Objective To investigate the correlation between hepatitis B virus (HBV)drug -resistance gene mutations and hepatocellular carcinoma (HCC).Methods The clinical data of treatment -experienced patients,who underwent examination for HBV drug -resistance gene mutations in Beijing Ditan Hospital from January 1 to December 31,2013,and still had detectable HBV DNA after being treated with nucleos(t)ide analogues,were collected.All the patients were followed up,and the development of HCC was considered as the clinical out-come.The correlation between drug -resistance gene mutations and the development of HCC in patients with HBV infection was analyzed. The chi -square test was used for comparison of categorical between groups,the t -test was used for comparison of continuous data between two groups,and the log -rank test was used for comparison of the incidence of HCC between two groups.Results A total of 227 patients were enrolled in this study.According to the results of the detection of HBV drug -resistance gene mutations,103 patients (103 /227, 45.37%)had no drug -resistance gene mutations and 124 (124 /227,54.63%)had drug -resistance gene mutations.There were no sig-nificant differences between the mutation group and the non -mutation group in HBV DNA load (5.19 ±1.60 log10 IU /ml vs 5.44 ±1.75 log10 IU /ml,t =-1.134,P =0.258)and the percentage of patients with liver cirrhosis (24.19% (30 /124)vs 16.50% (17 /103),χ2 =2.026,P =0.155).The median follow -up was 28 months (range 4 -58 months),and the incidence of HCC was 7.49% (17 /227).A-mong the patients with HBV drug -resistance gene mutations,12 (12 /124,9.68%)developed HCC,and among those without HBV drug-resistance gene mutations,5 (5 /103,4.85%)developed HCC.Among the patients who developed HCC,70.59% (12 /17)had HBV drug -resistance gene mutations at baseline;among the patients who did not develop HCC,53.33% (112 /210)had HBV drug -resistance gene mutations at baseline.Conclusion The patients with poor control of HBV DNA during antiviral therapy have a comparable incidence of HCC to those not treated with antiviral therapy,with a relatively high risk of developing HCC;the treated patients with HBV drug -resist-ance gene mutations may have a higher risk of HCC than those without such mutations,which needs to be confirmed by the studies with a longer follow -up period and a larger sample size.

Objective To construct the eukaryotic expression vector of HBEBP2 gene,and screen the exonic genes of proteins in hepatocytes interacting with HBEBP2.Methods The DNA fragment of HBEBP2 was amplified by PCR.The eukaryotic expression vector pGBKT7-HBEBP2 was constructed successfully by yeast-two hybrid system 3 and then transformed into yeast cells AH109.The transformed AH109 were then mated with yeast cells Y187 containing hepatic cDNA library plasmid.The diploid yeast cells were plated on synthetic dropout nutrient medium(SD/-Trp/-Leu/-His/-Ade) containing X-?-gal for the first selection.Library plasmids pACT2-DNA were extracted and co-transformed into yeast cell AH109 together with pGBKT7-HBEBP2.Then the yeast cells were plated on synthetic dropout nutrient medium(SD/-Trp/-Leu /-His/-Ade) containing X-?-gal for the second screening to eliminate false positive clones.The real positive clones were sequenced and analyzed by bioinformatics.Results Six proteins binding to HBEBP2 were screened,including human sapiens lactate dehydrogenase D,human sapiens mitochondrion,human sapiens mannose,human sapiens aldehyde oxidase,human sapiens serpin peptidase inhibitor and other two unknown proteins.Conclusions A novel class of proteins in hepatocytes interacting with HBEBP2 has been obtained.It is presumed that HBEBP2 protein is correlated with glycosylation,lipid metabolism and cell proliferation,etc.

Objective To explore the factors influencing the patients' treatment compliance infected with chronic hepatitis B virus, and provide some useful advices to improve patients compliance. Methods Data were collected through deep interviews with 9 patients and analyzed using a phenomenological hermeneutic method. Results Using generic analysis, the factors influencing patients' compliance fell in-to three themes: (1) The enforceability of the doctor's advice; (2)The factors of the patients their own, in-cluding the disease-related knowledge, the realization of how harmful the disease is, and past behavior habits; (3)The social factors, including economic situation, pressure of life, family care, and the supervision and guidance of health care workers. Conclusions In order to make the patients consciously adopt the doctor's advice, health workers should pay more attention to strengthen the enforceability of the doctor's ad-vice and health education, and focus on the impact of cognitive, psychological and social factors on pa-tients' compliance.

Cholestatic liver diseases (CHD) refers to a kind of liver disease in which accumulation of excessive bile due to various causes from inside and outside of the liver blocks the formation, secretion and excretion of bile, and thereby induce the normal bile flow unable to enter the duodenum. During the occurrence and development of CHD, intestinal microflora plays an important role in regulating bile acid metabolism, and immune response. In addition, CHD affects the composition, abundance and function of intestinal microflora, which in turn affects the synthesis and metabolism of bile acids. Hence, bile acids being an important signaling molecule for the occurrence and development of CHD plays role in the pathophysiological processes through bile acid transporters and nuclear receptors, such as farnesoid receptors. This paper briefly introduces the relationship between intestinal microecology and cholestatic liver disease based on the interrelationship among bile acid, intestinal flora and cholestatic liver disease, with a view to provide assistance in the treatment of cholestatic liver disease.

Normal intestinal microflora and microecology are essential for normal physiological functions in human body. Intestinal microflora imbalance is often observed in patients with alcoholic liver disease and manifests as abnormal number and constituent ratio of intestinal microflora, dysfunction of intestinal mucosal barrier, bacterial translocation, and intestinal endotoxemia, and it plays an important role in the development and progression of alcoholic liver disease. In addition, intestinal microflora also has influence on alcohol metabolism. Probiotics or fecal microbiota transplantation can regulate intestinal microflora and may play an active role in the treatment of alcoholic liver disease. Further studies are needed to discuss the standardized use of microecologics, dose selection, dosage form, and course of treatment during the prevention and treatment of alcoholic liver disease.

The clinical outcomes of chronic HBV infection are influenced by the interaction between virus, host and environmental factors. Several factors of host include age, sex, individual behavior, host genetic polymorphism and intestinal microflora, directly or indirectly affect the clinical outcome of chronic HBV infection. Therefore, in the management of chronic HBV infection, more attention need to be paid not only to antiviral therapy, but also to the impact of host factors in order to maximally improve the prognosis of patients.

HBV can interact with alcohol in various ways to cause liver damage. Heavy drinking can accelerate the progression of chronic hepatitis B and lead to a poorer prognosis; meanwhile, it can also affect the outcome and compliance in patients receiving antiviral therapy. The epidemiology of drinking in patients with chronic hepatitis B in China remains unclear, and further studies are needed to clarify the mechanism of interaction between alcohol and HBV. Drinking management should be strengthened in patients with chronic hepatitis B in clinical practice, in order to alleviate liver injury induced by alcohol.

BACKGROUNDTo construct recombinant vector expressing antisense RNA to CCR5 in eukaryotic cells and obtain recombinant pseudovirus, which will be used to block HIV-1 infection.

METHODSThe DNA fragment targeted against the initional part of CCR 5 mRNA translation was amplified by using RT-PCR from peripheral blood mononuclear cells (PBMCs) and cloned into retroviral vector pLXSN, then transfected into packaging cell (PA317) with lipofectAMINE. After 2-3 weeks selecting with G418, the pseudovirion in the survival cell's supernatant was detected with RT-PCR (FQ),then was used to infect NIH/3T3 cell.

RESULTSThe psuedovirion packed from expression vector of sense/antisense RNA to CCR5 had infected NIH/3T3 cell successfully. The vector had incorporated into its genome and transcripted into RNA.

CONCLUSIONSThe gene fragment of antisense RNA to CCR5 could be obtained from PBMCs and transfected into eukaryotic cell with retroviral vector. The results made a great foundation for studying its inhibiting effect on HIV-1 infection.

3T3 Cells ; Animals ; Eukaryotic Cells ; metabolism ; Gene Expression ; Genetic Vectors ; Mice ; Plasmids ; genetics ; RNA, Antisense ; genetics ; Receptors, CCR5 ; genetics ; Transfection

OBJECTIVETo study the quantity of anti-R7V in individuals infected with HIV and AIDS patients and its relation with the progression of disease.

METHODSELISA and precipitation and other methods were used to investigate the quantity of anti-R7V in asymptomatic long-term survivors and AIDS patients.

RESULTSPositive rate and quantity of anti-R7V were higher in the HIV active ones and AIDS. It showed that the quantity and positive rate of anti-R7V were rather high in dissolving test.

CONCLUSIONSIt is strong suggestion for anti-R7V to obstruct the replication of virus by interfering the connection between HIV with CCR5 or CXCR4 and so it impossible HIV entering to CD4+ T cells.

Acquired Immunodeficiency Syndrome ; immunology ; Adolescent ; Adult ; Aged ; Child ; Female ; Follow-Up Studies ; HIV Antibodies ; blood ; HIV Infections ; immunology ; HIV Long-Term Survivors ; HIV-1 ; immunology ; Humans ; Male ; Middle Aged ; Receptors, CCR5 ; physiology ; Receptors, CXCR4 ; physiology

Chronic HBV infection can generally be divided into four stages according to the natural course of disease. Clinically, the determination of different natural stages of chronic HBV infection is crucial for patients to start antiviral therapy and to avoid missing the antiviral opportunity and progressing to cirrhosis. In particular, it is a challenge for clinicians to distinguish the immune control stage from the reactive stage. As a novel marker of HBV, the quantitative detection of HBV core-associated antigen (HBcrAg) is of value for the identification of the HBV infection stages. This article reviews the research progress of HBcrAg in the identification of different stages of chronic HBV infection.