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Computer analysis of the amino acid sequences in gp41 of apathogenic African green monkey (AGM) virus, less pathogenic HIV-2 and highly pathogenic SIV and HIV-1 lentiviruses.

The bestfit computer program was used to compare the amino acid sequence of the gp160 envelope glycoprotein of an apathogenic AGM and the pathogenic SIVAGM monkey lentiviruses. It was found that the gp120 envelope glycoproteins of these viruses resembled each other in their functional domains. However, an insert of 40 amino acids was found in the gp41 envelope glycoproteins of the pathogenic SIVAGM virus in the amino acid sequence between the membrane anchoring sequence and the carboxyterminus. The insert introduced a new "RRIR" proteolytic cleavage signal into gp41. Comparing HIV-1 gp41 to that of the pathogenic SIVAGM virus revealed that the HIV-1 sequence contains an "RR" sequence that also serves as a signal for proteolytic cleavage. Comparing HIV-2 gp41 to the apathogenic and pathogenic simian immunodeficiency viruses revealed that HIV-2 gp41 lacks the above proteolytic cleavage signal. It is hypothesized that the pathogenic human and simian immunodeficiency lentiviruses can be proteolytically cleaved at the carboxyterminus of gp41, releasing two peptides: a) an "immunodeficiency" 58 amino acid peptide and b) an IL-2-like peptide. The apathogenic AGM virus and the less pathogenic HIV-2 lack one proteolytic cleavage signal in the gp41 amino acid sequence and therefore can release only the IL-2-like peptide but not the "immunodeficiency" peptide. If indeed the pathogenic SIVAGM and HIV-1 do release an "immunodeficiency" peptide, then such a peptide can be regarded as a toxin. Immunization of healthy individuals or HIV-1 patients against the toxic effect of the viral gp41 toxic peptide might prevent damage to the immune system when the virus reactivation leads to ARC and AIDS in infected individuals. Synthetic peptides modeled according to the immunodeficiency peptide (the toxin) can be used to produce anti-toxin antibodies in healthy HIV-1 infected individuals. Such anti-toxin antibodies can be used for passive immunization of AIDS patients or for active immunization of HIV-1 positive individuals prior to ARC or AIDS.

Amino Acid Sequence↗

Chromosome structure and sequence organization between pathogenic and non-pathogenic Leishmania spp.

We have used a chromosome fragmentation strategy based on systematic genomic insertions of the rare cutting yeast I-SceI endonuclease to assess structure and sequence organization of homologous chromosomes between evolutionary divergent pathogenic and non-pathogenic Leishmania species. This method was combined to physical mapping and hybridization studies using a number of specific chromosomal markers as probes. Our studies have concentrated on two different chromosomes of Leishmania major (L. major), L. donovani and L. infantum and of the non-pathogenic species L. tarentolae. Specific chromosome fragmentation events at the level of multiple I-SccI genomic integrations indicated that very similar distances separated internal genomic sequences between homologous chromosomes and that distances from chromosome ends were more variable. The order and orientation of genes along the homologous chromosomes were also conserved between species. With only few exceptions, genome organization between pathogenic and non-pathogenic Leishmania species was found to be highly conserved. Genomic comparison of pathogenic and non-pathogenic species may be useful for depicting regions involved in species-specific related pathologies.

Animals↗

Do plant and human pathogens have a common pathogenicity strategy?

Recently, a novel 'two-step' model of pathogenicity has been described that suggests host-cell-derived vasculoproliferative factors play a crucial role in the pathogenesis of bacillary angiomatosis, a disease caused by the human pathogenic bacterium Bartonella henselae. The resulting proliferation of endothelial cells could be interpreted as bacterial pathogens triggering the promotion of their own habitat: the host cell. Similar disease mechanisms are well known in the plant pathogen Agrobacterium tumefaciens, which causes crown gall disease. There are notable similarities between the pathogenicity of A. tumefaciens leading to tumourous disease in plants and to the B. henselae-triggered proliferation of endothelial cells in humans. Here, we hypothesize that this pathogenicity strategy might be common to several bacterial species in different hosts owing to shared pathogenicity factors.

Agrobacterium tumefaciens↗

Host-pathogen interactions: Host resistance factor Nramp1 up-regulates the expression of Salmonella pathogenicity island-2 virulence genes.

Nramp1 (Natural resistance-associated macrophage protein-1; also known as Slc11a1) is a host resistance gene that provides protection against several intracellular pathogens, including Salmonella enterica serovar Typhimurium. Little is known about the dynamic interplay that occurs between mammalian host resistance determinants such as Nramp1 and pathogens during infection. To explore these interactions, we examined the effect of Nramp1 on expression of Salmonella typhimurium (STM) virulence factors. We demonstrate that Salmonella pathogenicity island 2 (SPI2) is essential for replication of STM in spleens of infected Nramp1(+/+) mice. Furthermore, the presence of Nramp1 in transfected cell lines and congenic knockout mice resulted in the up-regulation of STM SPI2-associated virulence genes critical for intramacrophage survival. This Nramp1-dependent up-regulation of SPI2 was mimicked in vitro by chelation of iron, demonstrating the iron-responsive nature of expression of STM SPI2-associated virulence genes. We propose that acquisition of SPI2 by S. enterica not only enabled this bacterium to become an effective intracellular pathogen but also allowed the bacterium to withstand the effects of macrophage defense mechanisms such as Nramp1 early in the evolution of its pathogenic character. These dynamic Nramp1-pathogen interactions may be essential for regulating the course of an infection. This study demonstrates the presence of a previously undescribed direct influence of a mammalian innate host resistance locus on a pathogen at the genetic level.

2,2'-Dipyridyl↗

Protective immune responses induced by a non-pathogenic simian/human immunodeficiency virus (SHIV) against a challenge of a pathogenic SHIV in monkeys.

A simian/human immunodeficiency virus (SHIV)-NM3n containing the human nef, but not the monkey nef, and vpr genes of SIV was inoculated into two cynomolgus monkeys, resulting in systemic infection with a minimum level of transient virus load. In order to study the nature of immune responses associated with the prevention of a pathogenic SHIV, the SHIV-NM3n-inoculated monkeys and three naive monkeys were intravenously challenged with a pathogenic SHIV containing the envelope gene of HIV-1 89.6. After the heterologous virus challenge, all of the SHIV-NM3n-inoculated animals completely avoided the loss of CD4+ T lymphocytes in PBMC as well as lymphoid tissues compared to pathogenic SHIV-injected control animals. The inhibition of CD4+ cell depletion was associated with maintaining the proliferative response of helper T-cells against SIV p27 in the previously nonpathogenic virus-inoculated animals following the pathogenic virus challenge. Furthermore, the decline of CD28+ cells, the increase in CD95+ cells, and the enhancement of in vitro apoptosis in PBMC were inhibited in the non-pathogenic virus-inoculated animals. These results suggest that nonpathogenic SHIV-NM3n infection induces the protection of monkeys from heterologous pathogenic viruses that may be associated with blocking the change in immune responses and the cell loss induced by a pathogenic virus.

AIDS Vaccines↗

Pathogenicity islands and the evolution of bacterial pathogens.

The term pathogenicity island has been used to refer to large chromosomal regions in pathogenic bacteria that encode virulence genes. This article reviews the recent history of this term and considers what characteristics define a pathogenicity island. It appears that pathogenicity islands can confer complex virulence phenotypes and were acquired by bacteria from unrelated organisms, leading to interesting hypotheses about how bacterial pathogens evolved. It is likely that mechanisms that generate pathogenicity islands continue to operate and may contribute to the emergence of bacterial pathogens with new virulence properties.

Bacteria↗

Dynamics of antibiotic resistance genes co-occurrence with pathogenic and non-pathogenic bacteria throughout wastewater treatment processes.

Wastewater treatment plants (WWTPs) are recognized hotspots for antibiotic resistance genes (ARGs) and pathogenic bacteria. Despite advancements in treatment technologies, the persistence of ARGs and pathogenic bacteria remains a concern. In this study, we analyzed the dynamic changes in ARGs and bacterial communities throughout the treatment processes within an anaerobic-anoxic-oxic (AAO) WWTP over one week by using HT-qPCR coupled with 16S rRNA gene amplicon sequencing. The connectedness index, based on network analysis, showed that the dynamics of ARGs and mobile genetic elements (MGEs) were more strongly associated with potentially pathogenic bacteria than with non-pathogenic bacteria, suggesting that ARG immigration and dissemination in the WWTP were likely driven by potentially pathogenic taxa. The AAO treatment significantly reduced ARGs in final effluent (EF) (∼64 %) and residual sludge (RS) (∼81 %); however, potential hosts of ARGs such as Comamonas testosteroni and Clostridioides difficile persisted with minimal changes in relative abundance and remained detectable in EF and RS. Notably, the abundance of ARGs was lower in RS than in EF, and source tracking analysis identified influent as the primary source of ARGs and potentially pathogenic taxa in EF, underscoring the greater health risks associated with effluent discharge.

Wastewater↗

Prevalence of the "high-pathogenicity island" of Yersinia species among Escherichia coli strains that are pathogenic to humans.

The fyuA-irp gene cluster contributes to the virulence of highly pathogenic Yersinia (Yersinia pestis, Yersinia pseudotuberculosis, and Yersinia enterocolitica 1B). The cluster encodes an iron uptake system mediated by the siderophore yersiniabactin and reveals features of a pathogenicity island. Two evolutionary lineages of this "high pathogenicity island" (HPI) can be distinguished on the basis of DNA sequence comparison: a Y. pestis group and a Y. enterocolitica group. In this study we demonstrate that the HPI of the Y. pestis evolutionary group is disseminated among species of the family Enterobacteriaceae which are pathogenic to humans. It prevails in enteroaggregative Escherichia coli and in E. coli blood culture isolates (93 and 80%, respectively), but is rarely found in enteropathogenic E. coli, enteroinvasive E. coli, and enterotoxigenic E. coli isolates. In contrast, the HPI was absent from enterohemorrhagic E. coli, Shigella, and Salmonella enterica strains investigated. Polypeptides encoded by the fyuA, irp1, and irp2 genes located on the HPI could be detected in E. coli strains pathogenic to humans. However, these E. coli strains showed a reduced sensitivity to the bacteriocin pesticin, whose uptake is mediated by the FyuA receptor. Escherichia strains do not possess the hms gene locus thought to be a part of the HPI of Y. pestis. Deletions of the juA-irp gene cluster affecting solely the fyuA part of the HPI were identified in 3% of the E. coli strains tested. These results suggest horizontal transfer of the HPI between Y. pestis and some pathogenic E. coli strains.

Bacterial Outer Membrane Proteins↗

Animal health and foodborne pathogens: enterohaemorrhagic O157:H7 strains and other pathogenic Escherichia coli virotypes (EPEC, ETEC, EIEC, EHEC).

The majority of interactions between microorganisms and animals are based on convenient relations for both of them. Symbiotic microorganisms, like intestinal microbiota, produce important vitamins for animals and protects them from putative pathogens. In general, for monogastric animals, the main contribution of intestinal microorganisms is to supply with growth factors the animal diet, and in some cases they are responsible for providing essential vitamins (e.g. vitamin K). Some particular and relatively few microbes like viruses, bacteria, fungi, protozoa and algae are responsible for animal illness. Because microorganisms are easily dispersed, display physiological diversity, and tolerate extreme conditions, they are ubiquitous and may contaminate and grow in many products, including food and raw materials. Foodborne diseases are caused by consumption of contaminated food or beverages. Many different disease-causing pathogens can contaminate food, so there are many different foodborne infections. In addition, poisonous chemicals and biological toxins can cause disease if they are present in food. To know how a particular disease is spreading is an important matter to take appropriate steps to stop it. For example Escherichia coli O157:H7 infections can spread through contaminated food (meat, vegetables, cheese, etc.), contaminated drinking water or juices, contaminated swimming water and from person to person. Among foodborne pathogens, the most frequently detected are bacteria, but also parasitic protozoa and worms, viruses, natural toxins and other pathogenic agents like prions are important agents for foodborne diseases. Particular pathogenic types of E. coli, classified by their specific pathogenic mechanisms (toxins, adhesins, invasiveness, etc.) are actually known as E. coli virotypes. Enterohaemorrhagic E. coli (EHEC), which constitute the main part of this review, were also named verotoxigenic E. coli (VTEC) or Shiga toxigenic E. coli (STEC). EHEC strains cause haemorrhagic colitis (HC), haemolytic uremic syndrome (HUS) and thrombotic thrombocytopaenic purpura (TP) in humans. They synthetize shigatoxins (verotoxins) which are potent cytotoxic substances, adherence factors and enterohaemolysin. EHEC are responsible for many outbreaks of bloody diarrhoea caused by contaminated foods: beef, milk, fruits, juice, water, etc. The most important serogroups among EHEC are O26, O111 and O157, being O157:H7 the most relevant serotype in foodborne outbreaks. The normal intestinal microflora of cattle was found to be the most relevant reservoir of EHEC strains.

Animals↗

Effect of naturally occurring intramammary infections by minor pathogens on new infections by major pathogens in cattle.

New mammary infections were recorded in 3 dairy herds during a lactation period by bacteriologic examination of milk samples at 3-week intervals. Influences of the infection status of quarters at the time of new infection and of microorganisms responsible for bacterial invasion were analyzed. The new infection rate in uninfected quarters was about 3 times the rate in quarters already harboring bacterial considered minor pathogens (coagulase-negative staphylococci and Corynebacterium bovis) or major pathogens (Staphylococcus aureus, streptococci). The frequency of new infections with major pathogens was almost halved by preexisting infections with minor pathogens (P = 0.05), mainly because of coagulase-negative staphylococci (P = 0.05) and, to a lesser extent, C bovis (P = 0.19). New infections by minor pathogens also were less frequent in quarters harboring a major pathogen (P less than 0.05), indicating that the competition or antagonism between mammary infections was a general phenomenon.

Animals↗

In vivo interference between pathogenic and non-pathogenic viruses.

The interference among viruses is a well-documented biological phenomenon, both in animals and tissue culture systems. In two of our previous in vivo experiments and in four independent animal experiments, which are described in this presentation, interferences were successfully used to influence the outcomes of viral diseases by using non-pathogenic viruses. In this study, four pathogenic viruses were studied in their natural hosts, and against these viruses, in different combinations, 15 non-pathogenic viruses were tested. There was great variation in mutual effects among pathogenic and non-pathogenic viruses. In our four experiments, the viruses were either simultaneously inoculated or the non-pathogenic viruses were preinoculated. Newcastle disease vaccine (Strain H) had remarkable effects in the development of mouse ascites-associated lymphoma virus. The 50% mortality rate in mice caused by a vaccine strain of rabies virus was reduced to 15% using avian encephalitis virus. The clinical manifestations of rabbit myxoma virus effects were significantly delayed by Newcastle disease vaccine (Strain H). The 72% mortality rate due to Rous sarcoma virus in chickens was decreased to 33.3% when the animals were preinoculated with avian bursa virus vaccine.

Animals↗

Quinolone resistance in potentially pathogenic and non-pathogenic Escherichia coli strains isolated from healthy ruminants.

Quinolone resistance was studied in potentially pathogenic and non-pathogenic Escherichia coli strains from healthy ruminants. In cattle, 5.9% of the strains were resistant to nalidixic acid and 4.9% were resistant to enrofloxacin and ciprofloxacin, whereas in sheep and goats only 0.5% and 1.4%, respectively, of the strains were resistant to nalidixic acid and none to fluoroquinolones. Most of the strains resistant to quinolones were non-pathogenic strains isolated from cattle. However, the results of this study do not show that the potentially pathogenic E. coli strains isolated from healthy ruminants are more susceptible to quinolones than the non-pathogenic E. coli strains.

Animals↗

Determinants of pathogenicity in Xanthomonas campestris pv. vesicatoria are related to proteins involved in secretion in bacterial pathogens of animals.

One of the model systems investigated for studying plant bacterial pathogenesis is Xanthomonas campestris pv vesicatoria, the causal agent of bacterial spot disease of pepper and tomato. Genes necessary for both basic pathogenicity and the induction of the hypersensitive response in resistant plants (hrp genes) were previously isolated from X. c. pv. vesicatoria and characterized genetically. As a first step toward functional analysis, part of the hrp gene cluster, making up several loci, was sequenced. Here, we report the first indications of the function of hrp genes. Striking similarities to proteins from the mammalian pathogens Shigella flexneri, Yersinia enterocolitica, Y. pestis, and other bacteria were discovered. Proteins encoded by genes within the X. c. pv. vesicatoria loci hrpA, hrpB, and hrpC are similar to ATPases and to Yersinia Ysc and LcrD proteins, which are involved in secretion of Yop proteins, a particular class of essential pathogenicity factors produced by Yersinia species. This finding indicates, for the first time, that the fundamental determinants of pathogenicity may be conserved among bacterial pathogens of plants and animals. We hypothesize that hrp genes are involved in the secretion of molecules essential for the interaction of X. c. pv. vesicatoria with the plant.

Amino Acid Sequence↗

Douglas-fir root-associated microorganisms with inhibitory activity towards fungal plant pathogens and human bacterial pathogens.

A microbial culture collection composed of 1820 bacterial strains, including 298 actinomycete strains, was established from the roots of Douglas-fir (Pseudotsuga menziesii (Mirb.) Franco) seedlings harvested from conifer nurseries and forest sites. Two hundred and thirty-four strains inhibited the growth of Fusarium, Cylindrocarpon, and (or) Pythium spp. in in vitro assays. A significantly greater proportion of bacterial strains from actinomycete genera exhibited antifungal properties compared with bacterial strains from nonactinomycete genera. Eighty-nine percent of identified inhibitory strains were Streptomyces, Streptoverticillium, Bacillus, Pseudomonas, or Burkholderia species. The actinomycete species were isolated almost exclusively from forest seedlings. Recovery of inhibitory strains representing 29 microbial species was enhanced using a variety of methods to isolate microorganisms from the roots of seedlings from nursery and forest sites. Bacterial strains (including actinomycete strains) with antifungal activity were tested for in vitro growth inhibition of six clinical human bacterial pathogens (Enterococcus faecalis, Staphylococcus aureus, Klebsiella pneumoniae, Escherichia coli, Proteus mirabilis, and Pseudomonas aeruginosa). Forty-eight percent of the tested strains inhibited one or more human pathogens, Inhibitory activity towards fungal and bacterial pathogens was strain specific, not species specific, and many inhibitory strains exhibited broad-spectrum activity. Strains with antifungal activity against several conifer root pathogens were also more likely to inhibit multiple species of clinical bacterial pathogens.

Actinomycetales↗

Identification of pathogenic strains within serogroups of Yersinia pseudotuberculosis and the presence of non-pathogenic strains isolated from animals and the environment.

The existence of apathogenic strains of Yersinia pseudotuberculosis (Yp) has not so far been reported. Recently, the authors characterized new serogroups and a new subgroup in Yp, that is, O9, O10, O12, O13 and O14 and O1c, and the pathogenicity of these new strains was of interest. A total of 137 strains of serogroups O1c, O6, O7, O9, O10, O11, O12, O13 and O14 of Yp were investigated for their pathogenicity in vivo and in vitro. Although catalase activity and the inv gene were detected in all strains except those of groups O13 and O14, only a few strains, from serogroups O6 and O10 caused severe infection in mice. The remaining strains caused no mortality or severe infection even when they grew in limited tissues of infected mice. All the strains of Yp not possessing the virulence plasmid p YV caused no severe infection in mice. It is evident that less pathogenic Yp exists and that not only pathogenic but also less pathogenic Yp organisms exist in the same serogroup.

Animals↗

Plasma levels of the chemokine RANTES in macaque monkeys infected with pathogenic and non-pathogenic SIV/HIV-1 chimeric viruses at an early stage of infection.

Plasma levels of the chemokine RANTES were examined in monkeys infected with either a pathogenic simian and human immunodeficiency chimeric virus (SHIV) or a non-pathogenic SHIV to determine whether RANTES levels were related to the pathogenicity of the virus, the plasma viral load, or the kinetics of CD4+ T-cells. In the results no significant correlation was found between the RANTES kinetics and changes in the CD4+ T-cell numbers nor the plasma viral loads in any of the monkeys, although a transient decrease of the RANTES level was observed in the pathogenic virus-infected monkeys. At least, the plasma RANTES level can not be used as an index of the pathogenicity of the virus at the early stage of infection.

Animals↗

[Genetic differentiation with restriction patterns between pathogenic and non-pathogenic monoxenic Entamoeba histolytica].

UNLABELLED: Cysteine-proteinase of Entamoeba histolytica have been considered implicated like important virulence factors in the pathogenesis of amebiasis. On the basis of the differences in ethnic gene that encodes to 30 kDa proteinase. The present study validated a strategy to differentiate strains of pathogenic and non-pathogenic Entamoeba histolytica by restriction patterns. MATERIALS AND METHODS: Thirteen stool samples with Entamoeba histolytica cyst from 4 asymptomatic and 9 symptomatic patients ages and sex different into Robinson' medium were used. DNA obtained was used by amplified gene ethnic and it was cut with restriction enzyme Taq I and Hinf I. RESULTS: All strains were cultivated into Robinson's medium. A 530 bp fragment which hybridated with probe for Entamoeba histolytica was obtained. By the way valuation by restriction patterns with Taq I and Hinf I show that two of four samples of asymptomatic patients belong to pathogenic strain. It agrees with control strain positive HM-1:IMSS. Last 9 belonged to symptomatic patients with pathogenic strain. CONCLUSIONS: These results indicate that ethnic amplified by polymerase chain reaction is insufficiently to establish differential diagnostic. Therefore is necessary carry out enzyme digestion to identify pathogenic strain.

Animals↗