Academic literature on the topic 'Faible virulence'

Abstract Symptoms of Meloidogyne naasi invasion, development and reproduction were compared on 17 cloned ryegrass (Lolium multiflorum and L. perenne) plants, previously classified as susceptible (5 clones) or resistant (12) to a Welsh population. Observations on galling and reproduction confirmed the classification of most clones but some intermediate host status phenotypes were distinguished. Smaller root size at and immediately after inoculation was related to the generally poorer host status of L. perenne clones compared with those of L. multiflorum. Root axes number or size was not related to resistance and susceptiblity in either ryegrass species. In ryegrasses, resistance was expressed by slower nematode development rates, fewer females matured and those that laid eggs were less fecund. Gall numbers at 36 days after inoculation reliably predicted host status. A poor host cultivar of Phleum pratense included some plants on which a few galls with fully fecund females developed. The selected ryegrass clones maintained their phenotype when tested with populations of M. naasi from Belgium and France. Nonetheless, it cannot be concluded from these experiments that there is no heterogeneity for virulence in these nematode populations. Resistance du ray-grass, Lolium spp., a trois populations europeennes du nematode a galle Meloidogyne naasi - Les symptomes causes par la penetration, le developpement et la reproduction de Meloidogyne naasi ont ete compares chez 17 clones de ray-grass (Lolium multiflorum et L. perenne) dont 5 consideres auparavant comme sensibles et 12 comme resistants a une population provenant du Pays de Galles. Les observations relatives a la formation des galles et a la reproduction confirment la qualification de la plupart de ces clones mais quelques phenotypes a statut d'hote intermediaire ont ete detectes. Une longueur de racines plus faible au moment de et immediatement apres l'inoculation est en general correlee au statut d'hote mediocre des clones de L. perenne si on les compare a ceux de L. multiflorum. Le nombre et la taille des racines axiales ne sont correles ni a la resistance ni a la sensibilite chez aucune des especes de ray-grass. La resistance s'exprime chez le ray-grass par le taux plus faible du developpement du nematode, le moindre nombre de femelles matures et une fecondite moins elevee chez celles qui pondent des oeufs. Le nombre de galles releve 36 jours apres l'inoculation permet de predire le statut d'hote de facon fiable. Un cultivar de Phleum pratense a statut d'hote mediocre comportait cependant quelques plants presentant un petit nombre de galles contenant des femelles parfaitement fecondes. Les clones de ray-grass etudies ont conserve leur phenotype lors de tests envers des populations de M. naasi provenant de France et de Belgique. Ces experiences ne permettent cependant pas de conclure qu'il n'existe aucune heterogeneite dans la virulence de ces populations de nematode.

In this study we have tried to verify whether the interaction "in vitro" with bacteria or small pieces of normal hamster liver would modify the pathogenic behavior of axenic strains of E. histolytica: avirulent ones (ICB-32 and ICB-RPS), of attenuated virulence (ICB-CSP and HM1) and of mean virulence (ICB-462). Every attempt to render virulent, recover or increase the virulence of axenic strains of E. histolytica has failed

Abstract The present study describes different desiccation tolerance traits of three strains of Steinernema feltiae (IS-6, IS-15, and N8). A slow dehydration regime (pre-conditioning at 97% relative humidity \[RH] for 3 days at 23 degrees C) induced a quiescent anhydrobiosis state in all strains, which enabled them to survive at lower humidities (75% and 85% RH). The IS-6 strain isolated from the Negev desert region of Israel exhibited the best desiccation tolerance. The second best tolerance was observed in the IS-15 strain isolated from Galilee, in the northern part of Israel. The poorest tolerance was exhibited by the N8 strain, which was obtained from Germany. The higher desiccation tolerance of the IS-6 and IS-15 strains was associated with a dispersal response of the aggregated infective juveniles (IJs) at the slow dehydration regime. This allowed the coiled IJs to enter into anhydrobiosis individually, whereas the IJs of the N8 strain remained clumped together. In the present study, the IS-6 strain was chosen to determine the optimal conditions for induction into, and recovery from, anhydrobiosis. A high correlation (r = 0.875, P < 0.05) was found between the survival of individual IJs at 85% RH and the initial numbers of IJs (ranging from 70 to 7700) in the pre-conditioned clump. The same recovery rates of pre-conditioned IJs exposed to 85% RH over a period of 12 days were obtained with either direct immersion in distilled water or immersion in distilled water after 24 h exposure to 100% RH. No significant differences in virulence and ability to penetrate Tenebrio molitor larvae were observed between non-desiccated IJs and rehydrated IJs that had been pre-conditioned and desiccated for 5 days at 85% RH. Survie en etat de deshydratation du nematode entomopathogene Steinernema feltiae: induction de l'anhydrobiose - La presente etude decrit differents aspects de la tolerance a la dessiccation chez trois souches de Steinernema feltiae (IS-6, IS-15 et N8). Une deshydratation lente- preconditionnement a une humidite relative (RH) de 97% pendant 3 jours a 23 degrees C - induit un stade de quiescence anhydrobiotique chez toutes les souches, ce qui les rend capables de survivre a des humidites faibles (RH 75% et 85%). La souche IS-6 isolee dans le desert du Negev (Israel) fait montre de la meilleure tolerance a la dessiccation. Vient ensuite la souche IS-15 isolee en Galilee (partie nord d'Israel). La plus faible tolerance est celle de la souche N8 provenant d'Allemagne. La tolerance plus elevee a la dessiccation des souches IS-6 et IS-15 est associee a une reaction de separation des juveniles infestants (IJ) dans les agregats lors de la deshydratation lente. Cette separation est suivie d'une entree en anhydrobiose des separes, enroules sur eux-memes, tandis que les IJ de la souche N8 restent agglomeres. La souche IS-6 a ete choisie pour determiner les conditions optimales induisant l'anhydrobiose et la sortie de ce stade physiologique. Une forte correlation (r = 0,875, P < 0,05) a ete observee entre la survie des IJ separes a une RH de 85% et la presence d'agregats (comptant 70 a 7700 IJ) au moment du preconditionnement initial. Les memes taux de reviviscence sont obtenus, soit par immersion directe dans l'eau distillee, soit par exposition a une RH de 100% avant immersion dans l'eau. Aucune difference significative dans la virulence et la capacite a penetrer les larves de Tenebrio molitor n'a ete observee entre les IJ dessechees, apres le preconditionnement pendant 5 jours a une RH de 85% et les IJ n'ayant pas subi ce traitement.

ABSTRACTPrevious studies onCampylobacter jejunihave demonstrated the role of LuxS in motility, cytolethal distending toxin production, agglutination, and intestinal colonization; however, its direct involvement in virulence has not been reported. In this study, we demonstrate a direct role ofluxSin the virulence ofC. jejuniin two different animal hosts. The IA3902 strain, a highly virulent sheep abortion strain recently described by our laboratory, along with its isogenicluxSmutant andluxScomplement strains, was inoculated by the oral route into both a pregnant guinea pig virulence model and a chicken colonization model. In both cases, the IA3902luxSmutant demonstrated a complete loss of ability to colonize the intestinal tract. In the pregnant model, the mutant also failed to induce abortion, while the wild-type strain was highly abortifacient. Genetic complementation of theluxSgene fully restored the virulent phenotype in both models. Interestingly, when the organism was inoculated into guinea pigs by the intraperitoneal route, no difference in virulence (abortion induction) was observed between theluxSmutant and the wild-type strain, suggesting that the defect in virulence following oral inoculation is likely associated with a defect in colonization and/or translocation of the organism out of the intestine. These studies provide the first direct evidence that LuxS plays an important role in the virulence ofC. jejuniusing anin vivomodel of natural disease.

Lethal doses of 11 clinical and environmental isolates of Vibrio vulnificus were determined in suckling mice after oral challenge. With one exception, isolates that were virulent to iron-overloaded adult mice after intraperitoneal inoculation were highly lethal to the infant mice (>50% lethality at 105 CFU/mouse). The virulent isolate that failed to kill infant mice at 105 CFU had lost its invasiveness. Conditionally virulent isolates that were virulent only to simultaneously iron-overloaded and immunosuppressed adult mice required > 109 CFU to kill the infant mice. Avirulent isolates failed to kill at >109 CFU/mouse. There were no significant differences in the lethalities of clinical and environmental isolates. These findings demonstrated a close correlation between virulence in the iron-overloaded adult mouse and infectivity by the oral route.

In soybean, Rsv1, a single dominant resistance gene, invokes extreme resistance (ER) against most Soybean mosaic virus (SMV) strains, including SMV-N, but not SMV-G7, which provokes a virulent lethal systemic hypersensitive response (LSHR). The elicitor functions of the two viruses provoking Rsv1-mediated ER and LSHR have been mapped to the N-terminal 271 amino acids of P3 from SMV-N and SMV-G7, respectively, which differ by nine residues between the two strains. To identify amino acids of P3 from SMV-N provoking Rsv1-mediated ER, the unique residues of SMV-G7 were substituted with those of SMV-N. Of the mutants tested on Rsv1-genotype soybean, only SMV-G7I788R and SMV-G7T948A lost virulence. However, substitution of amino acids of SMV-N, individually or in combination, with the reciprocal residues from SMV-G7 at these two positions failed to confer virulence to SMV-N. In the search for additional virulence determinants, a series of SMV-N chimeras was generated in which fragments within a region from near the middle of the helper-component proteinase (HC-Pro) cistron to the 5′ end of the cytoplasmic inclusion cistron, nucleotides 1,605 to 3,787, were replaced with those of SMV-G7. Only SMV-N-derived chimeras harboring the 3′ region of HC-Pro, at least from nucleotide 2,013, and the entire 5′ end of P3 (nucleotides 2,430 to 3,237) from SMV-G7 were virulent whereas reciprocal exchanges resulted in loss of SMV-G7 virulence. This region of HC-Pro differs by three amino acids between SMV-N and SMV-G7. Analyses of SMV-G7-derived HC-Pro site-directed mutants showed that only SMV-G7M683R lost virulence on Rsv1-genotype soybean; however, SMV-NR682M failed to gain virulence. Nevertheless, an SMV-N derived mutant with three concurrent substitutions, R682M+R787I+A947T, gained virulence. The data indicate that both P3 and HC-Pro are involved in virulence of SMV on Rsv1-genotype soybean.

ABSTRACT The characterization of virulence determinants of pathogenic agents is of utmost relevance for the design of disease control strategies. So far, two classes of virulence determinants have been characterized for viral populations: those imprinted in the nucleotide sequence of some specific genomic regions and those that depend on the complexity of the viral population as such. Here we provide evidence of a virulence determinant that depends neither on a genomic sequence nor on detectable differences in population complexity. Foot-and-mouth disease virus is lethal for C57BL/6 mice showing the highest viral load in pancreas. Virus isolated from pancreas after one passage in mice showed an attenuated phenotype, with no lethality even at the highest dose tested. By contrast, virus from sera of the same mice displayed a virulence similar to that of the parental wild-type clone and virus isolated from spleen displayed an intermediate phenotype. However, viral populations from pancreas, spleen, and serum showed indistinguishable consensus genomic nucleotide sequences and mutant spectrum complexities, as quantified according to the mutation frequencies of both entire genomic nucleotide sequences of biological clones. The results show that the populations with differing virulences cannot be distinguished either by the consensus sequence or by the average complexity of the mutant spectrum. Differential harvesting of virus generated by cell transfection of RNA from serum and pancreas failed to reveal genetic differences between subpopulations endowed with differing virulences. In addition to providing evidence of hidden virulence determinants, this study underlines the capacity of a clone of an RNA virus to rapidly diversify phenotypically in vivo.

ABSTRACT Infectious bursal disease viruses (IBDVs), belonging to the familyBirnaviridae, exhibit a wide range of immunosuppressive potential, pathogenicity, and virulence for chickens. The genomic segment A encodes all the structural (VP2, VP4, and VP3) and nonstructural proteins, whereas segment B encodes the viral RNA-dependent RNA polymerase (VP1). To identify the molecular determinants for the virulence, pathogenic phenotype, and cell tropism of IBDV, we prepared full-length cDNA clones of a virulent strain, Irwin Moulthrop (IM), and constructed several chimeric cDNA clones of segments A and B between the attenuated vaccine strain (D78) and the virulent IM or GLS variant strain. Using the cRNA-based reverse-genetics system developed for IBDV, we generated five chimeric viruses after transfection by electroporation procedures in Vero or chicken embryo fibroblast (CEF) cells, one of which was recovered after propagation in embryonated eggs. To evaluate the characteristics of the recovered viruses in vivo, we inoculated 3-week-old chickens with D78, IM, GLS, or chimeric viruses and analyzed their bursae for pathological lesions 3 days postinfection. Viruses in which VP4, VP4-VP3, and VP1 coding sequences of the virulent strain IM were substituted for the corresponding region in the vaccine strain failed to induce hemorrhagic lesions in the bursa. In contrast, viruses in which the VP2 coding region of the vaccine strain was replaced with the variant GLS or virulent IM strain caused rapid bursal atrophy or hemorrhagic lesions in the bursa, as seen with the variant or classical virulent strain, respectively. These results show that the virulence and pathogenic-phenotype markers of IBDV reside in VP2. Moreover, one of the chimeric viruses containing VP2 sequences of the virulent strain could not be recovered in Vero or CEF cells but was recovered in embryonated eggs, suggesting that VP2 contains the determinants for cell tropism. Similarly, one of the chimeric viruses containing the VP1 segment of the virulent strain could not be recovered in Vero cells but was recovered in CEF cells, suggesting that VP1 contains the determinants for cell-specific replication in Vero cells. By comparing the deduced amino acid sequences of the D78 and IM strains and their reactivities with monoclonal antibody 21, which binds specifically to virulent IBDV, the putative amino acids involved in virulence and cell tropism were identified. Our results indicate that residues Gln at position 253 (Gln253), Asp279, and Ala284 of VP2 are involved in the virulence, cell tropism, and pathogenic phenotype of virulent IBDV.

ABSTRACT Highly virulent strains of Mycoplasma mycoides subsp.mycoides SC belonging to the African cluster contain an operon with the genes gtsA, gtsB, andgtsC, encoding membrane ATP binding cassette transporter proteins GtsA, GtsB, and GtsC, which are involved in glycerol transport. Strain Afadé from the African cluster incorporated [U-14C]glycerol with a time-dependent increase. The less virulent strain L2 of the European cluster, which lacksgtsB and gtsC, failed to incorporate glycerol. Antibodies against GtsB noncompetitively inhibited glycerol uptake.l-α-Glycerophosphate was not transported by M. mycoides subsp. mycoides SC. It is postulated to be synthesized by phosphorylation of glycerol during transport and subsequently metabolized further to dihydroxyacetone phosphate accompanied by release of H2O2. Peroxide production in glycerol-containing growth medium was high for the African strain Afadé but very low for the European strain L2. Virtually no H2O2 was produced by both strains without glycerol. Hence, the efficient glycerol uptake system found in the virulent strain of the African cluster leads to a strong release of peroxide, a potential virulence factor which is lacking in the less virulent European strains. M. mycoides subsp.mycoides SC might have adopted, as a strategy for virulence, a highly efficient uptake system for glycerol which allows the production of an active metabolic intermediate that damages host cells.

The pre-membrane protein (prM) of West Nile virus (WNV) functions as a chaperone for correct folding of the envelope (E) protein, and prevents premature fusion during virus egress. However, little is known about its role in virulence. To investigate this, we compared the amino acid sequences of prM between a highly virulent North American strain (WNVNY99) and a weakly virulent Australian subtype (WNVKUN). Five amino acid differences occur in WNVNY99 compared with WNVKUN (I22V, H43Y, L72S, S105A and A156V). When expressed in mammalian cells, recombinant WNVNY99 prM retained native antigenic structure, and was partially exported to the cell surface. In contrast, WNVKUN prM (in the absence of the E protein) failed to express a conserved conformational epitope and was mostly retained at the pre-Golgi stage. Substitutions in residues 22 (Ile to Val) and 72 (Leu to Ser) restored the antigenic structure and cell surface expression of WNVKUN prM to the same level as that of WNVNY99, and enhanced the secretion of WNVKUN prME particles when expressed in the presence of E. Introduction of the prM substitutions into a WNVKUN infectious clone (FLSDX) enhanced the secretion of infectious particles in Vero cells, and enhanced virulence in mice. These findings highlight the role of prM in viral particle secretion and virulence, and suggest the involvement of the L72S and I22V substitutions in modulating these activities.