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[Group tuberculous contamination in preschoolers].

The study of a new collective tuberculosis contamination is proper for us to report news about the antituberculosis fight. In 1997, an ill teacher with cavity produced 19 cases of tuberculin turnings in a class with 25 children, but none of them had tuberculosis. We tried to find an explanation. We studied another 3 epidemiological events. In 1970, a teacher from Holbav produced 80 tuberculin turnings with 42 ill children. In Săcele another teacher with cavity produced 39 tuberculin turnings with 5 ill children. In Prejmer, in 1988 a sick child with cavity made himself 28 tuberculin turnings with a single case of illness. We tried to explain these differences: similar sources (patients with cavities) and the same conditions of illness but different effects. Our epidemiological investigations showed that in Holbav only 3.6% of children had BCG vaccine; in Săcele were 18%; in Prejmer were 98%; in Codlea 96%. BCG vaccination prevents tuberculosis. But in this case is another problem, did all the tuberculin turnings signify a virulent infection? After a year when we tested again the children, we found that for 58% of tuberculin turnings the reaction diminished considerably. We consider that, this is the particularity of the evolution of the postvaccinal allergy. We conclude that hyperreactivity may be a transitory exacerbation of the postvaccinal allergy and not an evidence of the infection. BCG vaccination reduces the risk of tuberculosis even when the infection is important and virulent.

BCG Vaccine↗
PubMed2005

Simian immunodeficiency virus (SIV) envelope quasispecies transmission and evolution in infant rhesus macaques after oral challenge with uncloned SIVmac251: increased diversity is associated with neutralizing antibodies and improved survival in previously immunized animals.

BACKGROUND: Oral infection of infant macaques with simian immunodeficiency virus (SIV) is a useful animal model to test interventions to reduce postnatal HIV transmission via breast-feeding. We previously demonstrated that immunization of infant rhesus macaques with either modified vaccinia virus Ankara (MVA) expressing SIV Gag, Pol and Env, or live-attenuated SIVmac1A11 resulted in lower viremia and longer survival compared to unimmunized controls after oral challenge with virulent SIVmac251 (Van Rompay et al., J. Virology 77:179-190, 2003). Here we evaluate the impact of these vaccines on oral transmission and evolution of SIV envelope variants. RESULTS: Limiting dilution analysis of SIV RNA followed by heteroduplex mobility assays of the V1-V2 envelope (env) region revealed two major env variants in the uncloned SIVmac251 inoculum. Plasma sampled from all infants 1 week after challenge contained heterogeneous SIV env populations including one or both of the most common env variants in the virus inoculum; no consistent differences in patterns of env variants were found between vaccinated and unvaccinated infants. However, SIV env variant populations diverged in most vaccinated monkeys 3 to 5 months after challenge, in association with the development of neutralizing antibodies. CONCLUSIONS: These patterns of viral envelope diversity, immune responses and disease course in SIV-infected infant macaques are similar to observations in HIV-infected children, and underscore the relevance of this pediatric animal model. The results also support the concept that neonatal immunization with HIV vaccines might modulate disease progression in infants infected with HIV by breast-feeding.

Animals↗
PubMed2004

Using the genome to understand pathogenicity.

Genome sequencing, the determination of the complete complement of DNA in an organism, is revolutionizing all aspects of the biological sciences. Genome sequences make available for scientific scrutiny the complete genetic capacity of an organism. With respect to microbes, this means we now have the unprecedented opportunity to investigate the molecular basis of commensal and virulence behavior. We now have genome sequences for a wide range of bacterial pathogens (obligate, facultative, and opportunistic); this has facilitated the discovery of many previously unidentified determinants of pathogenicity and has provided novel insights into what creates a pathogen. In-depth analyses of bacterial genomes are also providing new perspectives on bacterial physiology, molecular adaptation to a preferred niche, and genomic susceptibility to the uptake of foreign DNA, three key factors that can play a significant role in determining whether a species, or a strain, will have pathogenic potential.

Bacteria↗
PubMed2002

Host versus in vitro signals and intrastrain allelic differences in the expression of a Candida albicans virulence gene.

The yeast Candida albicans is a harmless colonizer of mucosal surfaces in healthy people but can become a serious pathogen in immunocompromised patients, causing superficial as well as systemic infections. The evolution of gene families encoding pathogenicity-related functions, like adhesins and secreted aspartic proteinases (Saps), which are differentially induced by host signals at various stages of colonization and infection, may have allowed C. albicans an optimal adaptation to many different host niches. We found that even the two alleles of a single gene can be differentially regulated in the diploid C. albicans. In the model strain SC5314, the in vitro expression of one of the two SAP2 alleles, SAP2-1, depended on the presence of a functional SAP2-2 allele. In contrast, inactivation of SAP2-1 did not in-fluence the expression of SAP2-2. The proteinase encoded by the SAP2-2 allele serves as a signal sensor and amplifier to enhance its own expression as well as to induce the SAP2-1 allele to achieve maximal proteolytic activity under appropriate conditions. Using in vivo expression technology, we could demonstrate that the SAP2-1 allele is significantly activated only in the late stages of systemic candidiasis in mice, whereas the SAP2-2 allele is induced much earlier. The differential regulation of the two SAP2 alleles was due to differences in their pro-moters, which contained a variable number of two pentameric nucleotide repeats. Mutations that reduced or increased the copy number of these repeats diminished the inducibility of the SAP2 promoter during infection but not in vitro, suggesting that the mutations affected interactions of regulatory factors that are necessary for SAP2 activation in vivo but dispensable for its induction in vitro. Therefore, the signals and signal transduction pathways that mediate SAP2 expression within certain host niches may differ from those that activate the gene in vitro. In addition to the generation of gene families whose members exhibit functional and regulatory diversification, C. albicans seems to use its diploid genome to create further variability and host adaptation by differential evolution of even the two alleles of a single gene.

Alleles↗
PubMed2001

Complete DNA sequence and analysis of the large virulence plasmid of Shigella flexneri.

The complete sequence analysis of the 210-kb Shigella flexneri 5a virulence plasmid was determined. Shigella spp. cause dysentery and diarrhea by invasion and spread through the colonic mucosa. Most of the known Shigella virulence determinants are encoded on a large plasmid that is unique to virulent strains of Shigella and enteroinvasive Escherichia coli; these known genes account for approximately 30 to 35% of the virulence plasmid. In the complete sequence of the virulence plasmid, 286 open reading frames (ORFs) were identified. An astonishing 153 (53%) of these were related to known and putative insertion sequence (IS) elements; no known bacterial plasmid has previously been described with such a high proportion of IS elements. Four new IS elements were identified. Fifty putative proteins show no significant homology to proteins of known function; of these, 18 have a G+C content of less than 40%, typical of known virulence genes on the plasmid. These 18 constitute potentially unknown virulence genes. Two alleles of shet2 and five alleles of ipaH were also identified on the plasmid. Thus, the plasmid sequence suggests a remarkable history of IS-mediated acquisition of DNA across bacterial species. The complete sequence will permit targeted characterization of potential new Shigella virulence determinants.

Amino Acid Sequence↗
PubMed2026

Precision Engineering of Evolution-Resilient Rice against Bacterial Blight.

The persistent conflict between rice and Xanthomonas oryzae pv. oryzae (Xoo), the causal agent of bacterial blight, exemplifies a dynamic genetic arms race in agriculture. The cyclical deployment and erosion of major resistance (R) genes highlight the high adaptive potential of Xoo and the need for strategies that are durable rather than absolute. This review synthesizes a paradigm shift from reactive, single R-gene deployment toward proactive engineering of evolution-resilient resistance. We explore the molecular-genetic basis of Xoo adaptability, including TAL effector diversification, non-TAL virulence functions, genome variation, and immune suppression mechanisms. In response, we propose a framework for durable disease management with three connected components: precision disarmament through editing of susceptibility-gene effector-binding elements and executor/decoy designs; smart induction through targeted delivery and immune priming; and ecological fortification through protective microbiomes. We also discuss the limits, trade-offs, and field-validation requirements of these approaches. Integrating frontier technologies with evolutionary genetics, predictive genomics, and pathogen population dynamics can help develop rice varieties and deployment systems that are more difficult for Xoo populations to overcome.

CRISPR↗
PubMed1999

Influence of the genetic background on the pattern of lesions developed by resistant and susceptible mice infected with Paracoccidioides brasiliensis.

To compare the sequential evolution of lesions developed by resistant (A/Sn) and susceptible (B10.A) mice to Paracoccidioides brasiliensis infection we inoculated a virulent isolate of the fungus and collected the pancreas/peripancreatic omentum monthly (from 1 to 6 months) post infection. After fixation, tissue sections were stained by conventional methods for light microscopy to investigate the cellular composition, the extracellular matrix (ECM) patterns and the morphology of the yeasts in the lesions. In both strains, the fungal lesions were localized mostly in the omentum; a few lesions in the pancreatic parenchyma were observed, mostly in B10.A mice. In both strains, macrophages and plasmocytes were the predominant cells in all lesions, followed by neutrophils (PMN) and macrophages transformed into giant and epithelioid cells. Remarkable differences were observed between resistant and susceptible mice, specially related to the ECM structure of the granulomatous lesions. In A/Sn mice, from the 1st month on, the coexistence of two types of lesions was observed: one type showed a well-defined encapsulated nodule, constituted mainly of type I collagen. Neutrophils were abundant in areas of massive fungal destruction and few viable yeasts were observed. The other type showed residual characteristics, with sparse collagen deposits and presence of xantomatous-like macrophages, containing degenerated fungi. Such residual lesions predominated after the 2nd month and were the only type observed from the 4th month on, indicating the control of the infection. In B10.A mice, on the contrary, only one type of lesion was observed, showing less tendency to encapsulation and the formation of multiple small granulomatous foci, individualized by reticular type III collagen fibers. There were many plasmocytes in the periphery and large numbers of budding yeasts, with no evidence of fungal destruction. In the course of the infection the lesions progressively increased in number and size. Altogether, the comparative histopathological analysis demonstrates the influence of the genetic pattern of the host on the lesions developed by resistant and susceptible mice to P. brasiliensis infection.

Animals↗
PubMed2006

Insertion sequences in prokaryotic genomes.

Insertion sequences (ISs) are small DNA segments that are often capable of moving neighbouring genes. Over 1500 different ISs have been identified to date. They can have large and spectacular effects in shaping and reshuffling the bacterial genome. Recent studies have provided dramatic examples of such IS activity, including massive IS expansion during the emergence of some pathogenic bacterial species and the intimate involvement of ISs in assembling genes into complex plasmid structures. However, a global understanding of their impact on bacterial genomes requires detailed knowledge of their distribution across the eubacterial and archaeal kingdoms, understanding their partition between chromosomes and extra-chromosomal elements (e.g. plasmids and viruses) and the factors which influence this, and appreciation of the different transposition mechanisms in action, the target preferences and the host factors that influence transposition. In addition, defective (non- autonomous) elements, which can be complemented by related active elements in the same cell, are often overlooked in genome annotations but also contribute to the evolution of genome organisation.

Bacteria↗
PubMed2006

Combinatorial genetic evolution of multiresistance.

The explosion in genetic information, whilst extending our knowledge, might not necessary increase our conceptual understanding on the complexities of bacterial genetics, or why some antibiotic resistant genotypes such as blaCTX-M-15 and blaVIM-2 appear to dominate. However, the information we have thus far suggests that clinical isolates have 'hijacked' plasmids, primarily built of backbone-DNA originating from environmental bacteria. Additionally, the combinatorial presence of other elements such as transposons, integrons, insertion sequence (IS) elements and the 'new' ISCR (IS common region) elements have also contributed to the increase in antibiotic resistance - an antibiotic resistant cluster composing four or five genes has become commonplace. In some instances, the presence of antibiotics themselves, such as fluoroquinolones, can mediate a bacterial SOS cell response, subsequently amplifying and/or augmenting the transfer of large genetic entities therefore, potentially promoting long-term detrimental effects.

Anti-Bacterial Agents↗
PubMed2003

The evolutionary genomics of pathogen recombination.

A pressing problem in studying the evolution of microbial pathogens is to determine the extent to which these genomes recombine. This information is essential for locating pathogenicity loci by using association studies or population genetic approaches. Recombination also complicates the use of phylogenetic approaches to estimate evolutionary parameters such as selection pressures. Reliable methods that detect and estimate the rate of recombination are, therefore, vital. This article reviews the approaches that are available for detecting and estimating recombination in microbial pathogens and how they can be used to understand pathogen evolution and to identify medically relevant loci.

Animals↗
PubMed2004

Vesicular stomatitis virus evolution during alternation between persistent infection in insect cells and acute infection in mammalian cells is dominated by the persistence phase.

Vesicular stomatitis virus has the potential for very rapid evolution in the laboratory, but like many other arboviruses, it evolves at a relatively slow rate in the natural environment. Previous work showed that alternating replication in different cell types does not promote stasis. In order to determine whether other factors promote stasis, we compared the fitness trajectories of populations evolving during acute infections in mammalian cells, populations evolving during persistent infections in insect cells, and populations evolving during alternating acute and persistent infection cycles. Populations evolving under constant conditions increased in fitness in the environment in which they replicated. An asymmetric trade-off was observed such that acute infection had no cost for persistence but persistent replication had a dramatic cost for acute infection in mammalian cells. After an initial period of increase, fitness remained approximately constant in all the populations that included persistent replication, but fitness continuously increased in populations evolving during acute infections. Determination of the consensus sequence of the genes encoding the N, P, M, and G proteins showed that the pattern of mutation accumulation was coherent with fitness changes during persistence so that once fitness reached a maximum, the rate of mutation accumulation dropped. Persistent replication dominated both the genetic and the phenotypic evolution of the populations that alternated between acute infection of mammalian cells and persistence in insect cells, and fitness loss was observed in the mammalian environment despite periodic replication in mammalian cells. These results show that stasis can be achieved without good levels of adaptation to both the mammalian and the insect environments.

Adaptation, Physiological↗
PubMed1987

Rapid evolution of RNA viruses.

The high error rate inherent in all RNA synthesis provides RNA virus genomes with extremely high mutation rates. Thus nearly all large RNA virus clonal populations are quasispecies collections of differing, related genomes (14, 49). These rapidly mutating populations can remain remarkably stable under certain conditions of replication. Under other conditions, virus-population equilibria become disturbed, and extremely rapid evolution can result. This extreme variability and rapid evolution can cause severe problems with previously unknown virus diseases (such as AIDS). It also presents daunting challenges for the design of effective vaccines for the control of diseases caused by rapidly evolving RNA virus populations.

Acute Disease↗