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At least 973 records · Page 54Linked to original sources
PubMed2002

tRNA gene clusters at the 3' end of rRNA operons are specific to virulent subgroups of Streptococcus agalactiae strains, as demonstrated by molecular differential analysis at the population level.

The aim of this work was to characterize a 2.4 kb randomly amplified polymorphic DNA (RAPD) fragment described as a marker for a phylogenetic group of Streptococcus agalactiae strains significantly associated with neonatal meningitis. This fragment was analysed by cloning and sequencing, and showed that two types of tRNA gene cluster flank the 3' end of the rRNA operons in S. agalactiae strains. Both types of tRNA gene cluster act as markers for phylogenetic subgroups of strains within the species. One type could be used to distinguish two of the three virulent intraspecies subgroups to which most of the S. agalactiae strains able to invade the central nervous system of neonates belong. This raises the possibility that there is a link between these tRNA genes and the virulence of the bacterium. Based on this analysis, PCR primers were designed to determine whether S. agalactiae strains are likely to belong to lineages of organisms in which most of the highly virulent strains isolated from cerebrospinal fluid cluster. In addition, this work demonstrated that RAPD can be used to detect novel particularities within intraspecies variants of pathogens.

Bacterial Typing Techniques↗
PubMed2000

Phylogenetic comparison of the DEN-2 Mexican isolate with other flaviviruses.

Recent attention has focused on the geographic variation of dengue viruses, since major epidemies may follow introduction of a new virus strain into susceptible populations. We cloned and sequenced a very interesting Mexican isolate (200787/1983) which is antigenically unique by signature analysis with respect to all other dengue-2 topotype viruses. This strain is also unique in biological behavior (neurotropism) and is of epidemiological significance in Mexico. The dengue-2 Mexican isolate sequence information was compared with that of other flaviviruses, analyzing the branching structure of the phylogenetic tree reconstructed from the E gene amino acid sequences. The E glycoprotein, is target for neutralizing antibodies and T-cell responses, and defines the tropism and virulence of flaviviruses. In the phylogram, our strain was located in the position of greatest dissimilarity within serotype-2. Also, frequency analysis of amino acids revealed a very different signature pattern from that found in viral serotype-2.

Amino Acid Sequence↗
PubMed2001

Molecular evolution of human echovirus 9 isolated from patients with aseptic meningitis in northern Kyushu during the summer of 1997.

An epidemic of aseptic meningitis caused by human echovirus 9 (E-9) occurred in the summer of 1997 in northern Kyushu, Japan. Sequences of genome position 2504-3358, which encoded a part of VP1, of the nine isolated viruses were determined. An RGD motif and B-C loop were found in all. They were almost identical and closely related to the virulent strain Barty.

Amino Acid Sequence↗
PubMed2001

Complete genome sequence of enterohemorrhagic Escherichia coli O157:H7 and genomic comparison with a laboratory strain K-12.

Escherichia coli O157:H7 is a major food-borne infectious pathogen that causes diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome. Here we report the complete chromosome sequence of an O157:H7 strain isolated from the Sakai outbreak, and the results of genomic comparison with a benign laboratory strain, K-12 MG1655. The chromosome is 5.5 Mb in size, 859 Kb larger than that of K-12. We identified a 4.1-Mb sequence highly conserved between the two strains, which may represent the fundamental backbone of the E. coli chromosome. The remaining 1.4-Mb sequence comprises of O157:H7-specific sequences, most of which are horizontally transferred foreign DNAs. The predominant roles of bacteriophages in the emergence of O157:H7 is evident by the presence of 24 prophages and prophage-like elements that occupy more than half of the O157:H7-specific sequences. The O157:H7 chromosome encodes 1632 proteins and 20 tRNAs that are not present in K-12. Among these, at least 131 proteins are assumed to have virulence-related functions. Genome-wide codon usage analysis suggested that the O157:H7-specific tRNAs are involved in the efficient expression of the strain-specific genes. A complete set of the genes specific to O157:H7 presented here sheds new insight into the pathogenicity and the physiology of O157:H7, and will open a way to fully understand the molecular mechanisms underlying the O157:H7 infection.

Bacterial Proteins↗
PubMed1995

Convergent evolution within the V3 loop domain of human immunodeficiency virus type 1 in association with disease progression.

Phylogenetic analysis was used to study in vivo genetic variation of the V3 region of human immunodeficiency virus type 1 in relation to disease progression in six infants with vertically acquired human immunodeficiency virus type 1 infection. Nucleotide sequences from each infant formed a monophyletic group with similar average branch lengths separating the sets of sequences. In contrast to the star-shaped phylogeny characteristic of interinfant viral evolution, the shape of the phylogeny formed by sequences from the infants who developed AIDS tended to be linear. A computer program, DISTRATE, was written to analyze changes in DNA distance values over time. For the six infants, the rate of divergence from the initial variant was inversely correlated with CD4 cell counts averaged over the first 11 to 15 months of life (r = -0.87, P = 0.024). To uncover evolutionary relationships that might be dictated by protein structure and function, tree-building methods were applied to inferred amino acid sequences. Trees constructed from the full-length protein fragment (92 amino acids) showed that viruses from each infant formed a monophyletic group. Unexpectedly, V3 loop protein sequences (35 amino acids) that were found at later time points from the two infants who developed AIDS clustered together. Furthermore, these sequences uniquely shared amino acids that have been shown to confer a T-cell line tropic phenotype. The evolutionary pattern suggests that viruses from these infants with AIDS acquired similar and possibly more virulent phenotypes.

Acquired Immunodeficiency Syndrome↗
PubMed2005

Stealth proteins: in silico identification of a novel protein family rendering bacterial pathogens invisible to host immune defense.

There are a variety of bacterial defense strategies to survive in a hostile environment. Generation of extracellular polysaccharides has proved to be a simple but effective strategy against the host's innate immune system. A comparative genomics approach led us to identify a new protein family termed Stealth, most likely involved in the synthesis of extracellular polysaccharides. This protein family is characterized by a series of domains conserved across phylogeny from bacteria to eukaryotes. In bacteria, Stealth (previously characterized as SacB, XcbA, or WefC) is encoded by subsets of strains mainly colonizing multicellular organisms, with evidence for a protective effect against the host innate immune defense. More specifically, integrating all the available information about Stealth proteins in bacteria, we propose that Stealth is a D-hexose-1-phosphoryl transferase involved in the synthesis of polysaccharides. In the animal kingdom, Stealth is strongly conserved across evolution from social amoebas to simple and complex multicellular organisms, such as Dictyostelium discoideum, hydra, and human. Based on the occurrence of Stealth in most Eukaryotes and a subset of Prokaryotes together with its potential role in extracellular polysaccharide synthesis, we propose that metazoan Stealth functions to regulate the innate immune system. Moreover, there is good reason to speculate that the acquisition and spread of Stealth could be responsible for future epidemic outbreaks of infectious diseases caused by a large variety of eubacterial pathogens. Our in silico identification of a homologous protein in the human host will help to elucidate the causes of Stealth-dependent virulence. At a more basic level, the characterization of the molecular and cellular function of Stealth proteins may shed light on fundamental mechanisms of innate immune defense against microbial invasion.

Amino Acid Sequence↗
PubMed2003

The ability to replicate in macrophages is conserved between Yersinia pestis and Yersinia pseudotuberculosis.

Yersinia pestis, the agent of plague, has arisen from a less virulent pathogen, Yersinia pseudotuberculosis, by a rapid evolutionary process. Although Y. pestis displays a large number of virulence phenotypes, it is not yet clear which of these phenotypes descended from Y. pseudotuberculosis and which were acquired independently. Y. pestis is known to replicate in macrophages, but there is no consensus in the literature on whether Y. pseudotuberculosis shares this property. We investigated whether the ability to replicate in macrophages is common to Y. pestis and Y. pseudotuberculosis or is a unique phenotype of Y. pestis. We also examined whether a chromosomal type III secretion system (TTSS) found in Y. pestis is present in Y. pseudotuberculosis and whether this system is important for replication of Yersinia in macrophages. A number of Y. pestis and Y. pseudotuberculosis strains of different biovars and serogroups, respectively, were tested for the ability to replicate in primary murine macrophages. Two Y. pestis strains (EV766 and KIM10(+)) and three Y. pseudotuberculosis strains (IP2790c, IP2515c, and IP2666c) were able to replicate in macrophages with similar efficiencies. Only one of six strains tested, the Y. pseudotuberculosis YPIII(p(-)) strain, was defective for intracellular replication. Thus, the ability to replicate in macrophages is conserved in Y. pestis and Y. pseudotuberculosis. Our results also indicate that a homologous TTSS is present on the chromosomes of Y. pestis and Y. pseudotuberculosis and that this secretion system is not required for replication of these bacteria in macrophages.

Animals↗
PubMed2005

Evolution of the equine infectious anemia virus long terminal repeat during the alteration of cell tropism.

Equine infectious anemia virus (EIAV) is a lentivirus with in vivo cell tropism primarily for tissue macrophages; however, in vitro the virus can be adapted to fibroblasts and other cell types. Tropism adaptation is associated with both envelope and long terminal repeat (LTR) changes, and findings strongly suggest that these regions of the genome influence cell tropism and virulence. Furthermore, high levels of genetic variation have been well documented in both of these genomic regions. However, specific EIAV nucleotide or amino acid changes that are responsible for cell tropism changes have not been identified. A study was undertaken with the highly virulent, macrophage-tropic strain of virus EIAV(wyo) to identify LTR changes associated with alterations in cell tropism. We found the stepwise generation of a new transcription factor binding motif within the enhancer that was associated with adaptation of EIAV to endothelial cells and fibroblasts. An LTR that contained the new motif had enhanced transcriptional activity in fibroblasts, whereas the new site did not alter LTR activity in a macrophage cell line. This finding supports a previous prediction that selection for new LTR genetic variants may be a consequence of cell-specific selective pressures. Additional investigations of the EIAV(wyo) LTR were performed in vivo to determine if LTR evolution could be detected over the course of a 3-year infection. Consistent with previous in vivo findings, we observed no changes in the enhancer region of the LTR over that time period, indicating that the EIAV(wyo) LTR was evolutionarily stable in vivo.

Adaptation, Physiological↗
PubMed2004

Host nutritional status: the neglected virulence factor.

The emergence of new infectious diseases and old diseases with new pathogenic properties is a burgeoning worldwide problem. Severe acute respiratory syndrome (SARS) and acquired immune deficiency syndrome (AIDS) are just two of the most widely reported recent emerging infectious diseases. What are the factors that contribute to the rapid evolution of viral species? Various hypotheses have been proposed, all involving opportunities for virus spread (for example, agricultural practices, climate changes, rainforest clearing or air travel). However, the nutritional status of the host, until recently, has not been considered a contributing factor to the emergence of infectious disease. In this review, we show that host nutritional status can influence not only the host response to the pathogen, but can also influence the genetic make-up of the viral genome. This latter finding markedly changes our concept of host-pathogen interactions and creates a new paradigm for the study of such phenomena.

Animals↗
PubMed1995

Application of a monoclonal antibody recognizing protein p30 to detect African swine fever virus-infected cells in peripheral blood.

Monoclonal antibody (MAb) 174F11.8 recognizes an epitope of the African swine fever (ASF) virus-induced protein, p30, a protein expressed on the plasma membrane of infected cells. This MAb has been used to analyze infected cell populations in peripheral blood of experimentally inoculated pigs with a virulent or attenuated ASF virus. Flow cytometric analysis of peripheral blood at different days postinfection using this MAb, showed expression of p30 mainly in the monocyte/macrophage cell lineage. Additionally, a small percentage of granulocytes also expressed p30 during infection. This methodology allowed the quantification of fluctuations in the pool of infected monocyte/macrophage cells in the inoculated pigs, maximum percentages ranging between 6 and 31%. Significant differences in the percentages of cell populations expressing p30 were not found between virulent or attenuated virus infection. However, a 2- to 4-day delay in the maximum percentage of cells expressing p30 was observed during infection with the attenuated virus when compared to virulent virus infection. Percentages of infected cells detected by the expression of p30 and viral titres obtained in peripheral blood showed positive correlation. Consequently, MAb 174F11.8 constitutes a marker to follow evolution of ASF virus infection, allowing quantification of percentages of infected cells in peripheral blood.

African Swine Fever↗
PubMed2006

Asymptomatic bacteriuria Escherichia coli strain 83972 carries mutations in the foc locus and is unable to express F1C fimbriae.

Escherichia coli is the most common organism associated with asymptomatic bacteriuria (ABU). In contrast to uropathogenic E. coli (UPEC), which causes symptomatic urinary tract infection (UTI), very little is known about the mechanisms by which these strains colonize the urinary tract. Bacterial adhesion conferred by specific surface-associated adhesins is normally considered as a prerequisite for colonization of the urinary tract. The prototype ABU E. coli strain 83972 was originally isolated from a girl who had carried it asymptomatically for 3 years. This study characterized the molecular status of one of the primary adhesion factors known to be associated with UTI, namely F1C fimbriae, encoded by the foc gene cluster. F1C fimbriae recognize receptors present in the human kidney and bladder. Expression of the foc genes was found to be up-regulated in human urine. It was also shown that although strain 83972 contains a seemingly intact foc gene cluster, F1C fimbriae are not expressed. Sequencing and genetic complementation revealed that the focD gene, encoding a component of the F1C transport and assembly system, was non-functional, explaining the inability of strain 83972 to express this adhesin. The data imply that E. coli 83972 has lost its ability to express this important colonization factor as a result of host-driven evolution. The ancestor of the strain seems to have been a pyelonephritis strain of phylogenetic group B2. Strain 83972 therefore represents an example of bacterial adaptation from pathogenicity to commensalism through virulence factor loss.

Agglutination↗
PubMed2000

[Fulminant streptococcus infection of soft tissue].

BACKGROUND: In recent years there has been an apparent increase in severe infections produced by group A beta-hemolytic Streptococci in developed countries. Necrotizing fascitis and myositis are two rare but fearsome complications caused by this microorganism. METHODS: Two cases of fulminant soft tissue infection recently observed in the authors' center are presented and the clinical presentation and differential diagnosis commented upon. RESULTS: The first case was a necrotizing fascitis at a surgical wound which appeared following a gynecological surgery. The second case reports gluteal myositis following intramuscular injection. In both cases the evolution was disastrous. CONCLUSIONS: Streptococcus pyogenes may produce fulminant infections in patients without underlying disease either spontaneously or following minimum traumas. The most frequent involvement is of the soft tissues. This virulence at a local tissue and systemic level has been associated with the production of exotoxin.

Diagnosis, Differential↗
PubMed2002

The genome of swinepox virus.

Swinepox virus (SWPV), the sole member of the Suipoxvirus genus of the Poxviridae, is the etiologic agent of a worldwide disease specific for swine. Here we report the genomic sequence of SWPV. The 146-kbp SWPV genome consists of a central coding region bounded by identical 3.7-kbp inverted terminal repeats and contains 150 putative genes. Comparison of SWPV with chordopoxviruses reveals 146 conserved genes encoding proteins involved in basic replicative functions, viral virulence, host range, and immune evasion. Notably, these include genes with similarity to genes for gamma interferon (IFN-gamma) receptor, IFN resistance protein, interleukin-18 binding protein, IFN-alpha/beta binding protein, extracellular enveloped virus host range protein, dUTPase, hydroxysteroid dehydrogenase, superoxide dismutase, serpin, herpesvirus major histocompatibility complex inhibitor, ectromelia virus macrophage host range protein, myxoma virus M011L, variola virus B22R, four ankyrin repeat proteins, three kelch-like proteins, five vaccinia virus (VV) A52R-like family proteins, and two G protein-coupled receptors. The most conserved genomic region is centrally located and corresponds to the VV region located between genes F9L and A38L. Within the terminal 13 kbp, colinearity is disrupted and multiple poxvirus gene homologues are absent or share a lower percentage of amino acid identity. Most of these differences involve genes and gene families with likely functions involving viral virulence and host range. Three open reading frames (SPV018, SPV019. and SPV020) are unique for SWPV. Phylogenetic analysis, genome organization, and amino acid identity indicate that SWPV is most closely related to the capripoxvirus lumpy skin disease virus, followed by the yatapoxvirus yaba-like disease virus and the leporipoxviruses. The gene complement of SWPV better defines Suipoxvirus within the Chordopoxvirinae subfamily and provides a basis for future genetic comparisons.

Animals↗
PubMed2004

Innate immunity in plants and animals: striking similarities and obvious differences.

Innate immunity constitutes the first line of defense against attempted microbial invasion, and it is a well-described phenomenon in vertebrates and insects. Recent pioneering work has revealed striking similarities between the molecular organization of animal and plant systems for nonself recognition and anti-microbial defense. Like animals, plants have acquired the ability to recognize invariant pathogen-associated molecular patterns (PAMPs) that are characteristic of microbial organisms but which are not found in potential host plants. Such structures, also termed general elicitors of plant defense, are often indispensable for the microbial lifestyle and, upon receptor-mediated perception, inevitably betray the invader to the plant's surveillance system. Remarkable similarities have been uncovered in the molecular mode of PAMP perception in animals and plants, including the discovery of plant receptors resembling mammalian Toll-like receptors or cytoplasmic nucleotide-binding oligomerization domain leucine-rich repeat proteins. Moreover, molecular building blocks of PAMP-induced signaling cascades leading to the transcriptional activation of immune response genes are shared among the two kingdoms. In particular, nitric oxide as well as mitogen-activated protein kinase cascades have been implicated in triggering innate immune responses, part of which is the production of antimicrobial compounds. In addition to PAMP-mediated pathogen defense, disease resistance programs are often initiated upon plant-cultivar-specific recognition of microbial race-specific virulence factors, a recognition specificity that is not known from animals.

Animals↗
PubMed1995

The evolution of invasion by enteric bacteria.

Despite differences in disease pathologies and host range, many enteric pathogens, including Salmonella and Shigella spp., utilize a remarkably similar machinery to secrete proteins that promote their entry into host cells. Analogous structures are required for the export of virulence proteins in other animal and plant pathogens. While the structure and organization of the gene complexes specifying these secretory pathways are broadly conserved, their phylogenetic distribution and genomic locations suggest that these sequences arose independently in divergent pathogens.

Antigens, Bacterial↗
PubMed2006

Sexual reproduction and the evolution of microbial pathogens.

Three common systemic human fungal pathogens--Cryptococcus neoformans, Candida albicans and Aspergillus fumigatus--have retained all the machinery to engage in sexual reproduction, and yet their populations are often clonal with limited evidence for recombination. Striking parallels have emerged with four protozoan parasites that infect humans: Toxoplasma gondii, Trypanosoma brucei, Trypanosoma cruzi and Plasmodium falciparum. Limiting sexual reproduction appears to be a common virulence strategy, enabling generation of clonal populations well adapted to host and environmental niches, yet retaining the ability to engage in sexual or parasexual reproduction and respond to selective pressure. Continued investigation of the sexual nature of microbial pathogens should facilitate both laboratory investigation and an understanding of the complex interplay between pathogens, hosts, vectors, and their environments.

Animals↗
PubMed2005

Non-gamma-proteobacteria gene islands contribute to the Xanthomonas genome.

Horizontal gene transfer, a process through which genomes acquire sequences from distantly related organisms, is believed to be a major source of genetic diversity in bacteria. A central question concerning the impact of gene transfer on bacterial genome evolution is the proportion of horizontally transferred sequences within genomes. Through BLAST search, we found that the genomes of two phytopathogens, Xanthomonas campestris pv. campestris and Xanthomonas axonopodis pv. citri, have close to 40% of the genes with the highest similarity to genes from phylogenetically distant organisms (non-gamma-proteobacteria). Most of these genes are found to be contiguous in the genome, forming genome islands, which may have been transferred from other organisms. Overall, the total number of genes within genome islands corresponds to almost one quarter of the entire xanthomonad genomes. Interestingly, many of the genes in these islands are functionally related to plant pathogenesis and virulence. Thus, these results suggest that horizontally transferred genes are clustered in the genome, and may facilitate fitness in new environments, as in the case of plant-bacteria interaction.

Evolution, Molecular↗
PubMed2005

Phylogenetic characteristics, genomic heterogeneity and symptomatic variation of five closely related Japanese strains of Potato virus X.

To elucidate the genomic determinants of Potato virus X (PVX) strains, which cause diverse responses in host plants, we determined the complete genomic RNA sequences of four Japanese PVX strains: PVX-BS, -BH, -OG, and -TO. These four strains, plus the previously sequenced PVX-OS strain, differ in their pathogenicity in wild potato (Solanum demissum) and tobacco (Nicotiana tabacum cv. Samsun NN). The genomic sequences of these five PVX strains were highly homologous (i.e., the nucleotide sequence identity ranged from 95.4 to 98.5%). Phylogenetic analysis indicated that the Japanese PVX strains originated from an ancestral PVX strain in the European group, and that the virulence of these strains in both S. demissum and tobacco is not correlated with their phylogenetic relationships, suggesting that the pathogenicity of each strain in these host plants is determined by a relatively small number of nucleotides and can easily be altered independent of phylogenetic relationships. Particularly, OS, BH, and BS, which respectively produce markedly contrasting ringspot, mosaic, and asymptomatic infections in tobacco leaves, were the most closely related, suggesting that these three strains are an attractive model for analyzing the genetic determinants causing these symptoms. A possible correlation between the genomic and biological differences of these strains is discussed.

Amino Acid Sequence↗