Hepatitis B virus (HBV) is a major etiological agent for liver cirrhosis and hepatocellular carcinoma (1). The nature of the liver-specific HBV receptor(s) has been a longstanding puzzle in the field (2); this is partly attributable to the paucity of cell lines supporting productive HBV infection. Other than primary human hepatocytes (PHHs) and primary tupaia hepatocytes (PTHs), only the human liver progenitor cell line HepaRG could be infected with HBV after prolonged treatment with dimethyl sulfoxide (DMSO) (3). DMSO promotes the differentiation of HepaRG cell into foci of hepatocytes surrounded by biliary cells. Other human hepatoma cell lines such as HepG2 and Huh7 support HBV DNA replication and virion production upon transfection with cloned HBV genome but not after inoculation with HBV particles. HBV protein expression and genome replication are driven by several coterminal transcripts ranging from 0.7 to 3.5 kb (4). The subgenomic RNAs of 2.4 and 2.1 kb are responsible for the expression of three coterminal envelope proteins termed large (L), middle (M), and small (S), with the M protein having an extra preS2 domain than the S protein and the L protein having an extra preS1 domain than the M protein. In addition to their incorporation into virions, the envelope proteins, especially S and M, are secreted as capsid-free subviral particles that exceed virions by Ն1,000-fold. The large quantity of S protein associated with subviral particles is detected by enzyme-linked immunosorbent assay (ELISA) as hepatitis B surface antigen (HBsAg), which provides a sensitive serological marker of HBV infection. Another serological marker is hepatitis B e antigen (HBeAg), a secreted

Many Pseudomonas aeruginosa virulence traits that contribute to human infections are accepted as being associated with its environmental lifestyle. Therefore, identifying the molecular mechanisms that govern the lifestyle choice is of high significance. We previously reported that a mutation in suhB results in a decrease in swimming motility and increased biofilm formation compared to the wild-type strain. Yet, little is known about how this occurs. In this study, we demonstrated that SuhB inversely regulates motility and biofilm formation through the GacA-RsmY/Z-RsmA cascade. Mutations in gacA or the two small RNAs rsmY/rsmZ, or overproduction of the RsmA protein essentially rescued the motility defect of the suhB mutant. Additionally, we identified a c-di-GMP mediated mechanism for SuhB regulation of motility and biofilm formation. We showed that the ΔsuhB mutant displayed elevated levels of c-di-GMP, and the ΔsuhB motility and biofilm phenotypes could be switched by artificially decreasing c-di-GMP levels. Further experiments led to the identification of the diguanylate cyclase GcbA responsible for regulating the c-di-GMP concentration in ΔsuhB and hence the switch between planktonic and surface-associated growth. Together, our results demonstrate a novel mechanism for SuhB regulation of the lifestyle transition via the Gac/Rsm and c-di-GMP signaling networks in P. aeruginosa.

SUMMARY:The aim of this study was to analyze the molecular epidemiologic characteristics of Acinetobacter baumannii. A total of 398 isolates were collected in 7 regions of South China from January to June of 2012. Drug sensitivity was tested toward 15 commonly used antibiotics; thus, 146 multidrug-resistant strains (resistant to more than 7 drugs) were identified, representing 36.7z of all isolates. Pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MLST) were used for molecular subtyping. According to the PFGE results (with a cutoff of 70z similarity for the DNA electrophoretic bands), 146 strains were subdivided into 15 clusters, with cluster A being the largest (33.6z, distributed in all districts except Jiaxing). Cluster B was also widespread and included 14.4z of all strains. In addition, MLST results revealed 11 sequence types (ST), with ST208 being the most prevalent, followed by ST191 and ST729. Furthermore, 4 novel alleles and 6 novel STs were identified. Our results showed that multi-drug-resistant A. baumannii in South China shares the origin with other widespread strains in other countries. The nosocomial infections caused by A. baumannii have been severe in South China. Continuous monitoring and judicious antibiotic use are required.