There is around 10% people who can’t produce sufficient antibody after hepatitis B virus (HBV) vaccine injection. In order to find the mechanism of HBV vaccine non-responsiveness, 108 volunteers were unified injected HBV vaccine (10 μg/shot) three times. They were divided into non-responders with negative HBV surface antibody (HBsAb) titer and high responders with HBsAb titer about 1 000 mIU/ml. The plasma proteome were analyzed by two-dimensional fluorescence difference gel electrophoresis (2D-DIGE) technology after depletion of 14 high abundant proteins by multiple affinity removal system (MARS) column. 11 differential expressed proteins were identified by matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF-MS). Among these proteins, α1-microglobulin and kininogen-1 was up-regulated in nonresponders compared to high responders, while α1-antichymotrypsin, vitamin D binding protein, Afamin, antithrombin Ⅲ and vitronectin were down-regulated. After extensive validation by Western blotting and enzyme-linked immunosorbent assay (ELISA), the differential expression level of α1-antichymotrypsin, kininogen and α1-microglobulin were confirmed. These results suggest that those proteins are associated with the responsive state of HBV vaccine, thus may serve as potential biomarkers for assessing the immune response among diverse HBV vaccine responders and shed light on the mechanism of immunologic unresponsiveness.

To study the impact of coxsackievirus B3 2A protease on nuclear factor κB (NF-κB ), BHK cells were transfected with a plasmid pcDNA3.1-2A expressing CVB3 2A protease along with pGL3-NF-κB -promotor-luc. The activity of luciferase was detected to identify the relative effect of NF-κB upon tumor necrosis factor α (TNF-α) stimulation. The dimerization of NF-κB /p65 were also detected with Western blotting and translation of NF-κB /p65 was observed by immunofluorescence. The results showed that CVB3 2A protease not only inhibited the expression of luciferase activities from NF-κB /p65 promoter but also interfered the nuclear translocation of NF-κB /p65. CVB3 2A protease still inhibited the dimerization of NF-κB /p65. It is concluded that CVB3 protease 2A inhibits the activation of NF-κB pathway.

The classical dengue fever (DF) and dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS) caused by dengue virus (DV) are the most important infection diseases mediated by arthropod-borne viruses. The pathogenesis of DV infection is not completely clear and there is no licensed vaccine or specific antiviral drug available currently. Envelope (E) protein of DV plays an important role in pathogenesis and immunity response. In this study, the recombinant E/pGEX-6P-1 plasmid expressing E protein of dengue virus serotype 2 (DV2) was constructed. After optimizing the expression conditions, including the optimum temperature and incubation time, high purity of E protein could be obtained and it could induce high titre of specific antibodies against DV2 in BALB/c mice. This study will provide useful information to further understand the function and application of DV E protein.

Scirpusin A and Scirpusin B, two stilbene dimmers purified from medicinal plants, showed potent anti-viral activity. In this study, human immunodeficiency virus (HIV) envelope and vesicular stomatitis virus G protein (VSV-G)-pseudotyped HIV-1 as well as laboratory-adapted HIV-1 strain IIIB were used to evaluate the effects of these two compounds against HIV-1 in vitro. The results indicated that Scirpusin A and Scirpusin B prevented infection of TZM-bl cell line (susceptible to HIV-1 infection) by pseudotyped HIV-1 and laboratory strain IIIB in vitro. Scirpusin B showed a little higher activity than Scirpusin A. The 50% inhibitory concentration (IC50) of the latter was 1.33 μmol/L while the IC50 of the former was 4.77 μmol/L. Scirpusin A and Scirpusin B also showed similar effects on inhibiting VSV-G pseudotyped HIV-1 in TZM-bl cells, suggesting these two compounds can affect the cellular replication process of HIV-1. The preliminary study indicates that Scirpusin A could play antiviral roles after virus entering cell. The detailed mechanism is still a long way to go.

To investigate the drug resistance of Acinetobacter baumannii (A. baumannii) isolated from long-term hospitalized elderly patients in our hospital. A total of 52 isolates of A. baumannii were isolated from September, 2011 to August 2012 from elderly nosocomial patients in our hospital. The types of enzyme production, biofilm-forming ability, drug resistance and carrying resistance genes were tested. The infection of A. baumannii most frequently occurred in respiratory intensive care unit. The main separation sampling was sputum specimens (86.54%)．The multi-drug resistant A. baumannii strains were identified mostly (76.92%). A. baumannii isolates showed the lowest resistant rate to cefoperazone-sulbactam, which was 30.77%. The resistant rates to other antimicrobial agents were over 50%. The positive rate of enzyme production was 82.69%, and the most common production was other hydrolytic enzymes (63.46%). The biofilm-forming strains accounted for 5.77% of the isolates. 9 kinds of resistance genes were found in these 6 extensively drug-resistant strains. The study indicates that the grim situation of drug resistance of A. baumannii isolated from long-term hospitalized elderly patients. It is necessary to strengthen the monitoring of drug resistance, especially in respiratory intensive care unit. Meanwhile, drug resistance surveillance and disinfection and isolation should be strengthened in the endemic areas from where the biofilm-positive strains were isolated, so as to prevent and control the production and spread of multi-drug resistant and extensively drug resistant bacteria.

The pathogenesis of Staphylococcus epidermidis (S. epidermidis) in persistent infections is primarily attributed to its ability to form biofilms on the surface of indwelling medical devices. The antibiotic tolerance of biofilm is partly due to the presence of persister cells, however, the mechanism of bacterial persistence is poorly understood. In Escherichia coli (E. coli), PhoU was reported as a persistence switch involved in persister formation and tolerance to multiple antibiotics and stresses. There are two phoU homologues (serp0956 and serp0316) in S. epidermidis. As a component of pst operon, serp0956 was designated phoU1. The other phoU homologue serp0316 which encoded a hypothetical protein was named phoU2. Our previous study revealed that deletion of phoU1 in SE1457 had no effects on biofilm formation capacity. In this report a preliminary study on phoU2 was conducted. The relative transcriptional level of phoU2 in logarithmic phase (6 h) was higher than that in stationary phase (12 h) by using quantitative real-time polymerase chain reaction (PCR). PhoU2 was expressed in E. coli with a prokaryotic expression recombinant plasmid and purified to immunize BALB/c mice by intraperitoneal injection of anti-PhoU2 antiserum. Western blotting was carried out using PhoU2 polyclonal antibody as primary antibody to monitor PhoU2 expression in S. epidermidis. It was shown that there was continuous expression of PhoU2 in both exponential and plateau phases. The expression of PhoU2 was also detected in several clinical isolates of S. epidermidis. These results indicate that PhoU2 is conserved in different strains of S. epidermidis and suggeste that PhoU2 may function as a homologue of PhoU in S. epidermidis. These data allowe us to further characterize the role of PhoU2 in the formation of biofilm and persisters in S. epidermidis.

Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis (EBV-HLH) is a rapidly progressive disease with a high rate of mortality. In the patients with EBV-HLH, hypercytokinemia plays a major pathogenetic middle mechanism. The clinical manifestations were various and its diagnosis should meet HLH 2004 criteria as well as EBV-positive. In terms of treatment, the combination of dexamethasone, etoposide and cyclosporin A is the first choice. If they do not work，hematopoietic stem cell transplantation can be done. The recent progress on diagnosis and treatment of EBV-HLH is reviewed in the present paper.

Hepatitis C virus (HCV) is one of the most successful human pathogens. Most of acute HCV infections are rapidly developed to chronic infections, which leads to liver cirrhosis and ultimately to hepatocellular carcinoma (HCC). A protective vaccine is not yet available, and current therapeutic options can only result in sustained virus clearance in a small population. MicroRNAs (miRNAs) are small non-coding RNAs functioning as negative regulators of host gene expression. Until now, microRNA-122 (miR-122) and its application in HCV infection have been the focus of different published studies, leading to studying HCV infection and to identifying new therapeutic targets. This review will highlight the impacts of miR-122 on HCV replication and the possible miRNA targets for therapy of chronic hepatitis.

Since antiretroviral therapy was implemented in pregnant women infected with human immunodeficiency virus (HIV), the success rate of prevention of mother-to-child transmission (PMTCT) of HIV has been increased significantly. And some antiviral drugs, such as efavirenz and tenofovir, have gradually been proven to be safe for pregnant women and fetus. The range of options for PMTCT drugs is increased.