The potential impact of intestinal microbiota on human health and related diseases is an emerging research field. Growing evidence of the role of intestinal microbiota in host digestion, metabolism and immune function has drawn great attention from the scientific community. Changes of gut microbiota may lead to a variety of disorders in metabolic system, liver and intestinal tract. Therefore, further studies on how microbiota exactly affects host health and related diseases are of fundamental importance in providing valuable guidance in the prevention and treatment of many diseases which have no available effective therapeutics.

Hepatitis C virus (HCV) protease NS3/4A cleaves mitochondrial antiviral signaling protein (MAVS) to evade host innate recognition and interferon production. However, HCV infection induces interferon production in certain cell types and HCV could replicate in cells expressing NS3/4A cleavage-resistant MAVS. The roles of NS3/4A-mediated MAVS cleavage in host innate evasion and restriction of viral replication need to be clarified. In this study, by using an HCV NS3/4A-mediated MAVS cleavage reporter system, in which Huh7.5 cells express GFP-NLS-MAVS-TM462, we dissected the kinetics of MAVS cleavage during HCV infection. It was found that MAVS was barely cleaved during the early time but was efficiently cleaved only in the late time during viral infection. Using ypet-tagged HCV virus and Huh7.5 cells expressing RFP-NLS-MAVS-TM462, we dissected the MAVS cleavage in the HCV-positive (ypet-positive) cells on a single-cell manner. It was found that MAVS cleavage occurred only in part of the HCV-infected cells. We also assessed the MAVS cleavage by HCV NS3/4A from different genotypes, and found the cleavage efficiency was correlated with the protein level of HCV NS3/4A. Taken together, we found NS3/4A-mediated MAVS cleavage occurs in the late stage during viral replication and is correlated with NS3 protein level. We proposed HCV NS3/4A-mediated MAVS cleavage does not contribute to host innate evasion during early viral replication step.

The present paper aims to investigate the role of interleukin 23 (IL-23) in facilitating Th1, Th2 and Th17 differentiation during respiratory syncytial virus (RSV) infection of epithelial cells (BEAS-2B). Lymphocytes were treated by supernatants from BEAS-2B cells with RSV or mock infection. Then they were blocked by specific anti-IL-23R antibody, anti-IL-23p19 antibody and p38 mitogen-activated protein kinase (MAPK) inhibitor (SB203580). The concentrations of cytokines such as interferon γ (IFN-γ), IL-4 and IL-17 were detected by enzyme-linked immunosorbent assay (ELISA). The mRNA expressions of transcription factors (t-bet, gata3, rorγt), signal transducers (stat4, stat6, stat3) were determined by real-time polymerase chain reaction (PCR). The results showed that the concentrations of cytokines (IFN-γ， IL-4 and IL-17) were significantly increased after RSV infection, accompanied with the enhanced expressions of transcription factors. However, these cytokines and transcription factors were significantly decreased when IL-23 pathway was blocked by antibodies. The blockage of p38 MAPK signal pathway showed the same results. The results suggest that IL-23 could facilitate Th1, Th2 and Th17 differentiation in RSV-infected BEAS-2B cells, which might be associated with p38 MAPK signal pathway.

One H6N6 subtype avian influenza virus 〔A/environment/Zhenjiang/zj18/2013 (en/zj18)〕 was isolated from a live poultry market in Zhenjiang in an epidemiological surveillance and was subjected to genome sequencing and further analysis. Next-generation sequencing (NGS) by Illumina MiSeq Platform was used to obtain the complete genome sequence from the isolated virus. MEGA5.0 software was used to align the eight fragments respectively. The phylogenetic and molecular characteristics of the isolate were analyzed by Neighbor-Joining method. BLAST searches demonstrated that the 8 genes (PB2, PB1, PA, HA, NP, NA, M and NS) had 96.7%－99.6% nucleotide identity with the ones on the H6N6 subtype reference viruses circulating in southeast China. The enzyme cleavage site on HA was PQIETR↓GL, which was the typical characteristic of the low pathogenic avian influenza virus (LPAIV). The key HA receptor binding sites were E190 and G228, indicating a preference binding for α2-3-linked sialic acids. The results suggest that it is necessary to strengthen the continuous surveillance of avian influenza A viruses.

To establish the characteristics of bacterial colonization and antibiotic resistance in the newborn in Neonatal Intensive Care Unit (NICU) of Beijing Obstetrics and Gynecology Hospital, Capital Medical University, pharyngeal swab specimens of hospitalized newborns in NICU were collected from August 1, 2014 to May 31, 2015, and subjected to bacterial culture and drug resistance analysis. A total of 677 swabs were included in this study and 34.0% were positive on culture detection. Among these positive cases, 159 (69.1%) were Gram-positive cocci, and 71 (30.9%) were Gram-negative bacilli. Streptococcus viridans, Kocuria kristinae and Staphylococcus epidermidis were the main colonized Gram-positive cocci. Escherichia coli, Acinetobacter baumannii and Klebsiella pneumoniae were the main colonized Gram-negative bacilli. Drug resistance of the isolates to commonly used antibiotics was studied and presented.

To analyze the bloodstream infection caused by extended-spectrum β-lactamase (ESBL)-producing Klebsiella pneumoniae (K. pneumoniae) in Shenzhen Nanshan District People’s Hospital, and investigate the risk factors and antimicrobial resistance characteristics of such infections, 107 cases with bloodstream infection caused by K. pneumoniae between January 2012 to September 2016 were selected for this study. According to the results of drug susceptibility testing, the patients were divided into the ESBL group (20 cases) and the non-ESBL group (87 cases). SPSS 19.0 software was used to analyze the data. Two of the leading causes for K. pneumoniae bloodstream infection were secondary infection by pulmonary (38.32%) and urinary tract (14.02%) respectively. Univariate analysis and logistic regression analysis confirmed that trauma and nosocomial infection were the risk factors of bloodstream infection caused by ESBL-producing K. pneumoniae. Antibiotic resistance in the ESBL group was significantly higher than the non-ESBL group. The isolates were sensitive to carbapenems. The mortality rate for all patients was 17.76%: 25% (5 of 20) for the ESBL group and 16.09% (14 of 87) for the non-ESBL group respectively. The results indicated that ESBL production is not the independent factor of mortality of K. pneumoniae bloodstream infection.

Rifampicin is mainly used for the treatment of tuberculosis. Early studied indicated it can cause adverse reactions such as thrombocytopenia in clinical applications, and we reported a severe thrombocytopenia in this case. Following the use of rifampicin, patient’s platelet count decreased to 4×10⁹/L. After immediate withdrawal of rifampicin plus other treatments, platelet count returned to the normal. The case suggested that in the process of rifampicin treatment, side effects should be closely observed. Routine blood biochemical examination, liver and kidney function should be monitored. When platelet count significantly decreased (less than 30×10⁹/L), rifampicin should be withdrawn immediately, and supplementary treatment such as platelet infusion should be given, and rifampicin should not be administered to such patients any more.

Hepatitis C virus (HCV) is a leading cause of hepatocellular carcinoma (HCC). HCV-induced hepatocarcinogenesis is a sequential process caused by viral factors and (or) chronic host inflammation status. Host genetic variation is now emerging as an additional element that contributes to one’s risk of developing HCC. Therefore, a comprehensive understanding of the molecular mechanisms for HCV-induced HCC will help to solve this problem.

In practice, Klebsiella pneumoniae (K. pneumoniae) can be divided into classic K. pneumoniae and hypervirulent K. pneumoniae with higher frequency of existence and characteristic performance of characterized virulence factors, such as capsules, lipopolysaccharides, adhesins and siderophores. Current research and clinical progresses on hypervirulent K. pneumoniae and associated virulence factors were reviewed and discussed.