Age-specific salivary immunoglobulin A response to Streptococcus mutans GbpB

In a follow-up study of children infected with Streptococcus mutans at an early age (children previously shown to respond poorly to S. mutans GbpB), there was a delay in their immune response, rather than a complete inability to respond to this antigen. Epitopes in the N-terminal third of GbpB were identified as targets for naturally induced immunoglobulin A antibody in children at an early age.14680480

Class II Transactivator (CIITA) Enhances Cytoplasmic Processing of HIV-1 Pr55Gag

The Pr55(gag) (Gag) polyprotein of HIV serves as a scaffold for virion assembly and is thus essential for progeny virion budding and maturation. Gag localizes to the plasma membrane (PM) and membranes of late endosomes, allowing for release of infectious virus directly from the cell membrane and/or upon exocytosis. The host factors involved in Gag trafficking to these sites are largely unknown. Upon activation, CD4+ T cells, the primary target of HIV infection, express the class II transcriptional activator (CIITA) and therefore the MHC class II isotype, HLA-DR. Similar to Gag, HLA-DR localizes to the PM and at the membranes of endosomes and specialized vesicular MHC class II compartments (MIICs). In HIV producer cells, transient HLA-DR expression induces intracellular Gag accumulation and impairs virus release.Here we demonstrate that both stable and transient expression of CIITA in HIV producer cells does not induce HLA-DR-associated intracellular retention of Gag, but does increase the infectivity of virions. However, neither of these phenomena is due to recapitulation of the class II antigen presentation pathway or CIITA-mediated transcriptional activation of virus genes. Interestingly, we demonstrate that CIITA, apart from its transcriptional effects, acts cytoplasmically to enhance Pr160(gag-pol) (Gag-Pol) levels and thereby the viral protease and Gag processing, accounting for the increased infectivity of virions from CIITA-expressing cells.This study demonstrates that CIITA enhances HIV Gag processing, and provides the first evidence of a novel, post-transcriptional, cytoplasmic function for a well-known transactivator

Biology of Streptococcus mutans-Derived Glucosyltransferases: Role in Extracellular Matrix Formation of Cariogenic Biofilms

The importance of Streptococcus mutans in the etiology and pathogenesis of dental caries is certainly controversial, in part because excessive attention is paid to the numbers of S. mutans and acid production while the matrix within dental plaque has been neglected. S. mutans does not always dominate within plaque; many organisms are equally acidogenic and aciduric. It is also recognized that glucosyltransferases from S. mutans (Gtfs) play critical roles in the development of virulent dental plaque. Gtfs adsorb to enamel synthesizing glucans in situ, providing sites for avid colonization by microorganisms and an insoluble matrix for plaque. Gtfs also adsorb to surfaces of other oral microorganisms converting them to glucan producers. S. mutans expresses 3 genetically distinct Gtfs; each appears to play a different but overlapping role in the formation of virulent plaque. GtfC is adsorbed to enamel within pellicle whereas GtfB binds avidly to bacteria promoting tight cell clustering, and enhancing cohesion of plaque. GtfD forms a soluble, readily metabolizable polysaccharide and acts as a primer for GtfB. The behavior of soluble Gtfs does not mirror that observed with surface-adsorbed enzymes. Furthermore, the structure of polysaccharide matrix changes over time as a result of the action of mutanases and dextranases within plaque. Gtfs at distinct loci offer chemotherapeutic targets to prevent caries. Nevertheless, agents that inhibit Gtfs in solution frequently have a reduced or no effect on adsorbed enzymes. Clearly, conformational changes and reactions of Gtfs on surfaces are complex and modulate the pathogenesis of dental caries in situ, deserving further investigation

Association between caries prevalence and clinical, microbiological and dietary variables in 1.0 to 0.5-year-old Brazilian children

The association between caries prevalence and clinical (presence of visible plaque in the labial surfaces of maxillary incisors), microbiological (salivary levels of mutans streptococci) and dietary variables was evaluated in 142 1.0- to 2.5-year-old children attending public day-care nurseries in the city of Piracicaba - Sao Paulo. A significant difference in caries prevalence was observed between those children with and without visible plaque (chi(2) = 12.08, p < 0.001). The mean ds (decayed surfaces) was significantly higher in children with visible plaque on the maxillary incisors than in children without it (p < 0.001). Mutans streptococci were detected in 114 (80.3%) of the children. A significantly higher caries prevalence was observed in children with high levels of mutans streptococci compared to children with low levels (chi(2) = 28.67, p < 0.001). The mean ds was significantly higher in children with levels of mutans streptococci greater than 50 CFU when compared to children with 0 CFU or 1-50 CFU of mutans streptococci (p < 0.05). Children who were either never breast-fed or only until 3 months exhibited a significantly higher caries prevalence than those breast-fed for a longer time (chi(2) = 4.11, p < 0.05). A significantly higher caries prevalence was also observed between children that used bottle containing milk with sucrose and cereal than children using bottle with milk with or without sucrose (chi(2) = 6.24, p < 0.05). Children who started to eat salty meals at or after 7 months of age showed a significant higher caries prevalence than children who started earlier (chi(2) = 10.30, p < 0.01). These data support the evidence of an association between caries prevalence in young children and mutans streptococci levels, clinical and dietary factors.32531932