D组的TC、TG水平均较B组、C组明显升高(P＜0.05),且LDL水平也高于B组(P＜0.05);D组的Leptin水平较B组上升更明显,APN水平较B组、C组下降更明显,差异均有统计学意义(P＜0.05).[结论]脂肪细胞因子与单纯性肥胖及非酒精性脂肪肝相关,其可能参与了单纯性肥胖患者非酒精性脂肪肝病的病理生理过程.

Background: A recent genome-wide scan has identified two genetic variants in the HLA-DP region strongly associated with hepatitis B infection in Japanese. This study evaluates the effects of these risk variants in Chinese, where the HBV infection is the most popular in the world.Methods and Findings: We have assessed the relationship between these two single nucleotide polymorphisms (rs3077 and rs9277535) and chronic hepatitis B infection in two independent case-control studies. The first population in Chinese Han included 736 patients and 782 spontaneously recovered controls. The second set was established in Chinese Zhuang minority of 177 patients and 208 controls. Both A alleles of rs3077 and rs9277535 significantly deceased the risk to CHB in Chinese Han (OR = 0.540, 95% CI: 0.464-0.628, P = 4.068x10(-16) and OR = 0.696, 95% CI: 0.601-0.806, P = 1.062x10(-26), respectively). Conceivably, rs9277535 was found to be associated with decreased risk of the disease in Chinese Zhuang, with an OR of 0.606 (95% CI, 0.441-0.833, P = 0.002).Conclusion: Chronic hepatitis B susceptibility loci in HLA-DP region (rs3077 and rs9277535) identified by genome-wide scan in Japanese population were validated in Chinese population. These findings might provide clues to develop screening and surveillance strategies.

Natural killer (NK) cells are important antiviral effectors of innate immunity because of their contribution to virus elimination. NK cell-mediated immunological reaction to hepatitis B virus (HBV) infection depends on a fine balance between inhibitory and activating receptors. The aim of the study was to investigate genetic polymorphisms in NK cell receptors (NKR)-KLRD1 (CD94), KLRK1 (NKG2D), KLRC4 (NKG2F), and KLRC1 (NKG2A)-to evaluate the association of NKR genetic polymorphisms with susceptibility to chronic hepatitis B in a Han Chinese population. Twelve single nucleotide polymorphisms (SNPs), including rs2302489 in CD94; rs2255336, rs2617160, rs7980470, rs 2734565, and rs17513986 in NKG2D; rs2617170, rs17549004, and rs3825295 in NKG2F; rs2734414, rs7301582, and rs2734440 in NKG2A, were selected in the present study. SNP genotyping was undertaken in 500 Han Chinese patients (285 patients with chronic hepatitis B and 215 patients who cleared HBV spontaneously) by a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and by the TaqMan method. Single marker association analysis was conducted and the SNP rs2617160 with a TT genotype in NKG2D was associated significantly with an increased risk of chronic hepatitis B (P=0.044; OR=1.49; 95% CI=1.01-2.19). Haplotype analysis with multiple loci indicated that there was no significant association between the haplotypes of the NKR genes and susceptibility to chronic hepatitis B. The SNP rs2617160 in NKG2D associated with susceptibility to chronic hepatitis B in a Han Chinese population. J. Med. Virol. 82:1501-1507, 2010. (C) 2010 Wiley-Liss, Inc.

Objective To determine potential gene-gene interactions of TNF-α and VDR loci with outcomes of hepatitis B virus(HBV) infection.Methods A total of 391 chronic hepatitis B(HB) patients as a case group and 212 HBV self-limited infected subjects as a control group were recruited to conduct a case-control study.TNF-α-238G/A,-857C/T,-863C/A,VDR-TaqⅠT/C and FokⅠC/T gene polymorphisms were examined by polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP).The interactions between TNF-α and VDR genes were analyzed by multiple model.Results There were positive gene-gene interactions between TNF-α-238 GA and FokⅠ CT/CC(ORint=4.04),between-863 CC and-857 CC(ORint=1.26) and between-857 CC and FokⅠ CT/CC(ORint=1.37),respectively,which increase the risk of chronic hepatitis B.There were negative gene-gene interactions between TNF-α-238 GA and-857 CC(ORint=0.92)and between FokⅠ CT/CC and TNF-α-863 CC(ORint=0.95),which decrease the risk of chronic hepatitis B.Conclusion Interaction between TNF-α loci and VDR loci potentially increase the risk of chronic hepatitis B after HBV infection.

OBJECTIVE To explore the effect of use of lens culinaris agglutinin (LCA)-coupled spin column (ACSC) in detection of alpha-fetoprotein (AFP) isoform AFP-L3 and to evaluate the value of AFP-L3 as a biomarker in diagnosis of hepatocellular-carcinoma (HCC). METHODS The serum samples of 132 patients with elevated AFP level (20-1000 microg/L), 79 diagnosed as with HCC and 53 with benign liver diseases (35 with liver cirrhosis and 18 with chronic hepatitis) underwent ACSC to isolate the fraction of AFP-L3. The contents of AFP and AFP-L3 were detected by micro-particle immunoassay. The ratio of AFP-L3 to total AFP, AFP-L3%, was calculated. Correlation between the abnormally elevated AFP-L3% and HCC was analyzed. RESULTS Detection of AFP-L3% using ACSC method was operating friendly. The average value of AFP-L3% in the patients with HCC was 36.4%, significantly higher than those of the patients with benign liver diseases (5.3% respectively, P < 0.01). The area under the receiver operating characteristic (ROC) curve of AFP-L3% was 0.807. Taking AFP-L3% > or = 10% as diagnostic criteria, the sensitivity of AFP-L3% in HCC diagnosis was 84.8% (67/79) and the specificity was 92.5% (49/53), with a total conformity rate of 87.9% compared to the confirmed clinical diagnosis. Conclusion ACSC is of clinical value in detecting AFP-L3. AFP-L3% is a valuable biomarker in diagnosis and prediction of prognosis of HCC.

BACKGROUND Host genetic factors and environmental factors including hepatitis B virus (HBV) genotype are widely studied for the different outcomes of HBV infection. Human leukocyte antigen (HLA) plays an important role in the immunological reaction to HBV infection. AIMS To explore whether the HLA-DQB1 allele polymorphisms are associated with the outcome of HBV infection in a Chinese Han population. PATIENTS One hundred and thirty three HBV subjects with spontaneous recovery and 151 chronic hepatitis B patients were recruited into this case-control study in the Beijing area of China. METHODS Sequence specific primer-polymerase chain reaction (SSP-PCR) was used to detect 13 alleles of HLA-DQB1 gene and 13 alleles of HLA-DRB1 gene. Multivariate logistic regression model was performed to detect the association of candidate factors with outcome of HBV infection by SAS 9.1.2 software package. RESULTS The frequency of HLA-DQB1*0502 allele in the chronic hepatitis B group was significantly higher than that in the group with spontaneous recovery independent of HLA-DRB1 (odds ratio 95%CI 1.8-190). In this study there was no evidence to indicate that cigarette smoking or alcohol consumption was associated with the outcome of HBV infection. CONCLUSION HLA-DQB1*0502 is independently associated with the outcome of HBV infection and is one host genetic factor affecting HBV infection outcome. At the same time, we can not rule out the possibility that excluded genes and alleles may also affect outcome.

Objective To determine whenther-238G/A,-857T/C and-863C/A polymorphisms of tumor necrosis factor-alphya(TNF-α) gene promoter were associated with outcomes of hepatitis B virus(HBV) infection.Methods A total of 244 HBV self-limited infected subjects,212 asymptomatic HBsAg carriers(HBsAg carriers) and 391 chronic hepatitis B(HB) patients were recruited to conduct a case-control study.TNF-α-238G/A,-857C/T and-863C/A gene promoter polymorphisms were examined by polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP).Results The frequency of-238 allele A in self-limited individuals was 2.6%,significantly lower than 5.0% in chronic HB patients and 5.3% in HBsAg carriers(P=0.04 and P=0.047),respectively.The frequency of TNF-α-857 allele C in chronic HB patients was 87.5%,significantly higher than 80.5% in HBsAg carriers and 82.8% in self-limited individuals(P=0.0008 and P=0.03),respectively.The frequency of TNF-α-863 allele A in chronic HB group was(77.5%,)significantly higher than 71.5% in HBsAg carriers(P=0.02).Multiple logistic regression analyses indicated an increased risk of chronic HB associated with TNF-α-238GA and-857CC after gender and age adjusting(OR=1.53,P=0.044;OR=2.11,P=0.045),and HBsAg carriers with-857CC significantly increasing risk of chronic HB associated with TNF-α-238GA and-857CC after gender and age adjusting(OR=1.53,P=0.044;OR=2.11,P=0.045),an HBsAg carriers with-857CC significantly increasing risk of chronic HB(OR=1.92,P=0.004),and-238GA associated with and increasing risk of HBsAg carriers(OR=2.34,P=0.020).Conclusion TNF-α promoter polymorphism is probably an important risk factor of the influence of outcome of HBV infection.

OBJECTIVE:To determine whether Taq I T/C and Fok I C/T polymorphisms of vitamin D Receptor (VDR) gene was associated with the outcomes of hepatitis B virus (HBV) infection.METHODS:A total of 212 HBV self-limited infection individuals, 244 asymptomatic HBsAg carriers and 391 chronic hepatitis B (HB) patients were recruited to conduct a case-control study. VDR-Taq I T/C and VDR-Fok I C/T polymorphisms were examined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).RESULTS:The frequency of VDR-Fok I allele C in the chronic HB patients was 45.8%, significantly higher than 38.2% of the self-limited infection individuals (chi(2) = 6.43, P = 0.01). The frequencies of VDR-Fok I genotypes TT, TC, and CC in HB patients were 30.7%, 47.1%, and 22.2% respectively, and 41.0% (TT), 41.5% (TC), and 17.5% (CC) in the self-limited infection individuals. There was a statistically significant difference between HB patients and self-limited infection individuals (chi(2) = 6.76, P = 0.03). The results of univariate analysis showed that the subjects carrying VDR-Fok I CC/TC genotype had 1.57-fold elevated risk for developing chronic HB when they were infected HBV (OR = 1.57, P = 0.01). A multiple logistic regression analysis revealed that VDR-Fok I CC/CT was independently associated with chronic HB after adjusting both potential confounding effects of gender (OR = 1.70, P = 0.021). The statistically significant association between TaqI T/C polymorphism and outcome of HBV infection was not demonstrated in the study. The frequency of haplotype TC of VDR-TaqI and Fok I in HB patients was 2.3080%, significantly higher than 0.5391% of the self-limited infection individuals (chi(2) = 6.08, P = 0.01). However, the frequency of haplotype TT in the HB patients was 1.5283%, significantly lower than 3.7061% of the self-limited infection individuals (chi(2) = 5.65, P = 0.02) and 3.4820% of the HBV carriers (chi(2) = 5.12, P = 0.02).CONCLUSION:VDR gene polymorphism is probably an influence factor on the genetic susceptibility of HBV infection.

Objective To clone human CCL3L1 cDNA and to express and purify the glutathione-S-transferase (GST) fusion protein and human CCL3L1 protein. Methods Total RNA was isolated from breast cancer cell line MCF7. CCL3L1 cDNA including open reading frame was obtained by RT-PCR. PCR product was digested with EcoR I and cloned into the pGEX-4T-1 vector. The plasmids from positive clone was prepared and sequenced to confirm the CCL3L1 in correct fusion form. pGEX-4T-CCL3L1 was transfected to BL21 E. coli via isopropyl-beta-D-thiogalactoside (IPTG) induction to produce GST-CCL3L1 fusion protein, which was further detected by SDS-PAGE and Western blotting. Results As shown and confirmed by restriction endonuclease digestion analysis, CCL3L1 was correctly inserted into pGEX-4T-1 vector. The expressed fusion protein had a relative molecular weight of approximately 34 kD. Conclusion GST-CCL3L1 fusion protein can be successfully expressed using appropriate vector.

OBJECTIVETo determine whether -Taq I T/C and -Fok I C/T polymorphisms of vitamin D receptor (VDR) gene are associated with the familial aggregation of hepatitis B virus (HBV) infection.METHODSBased on a population-based case-control family design, 288 family members from 27 case families and 230 family members from 27 control families were recruited. VDR gene polymorphisms were analyzed. VDR-Taq I T/C and VDR-Fok I C/T polymorphisms were examined by polymerase chain reaction-restriction fragment length polymorphism.RESULTSThe frequency of VDR-Taq I TT genotype in the case families was significantly higher than that in the control families (P < 0.05) , however, the frequency of VDR-Fok I CC genotype in the case families was significantly higher than that in the control families (P < 0.05). The frequency of family members carriying Taq I T-Fok I C haplotype in the case families was significantly higher than that in the control families (OR = 1.67, P < 0.05), however, the frequency of family members carrying Taq I C-Fok I T haplotype in the case families was significantly lower than that in the control families (OR = 0. 24, P < 0.05). The similar results were found in the familial biological kinship relatives with any HBV-infected makers.CONCLUSIONVDR-Taq I and -Fok I gene polymorphisms are likely to play a substantial role in HBsAg familial aggregation.

AIM: To investigate the correlation between the polymorphism of interleukin-10 (IL-10) gene promoters and the clinical phenotypes of hepatitis B virus (HBV) infection in Chinese population. METHODS: The genotypes of -819 locus in IL-10 promoter region were determined by polymerase chain reaction-sequence specific primer analysis (PCR-SSP), and those of -1082 and -592 loci in IL-10 promoter region were detected by polymerase chain restriction fragment length polymorphism analysis (PCR-RFLP) in patients with chronic hepatitis B (CHB, n = 478), selflimited HBV infection (SHI, n = 267) and chronic asymptomatic HBV carrier (AsC, n = 223). RESULTS: The allele A and genotype AA frequencies of -1082 locus in IL-10 promoter region were significantly higher in CHB patients than those in SHI patients and AsC (A: χ = 37.72, P = 0.000; χ = 45.23, P = 0.000; AA: χ = 20.53, P = 0.000; χ = 19.14, P = 0.000). The allele T and genotype TT of -819 locus in IL-10 promoter region were also markedly higher in CHB patients than those in SHI patients and AsC (T: χ = 10.5, P < 0.001; χ = 17.38, P < 0.001; TT: χ = 8.76, P = 0.003; χ = 5.656, P = 0.017). The polymorphism of -592 loci locus in IL-10 promoter region was not significantly different between the three groups (P > 0.05). CONCLUSION: The genetic polymorphism of interleukin-10 may be associated with the clinical phenotypes of HBV infection.

OBJECTIVE:To explore whether the vitamin D receptor gene (VDR) polymorphisms are associated with the outcomes of hepatitis B virus (HBV) infection in Chinese Han population.METHODS:Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to detect the polymorphisms of Fok I locus in exon 2 and Taq I locus in exon 9 of VDR gene. One hundred and eighty-four chronic hepatitis B patients and 205 asymptomatic HBV carriers were recruited to make the comparison of frequencies of genotype and haplotype of the VDR gene between the patients and the carriers.RESULTS:The univariate analysis showed a significant difference in Fok I polymorphism between chronic hepatitis B patients group and asymptomatic HBV carriers group. The FF genotype frequency in chronic hepatitis B patients group was 44.6%,higher than 31.7% in asymptomatic HBV carriers group (P<0.05). After adjusting the confounders by multiple logistic regression analysis, the result still showed a significant difference in Fok I site polymorphism between chronic hepatitis B patients group and asymptomatic HBV carriers group (OR=1.95, P<0.05). The FT haplotype frequency in chronic hepatitis B patients group was higher than that in asymptomatic HBV carriers group (OR=1.45, P<0.05). The fT haplotype frequency in chronic hepatitis B patients group was lower than that in asymptomatic HBV carriers group (OR=0.72, P<0.05).CONCLUSION:VDR gene polymorphism may be an influence factor of genetic susceptibility to HBV infection.

OBJECTIVE To explore whether the TNFA promoter single nucleotide polymorphisms (SNPs) are associated with the outcomes of hepatitis B virus(HBV) infection in Chinese Han population. METHODS One hundred and forty-eight self-limited HBV infection subjects and 207 chronic hepatitis B patients were recruited. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and sequence specific primer-PCR(PCR-SSP) were used to detect the SNPs of five sites in TNFA promoter (-238G/A, -308G/A, -857C/T, -863C/A, -1031T/C). The frequency distributions of genotypes and haplotypes in different groups were analyzed by EPI and EH programs. RESULTS The frequencies of -238GG genotype in chronic hepatitis B patients were significantly higher than that in self-limited infection subjects (P=0.02). The frequencies of -857TT genotype in chronic hepatitis B patients were clearly lower than that in self-limited infection subjects (P=0.02). Haplotypic frequencies of GGCCT (-238/-308/-857/-863/-1031) in chronic hepatitis B patients was significantly lower than that in self-limited infection subjects (P=0.03), and the frequencies of haplotype GGCAT or GGTAT in chronic hepatitis B patients were clearly higher than those in self-limited infection subjects (P=0.0001; P=0.004). CONCLUSION TNFA promoter polymorphisms are important host genetic factors affecting the outcomes of HBV infection.