J Clin Microbiol 2011,49(2):539–548.PubMedCrossRef 56. Kremer K, Arnold C, Cataldi A, Gutierrez MC, Haas WH, Panaiotov S, Skuce RA, Supply P, van der Zanden AGM, van Soolingen D: Discriminatory power and reproducibility of novel DNA typing methods for Mycobacterium tuberculosis

complex strains. J Clin Microbiol 2005,43(11):5628–5638.PubMedCrossRef Competing interests The other authors declare that they have no competing interests. Authors’ contributions PS, MM, JVV and PDV conceived the study and GW2580 chemical structure participated in its design and coordination. JVV and PDV provided the bacterial culture collection for the study. JZ participated in the design of the study, carried out the molecular work, performed the data analysis selleck chemicals llc and drafted the manuscript. PS coordinated the work and performed the statistical analysis.

All authors read and approved the final manuscript.”
“Background Toxoplasma gondii is an intracellular protozoan that infects many types of nucleated cells. It is estimated that approximately one-third of the world’s population is chronically infected with tissue cysts of this parasite [1]. Humans may be infected through ingestion of uncooked or under-cooked meat of intermediate hosts or the oocysts excreted by the definitive host, Felis catus. Ingested bradyzoites and tachyzoites invade host cells and cause acute infection. In humans, T. gondii infections may cause disseminating damage to the brain, eyes, lymph nodes and

even death in some immunocompromised individuals [2]. In pregnant women, this parasite can be transmitted to the fetus, resulting in tissue destruction, as well as developmental defects of the fetus or newborn [2]. In immunocompetent hosts, tachyzoites are converted into bradyzoites quickly, and a lifelong chronic infection is established. The molecular mechanism of host cell invasion by T. gondii has been extensively investigated [2]. During invasion, a T. gondii MGCD0103 clinical trial tachyzoite attaches to the host cell membrane and forms a moving junction (MJ) between the tachyzoite and the host Molecular motor cell membrane by releasing microneme proteins (MIC) and rhoptry neck proteins (RON) at the interface of the tachyzoite-host cell surface. Afterwards, the tachyzoite membrane and the host cell membrane remain in contact so that the MJ moves along the parasite’s surface until the parasitophorous vacuole (PV) is finally formed [3, 4]. The MJ works as a sieve to exclude many of the host transmembrane proteins but retains GPI-anchored or raft-associated multipass transmembrane proteins on the PV membrane (PVM) [3, 4].