The Mycobacterium tuberculosis complex (MTBC) consists of closely related species that cause tuberculosis in both humans and animals. This illness, still today, remains to be one of the leading causes of morbidity and mortality throughout the world. The mycobacteria enter the host by air, and, once in the lungs, are phagocytated by macrophages. This may lead to the rapid elimination of the bacillus or to the triggering of an active tuberculosis infection. A large number of different virulence factors have evolved in MTBC members as a response to the host immune reaction. The aim of this review is to describe the bacterial genes/proteins that are essential for the virulence of MTBC species, and that have been demonstrated in an in vivo model of infection. Knowledge of MTBC virulence factors is essential for the development of new vaccines and drugs to help manage the disease toward an increasingly more tuberculosis-free world.

Brucella spp., like other pathogens, must cope with the environment of diverse host niches during the infection process. In doing this, pathogens evolved different type of transport systems to help them survive and disseminate within the host. Members of the TolC family have been shown to be involved in the export of chemically diverse molecules ranging from large protein toxins to small toxic compounds. The role of proteins from the TolC family in Brucella and other ␣-2-proteobacteria has been explored little. The gene encoding the unique member of the TolC family from Brucella suis (BepC) was cloned and expressed in an Escherichia coli mutant disrupted in the gene encoding TolC, which has the peculiarity of being involved in diverse transport functions. BepC fully complemented the resistance to drugs such as chloramphenicol and acriflavine but was incapable of restoring hemolysin secretion in the tolC mutant of E. coli. An insertional mutation in the bepC gene strongly affected the resistance phenotype of B. suis to bile salts and toxic chemicals such as ethidium bromide and rhodamine and significantly decreased the resistance to antibiotics such as erythromycin, ampicillin, tetracycline, and norfloxacin. Moreover, the B. suis bepC mutant was attenuated in the mouse model of infection. Taken together, these results suggest that BepC-dependent efflux processes of toxic compounds contribute to B. suis survival inside the host.Brucella spp. are responsible for a zoonosis that causes a serious economical impact worldwide and a human disease that is difficult to treat (8,16,22). Brucella enters the host via the nasal, oral, and pharyngeal cavities, and after penetrating the mucosal epithelium, the organism is transported to the lymph nodes. During early infection, innate immunity mechanisms from the host contribute to reduce the initial number of infecting Brucella cells (38). Brucella has the ability to invade and survive within macrophages and nonphagocytic cells. After entering the host cell, Brucella is found in a membrane-associated vacuole (phagosome). Brucella subverts the intracellular endocytic pathway, bypassing the classical lysosomal pathway; the bacteria multiplicate and survive in a compartment associated with rough endoplasmic reticulum (for recent reviews, see references 33 and 69). By using this strategy, the bacterium escapes some bactericidal mechanisms (10).The outer membrane of Brucella is considerably hydrophobic compared to those of other ␣-2-proteobacteria and therefore more permeable to lipophilic compounds (54). Conversely, the hydrophobic character of the outer membrane makes Brucella relatively resistant to polycationic peptides. In other species, low permeability to hydrophobic compounds goes together with efflux systems to increase protection against toxic molecules (47). Therefore, this unusual characteristic of the outer membrane raises interesting questions about the physiology of Brucella spp. Some outer membrane proteins (76) and the O side chain component of the lipopolysaccharid...

The morphology and physiology of the oogenesis have been well studied in the vector of Chagas disease Rhodnius prolixus. However, the molecular interactions that regulate the process of egg formation, key for the reproductive cycle of the vector, is still largely unknown. In order to understand the molecular and cellular basis of the oogenesis, we examined the function of the gene Bicaudal C (BicC) during oogenesis and early development of R. prolixus. We show that R. prolixus BicC (Rp-BicC) gene is expressed in the germarium, with cytoplasmic distribution, as well as in the follicular epithelium of the developing oocytes. RNAi silencing of Rp-BicC resulted in sterile females that lay few, small, non-viable eggs. The ovaries are reduced in size and show a disarray of the follicular epithelium. This indicates that Rp-BicC has a central role in the regulation of oogenesis. Although the follicular cells are able to form the chorion, the uptake of vitelline by the oocytes is compromised. We show evidence that the polarity of the follicular epithelium and the endocytic pathway, which are crucial for the proper yolk deposition, are affected. This study provides insights into the molecular mechanisms underlying oocyte development and show that Rp-BicC is important for de developmental of the egg and, therefore, a key player in the reproduction of this insect.

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