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At least 127 records · Page 7Linked to original sources

PubMed1994

Secretion of human epidermal growth factor (EGF) in autotrophic culture by a recombinant hydrogen-utilizing bacterium, Pseudomonas pseudoflava, carrying broad-host-range EGF secretion vector pKSEGF2.

We constructed the broad-host-range human epidermal growth factor (EGF) secretion plasmid pKSEGF2 by inserting the Escherichia coli tac promoter, the signal sequence of Pseudomonas stutzeri amylase, and the synthesized EGF gene into the broad-host-range vector pKT230. E. coli JM109 carrying pKSEGF2 secreted EGF into the periplasm and the culture medium under the control of the tac promoter. Pseudomonas aeruginosa PAO1161 carrying pKSEGF2 and Pseudomonas putida AC10 carrying pKSEGF2 secreted EGF into the culture medium constitutively. Four hydrogen-utilizing bacteria, Pseudomonas pseudoflava, Alcaligenes eutrophus, Alcaligenes paradoxus, and Paracoccus denitrificans, were transconjugated with pKSEGF2 from eight hydrogen-utilizing bacteria tested. In these transconjugated hydrogen-utilizing bacteria, P. pseudoflava carrying pKSEGF2 grew autotrophically and secreted EGF, confirmed by Western blot (immunoblot) analysis, into the culture medium constitutively.

Alcaligenes↗

PubMed1992

Restricted replication of ectromelia virus in cell culture correlates with mutations in virus-encoded host range gene.

Ectromelia virus (strain Moscow) was shown to replicate poorly or not at all in cell lines derived from the rabbit or hamster. The failure of ectromelia virus to replicate in cell lines derived from the hamster suggested that the virus lacked a functional CHO host range (hr) gene required for multiplication in these cells. A DNA fragment which hybridized to the CHO hr gene was cloned from the ectromelia virus genome and shown by sequence analysis to be deleted of 506 bp within the ectromelia virus CHO hr homologue. Two additional ectromelia viruses (Hampstead and Mill Hill strains) were also shown to lack an intact CHO hr gene. Insertion of the CHO gene from cowpox virus into the ectromelia virus genome extended the host range of ectromelia virus in tissue culture. These results demonstrate that an intact CHO hr gene is not required for maintenance of ectromelia virus in nature and provide a partial explanation for ectromelia virus' narrow host range, as opposed to the broad host range of cowpox virus, which has a functional CHO hr gene.

Animals↗

PubMed1988

Pathogenic and host range determinants of the feline aplastic anemia retrovirus.

Feline leukemia virus (FeLV) C-Sarma (or FSC) is a prototype of subgroup C FeLVs, which induce fatal aplastic anemia in outbred specific-pathogen-free (SPF) cats. FeLV C isolates also possess an extended host range in vitro, including an ability, unique among FeLVs, to replicate in guinea pig cells. To identify the viral determinants responsible for the pathogenicity and host range of FSC we constructed a series of proviral DNAs by exchanging gene fragments between FSC and FeLV-61E (or F6A), the latter of which is minimally pathogenic and whose host range in vitro is restricted to feline cells. Transfer of an 886-base-pair (bp) fragment of FSC, encompassing the codons for 73 amino acids at the 3' end of pol (the integrase/endonuclease gene) and the codons for 241 amino acids of the N-terminal portion of env [the extracellular glycoprotein (gp70) gene], into the F6A genome was sufficient to confer onto chimeric viruses the ability to induce fatal aplastic anemia in SPF cats. In contrast, no chimera lacking this sequence induced disease. When assayed in vitro, all chimeric viruses containing the 886-bp fragment of FSC acquired the ability to replicate in heterologous cells, including dog and guinea pig cells. Thus, the pathogenic and the host range determinants of the feline aplastic anemia retrovirus colocalize to a 3' pol-5' env region of the FSC genome and likely reside within a region encoding 241 amino acid residues of the N terminus of the extracellular glycoprotein.

Anemia, Aplastic↗

PubMed1995

Infection by retroviral vectors outside of their host range in the presence of replication-defective adenovirus.

Retrovirus infection is normally limited to cells within a specific host range which express a cognate receptor that is recognized by the product of the env gene. We describe retrovirus infection of cells outside of their normal host range when the infection is performed in the presence of a replication-defective adenovirus (dl312). In the presence of adenovirus, several different ecotropic vectors are shown to infect human cell lines (HeLa and PLC/PRF), and a xenotropic vector is shown to infect murine cells (NIH 3T3). Infectivity is demonstrated by 5-bromo-4-chloro-3-indolyl-beta-D-galactopyranoside (X-Gal) staining, selection with G418 for neomycin resistance, and PCR identification of the provirus in infected cells. Infectivity is quantitatively dependent upon both the concentration of adenovirus (10(6) to 10(8) PFU/ml) and the concentration of retrovirus. Infection requires the simultaneous presence of adenovirus in the retrovirus infection medium and is not stimulated by preincubation and removal of adenovirus from the cells before retrovirus infection. The presence of adenovirus is shown to enhance the uptake of fluorescently labeled retrovirus particles into cells outside of their normal host range, demonstrating that the adenovirus enhances viral entry into cells in the absence of the recognized cognate receptor. This observation suggests new opportunities for developing safe retroviral vectors for gene therapy and new mechanisms for the pathogenesis of retroviral disease.

3T3 Cells↗

PubMed1990

Infection of CV1 cells expressing the polyoma virus middle T antigen or the SV40 agnogene product with simian virus 40 host-range mutants.

SV40 viruses bearing mutations at the carboxy-terminus of large T antigen exhibit a host-range phenotype: such viruses are able to grow in BSC monkey kidney cells at 37 degrees C, but give at least 10,000-fold lower yields than wild type virus in BSC cells at 32 degrees C or in CV1 monkey kidney cells at either temperature. The block to infection in the nonpermissive cell type occurs after the onset of viral DNA replication. Infectious progeny virions are produced at very low efficiency. Although capsid proteins are synthesized at decreased levels, this does not account for the magnitude of the defect. Presumably some step of virion assembly or maturation is affected in these mutants. We have previously reported that the viral agnogene product, a protein thought to be involved in viral assembly or release, fails to accumulate in CV1 cells infected with host-range mutants. In polyoma virus the middle T antigen plays a role in virion maturation by influencing the phosphorylation of capsid proteins. In this communication we show that host-range mutants fail to undergo productive infection of CV1 cells expressing middle T antigen. These mutants do form plaques on an agnoprotein-expressing cell line. However, the agnoprotein does not seem to act by correcting the mutational block but rather increases the efficiency of plaque formation.

Animals↗

PubMed1990

Nucleotide sequence analyses of the genes encoding the HN, M, NP, P, and L proteins of two host range mutants of Sendai virus.

Comparative nucleotide sequence analyses of the genome of Sendai virus (strain Z) and two host range mutants, ts-f1 and F1-R, previously described revealed that the ts defect of ts-f1 can be attributed to two nucleotide exchanges in the NP gene. These exchanges lead to a single amino acid substitution. A single base pair change was found in both the P and L genes of F1-R, but not of ts-f1. Both host range mutants have the two same exchanges in the M gene. These additional mutations are discussed concerning their significance in the pantropic properties of the host range mutants.

Animals↗

PubMed1985

Mapping of a vaccinia host range sequence by insertion into the viral thymidine kinase gene.

A vaccinia virus mutant deleted of ca. 18 kilobase pairs at the left-hand end of the genome is unable to multiply on many human cell lines. To determine whether all or some of the deleted sequences were responsible for the host range property, the corresponding region from wild-type DNA was cloned in three pieces into a vaccinia transplacement vector containing the thymidine kinase gene on the HindIII J fragment. The next step was to transfer these pieces to the genome of the host range deletion mutant by in vivo homologous recombination around the thymidine kinase locus. Transfer of one 5.2-kilobase-pair EcoRI fragment was found to restore a wild-type phenotype on the host range mutant, thus demonstrating that only a small portion of the 18-kilobase-pair deletion contains the host range function(s). This result also illustrates that the method initially devised for inserting foreign genes into vaccinia virus DNA is useful for studies of the vaccinia genome.

Cell Line↗

PubMed1994

The SPI-1 gene of rabbitpox virus determines host range and is required for hemorrhagic pock formation.

Wild-type rabbitpox virus (RPV) and cowpox virus (CPV) produce red hemorrhagic lesions or pocks upon infection of the chicken chorioallantoic membrane (CAM) of 11-day-old embryonated chicken eggs. However, white, nonhemorrhagic pock variants arise spontaneously within wild-type (wt) populations of either virus at a frequency of about 1%, reflective of complex deletions/rearrangements in the termini of the viral DNA. A subpopulation of the RPV white-pock mutants fail to plaque on pig kidney (PK-15) cells and are referred to as host-range (hr) mutants. In the case of CPV, white-pock formation has been linked to mutations in the SPI-2 (crmA) gene. We show that five spontaneous RPV white-pock host-range mutants (RPV mu hr8sm, RPV mu hr23, RPV mu hr28, RPV mu hr30, and RPV mu hr31) each contain a SPI-2 (crmA) gene and express the crmA protein but lack instead a functional SPI-1 gene. Two other spontaneous RPV white-pock mutants, RPV mu 9 and RPV mu 12, which plaque on PK-15 cells (nonhost-range mutants) contain and express a SPI-1 gene but lack instead a functional SPI-2 gene. Targeted disruption of either the SPI-1 or SPI-2 genes of wtRPV, but only the SPI-2 gene of wtCPV, generates mutants which produce white pocks. The RPV delta SPI-1 mutant fails to plaque on PK-15 or human A549 cells, whereas the RPV delta SPI-2 mutant has a normal host range. No changes in host range compared to wtCPV for either the CPV delta SPI-1 or CPV delta SPI-2 mutants were noted. These differences in phenotypes observed between the two viruses may be reflective of either small sequence variations between the highly conserved SPI-1 or SPI-2 genes or the aggregate phenotypes provided by the other remaining genes.

Amino Acid Sequence↗

PubMed1992

Inhibition of bacteriophage lambda development by the klaA gene of broad-host-range plasmid RK2.

The kil-kor regulon of broad-host-range plasmid RK2 is an unusual array of eight co-regulated operons that express at least 21 genes, including the plasmid replication initiator gene. Some of the operons were first identified as kil loci because uncontrolled expression in the absence of certain kor regulatory genes leads to death of the host cells. The functions of kilA, C and E are unknown, although co-regulation with the replication initiator gene suggests that they may have importance in the maintenance or host range of the plasmid. Here we report studies on the function of klaA, the first of three host-lethal genes in the kilA operon. We found that lambda pklaA-1, a lambda phage containing the klaA gene, is unable to form plaques unless the host expresses the KorA and KorB repressors needed to regulate transcription from the klaA promoter. The failure to form plaques depends on the klaA gene product and results from the inability of infected cells to produce viable phage particles. Transcription of early, delayed early and late genes or processing of lambda DNA are not affected by klaA overexpression, while cell lysis, lambda DNA replication and production of functional phage heads are reduced. However, the failure to produce viable phage is best explained by the inability to synthesize lambda tails. The finding that klaA strongly inhibits a specific morphogenetic step in the assembly of lambda phage particles has significance with respect to the function of klaA on plasmid RK2.

Bacterial Proteins↗

PubMed1998

Analysis of host range restriction determinants in the rabbit model: comparison of homologous and heterologous rotavirus infections.

The main limitation of both the rabbit and mouse models of rotavirus infection is that human rotavirus (HRV) strains do not replicate efficiently in either animal. The identification of individual genes necessary for conferring replication competence in a heterologous host is important to an understanding of the host range restriction of rotavirus infections. We recently reported the identification of the P type of the spike protein VP4 of four lapine rotavirus strains as being P[14]. To determine whether VP4 is involved in host range restriction in rabbits, we evaluated infection in rotavirus antibody-free rabbits inoculated orally with two P[14] HRVs, PA169 (G6) and HAL1166 (G8), and with several other HRV strains and animal rotavirus strains of different P and G types. We also evaluated whether the parental rhesus rotavirus (RRV) (P5B[3], G3) and the derived RRV-HRV reassortant candidate vaccine strains RRV x D (G1), RRV x DS-1 (G2), and RRV x ST3 (G4) would productively infect rabbits. Based on virus shedding, limited replication was observed with the P[14] HRV strains and with the SA11 Cl3 (P[2], G3) and SA11 4F (P6[1], G3) animal rotavirus strains, compared to the homologous ALA strain (P[14], G3). However, even limited infection provided complete protection from rotavirus infection when rabbits were challenged orally 28 days postinoculation (DPI) with 10(3) 50% infective doses of ALA rabbit rotavirus. Other HRVs did not productively infect rabbits and provided no significant protection from challenge, in spite of occasional seroconversion. Simian RRV replicated as efficiently as lapine ALA rotavirus in rabbits and provided complete protection from ALA challenge. Live attenuated RRV reassortant vaccine strains resulted in no, limited, or productive infection of rabbits, but all rabbits were completely protected from heterotypic ALA challenge. The altered replication efficiency of the reassortants in rabbits suggests a role for VP7 in host range restriction. Also, our results suggest that VP4 may be involved in, but is not exclusively responsible for, host range restriction in the rabbit model. The replication efficiency of rotavirus in rabbits also is not controlled by the product of gene 5 (NSP1) alone, since a reassortant rotavirus with ALA gene 5 and all other genes from SA11 was more severely replication restricted than either parental rotavirus strain.

Animals↗

PubMed1994

An analysis of the complete nucleotide sequence of the Haemophilus ducreyi broad-host-range plasmid pLS88.

We present an analysis of the complete nucleotide sequence of pLS88, a naturally occurring, 4.8-kb broad-host-range plasmid isolated from Haemophilus ducreyi and encoding resistance to sulfonamides, streptomycin, and kanamycin. Sequence analysis of the genes encoding sulfonamide and streptomycin resistance revealed homology to the RSF1010 sulII and strA genes. The sulII-strA intergenic region of pLS88 has a 38-bp deletion identical to that of the RSF1010-like plasmid pHD8.1, isolated from Actinobacillus pleuropneumoniae. The kanamycin resistance gene shows strong homology to Tn903, but lacks the inverted repeats of the transposon. No other genes have been identified. The region downstream of the kanamycin resistance gene shows homology to the RSF1010 oriV region; however, this region is not essential to plasmid replication. The ori of pLS88 is contained within a 1060-bp region and does not appear to contain structures typical of plasmid origins. This region is flanked by DNA showing strong homology to regions both upstream and downstream of the Haemophilus influenzae ROB-1 beta-lactamase gene. Because of the small size of the origin, pLS88 appears to resemble the structure of narrow-host-range plasmids, but replicates, via an as yet unidentified mechanism, as a broad-host-range plasmid.

Base Sequence↗

PubMed1998

A series of broad host range shuttle vectors for constitutive and inducible expression of heterologous proteins in insect cell lines.

A series of shuttle vectors have been constructed that allow expression of heterologous proteins in either dipteran or lepidopteran insect cell lines. Constitutive expression in a broad range of host cells is mediated by the Orgyia pseudotsugata multicapsid nucleopolyhedrosis virus (OpMNPV) immediate-early 2 (ie2) promoter. Alternatively, if inducible expression is required, for example to express cytotoxic proteins, a vector has been constructed that uses the Drosophila metallothionein (Mtn) promoter for metal-inducible protein expression in dipteran cell lines. A chimeric synthetic bacterial-OpMNPV ie promoter-Zeocin resistance gene cassette has been included to facilitate cloning in E. coli as well as the generation of stably transformed insect cell lines. The utility of the system is demonstrated by the constitutive and inducible expression of the highly processed glycosylphosphatidylinositol-anchored glycoprotein, human melanotransferrin, in transformed insect cell lines.

Animals↗

PubMed2004

The broad host range pathogen Pseudomonas aeruginosa strain PA14 carries two pathogenicity islands harboring plant and animal virulence genes.

The ubiquitous bacterium Pseudomonas aeruginosa is the quintessential opportunistic pathogen. Certain isolates infect a broad range of host organisms, from plants to humans. The pathogenic promiscuity of particular variants may reflect an increased virulence gene repertoire beyond the core P. aeruginosa genome. We have identified and characterized two P. aeruginosa pathogenicity islands (PAPI-1 and PAPI-2) in the genome of PA14, a highly virulent clinical isolate. The 108-kb PAPI-1 and 11-kb PAPI-2, which are absent from the less virulent reference strain PAO1, exhibit highly modular structures, revealing their complex derivations from a wide array of bacterial species and mobile elements. Most of the genes within these islands that are homologous to known genes occur in other human and plant bacterial pathogens. For example, PAPI-1 carries a complete gene cluster predicted to encode a type IV group B pilus, a well known adhesin absent from strain PAO1. However, >80% of the PAPI-1 DNA sequence is unique, and 75 of its 115 predicted ORF products are unrelated to any known proteins or functional domains. Significantly, many PAPI-1 ORFs also occur in several P. aeruginosa cystic fibrosis isolates. Twenty-three PAPI ORFs were mutated, and 19 were found to be necessary for full plant or animal virulence, with 11 required for both. The large set of "extra" virulence functions encoded by both PAPIs may contribute to the increased promiscuity of highly virulent P. aeruginosa strains, by directing additional pathogenic functions.

Animals↗

PubMed2000

Improved gfp and inaZ broad-host-range promoter-probe vectors.

A new set of broad-host-range promoter-probe vectors has been constructed. One subset contains the pVS1 and p15a replicons and confers resistance to either gentamicin or kanamycin. The other set contains the broad-host-range replicon from pBBR1 and confers resistance to kanamycin, tetracycline, ampicillin, or spectinomycin/streptomycin. Both plasmid sets are highly stable and are maintained without selection for more than 30 generations in several bacterial taxa. Each plasmid contains a promoter-probe cassette that consists of a multicloning site, containing several unique restriction sites, and gfp or inaZ as a reporter gene. The cassette is bound by transcriptional terminators to permit the insertion of strong promoters and to insulate the cassette from external transcription enabling the detection of weak or moderate promoters. The vector suite was augmented with derivatives of the kanamycin-resistant gfp promoter-probe plasmids that encode Gfp variants with different half-life times.

Bacterial Outer Membrane Proteins↗

PubMed1999

Natural host range and prevalence of the genus strongwellsea (Zygomycota: entomophthorales) in denmark

The natural occurrence and host range of species of the insect pathogenic fungal genus Strongwellsea [Zygomycota: Entomophthorales] were studied by extensive sampling and examination of adult Diptera [Cyclorrhapha]. The host range for Strongwellsea spp. was significantly enlarged. Three families were documented as new hosts: Muscidae (three species), Calliphoridae (one species), and Sarcophagidae (one species). Further, within the family Anthomyiidae six new host species were recorded and three new host species were documented in the Fanniidae. Strongwellsea castrans was identified as the pathogen in the Anthomyiids, while records from Fanniidae belonged to S. magna. The records of S. magna were the first outside the type locality (California). Primary conidia morphology indicated that muscid and calliphorid species were infected by three undescribed species of Strongwellsea. For the sarcophagid fly, no conidia were encountered, so the Strongwellsea species could not be identified. The tested sampling methods had each different advantages. Sweep netting and diagnosis in situ gave the best opportunity to sample a high number of infected dipterans per time unit spend, while sweep netting followed by incubation in the laboratory was the only method for the documentation of resting spores. The prevalence of S. castrans in the cabbage root fly Delia radicum was obtained by two methods: Samples collected by sweep net and incubated and water trap samples. Water trap captures gave higher prevalences of conidial infections than sweep-net captures. Measured prevalences of Strongwellsea spp. infections are therefore highly dependent on sampling method. The occurrence of resting spores of S. castrans in D. radicum was almost exclusively restricted to females and varied during the season. In samples from 1988 through 1993, no infected females in June contained resting spores, while 43.0% of the S. castrans-infected females from samples in August contained resting spores. During September and October, a decreasing proportion of S. castrans-infected D. radicum contained resting spores. The results document that species from the genus Strongwellsea are common fungal pathogens of adult flies from different families, occasionally with high prevalences. It also appears that the two described species of Strongwellsea, S. castrans and S. magna, have a range of dipterous host species that may always belong to a single family, Anthomyiidae and Fanniidae, respectively. Our data shows also that the host family Muscidae may be exploited by two new species of Strongwellsea. Copyright 1999 Academic Press.

Journal Article↗

PubMed1995

Evolution of the feline-subgroup parvoviruses and the control of canine host range in vivo.

A related group of parvoviruses infects members of many different carnivore families. Some of those viruses differ in host range or antigenic properties, but the true relationships are poorly understood. We examined 24 VP1/VP2 and 8 NS1 gene sequences from various parvovirus isolates to determine the phylogenetic relationships between viruses isolated from cats, dogs, Asiatic raccoon dogs, mink, raccoons, and foxes. There were about 1.3% pairwise sequence differences between the VP1/VP2 genes of viruses collected up to four decades apart. Viruses from cats, mink, foxes, and raccoons were not distinguished from each other phylogenetically, but the canine or Asiatic raccoon dog isolates formed a distinct clade. Characteristic antigenic, tissue culture host range, and other properties of the canine isolates have previously been shown to be determined by differences in the VP1/VP2 gene, and we show here that there are at least 10 nucleotide sequence differences which distinguish all canine isolates from any other virus. The VP1/VP2 gene sequences grouped roughly according to the time of virus isolation, and there were similar rates of sequence divergence among the canine isolates and those from the other species. A smaller number of differences were present in the NS1 gene sequences, but a similar phylogeny was revealed. Inoculation of mutants of a feline virus isolate into dogs showed that three or four CPV-specific differences in the VP1/VP2 gene controlled the in vivo canine host range.

Amino Acid Sequence↗

PubMedDate not supplied

Use of digoxigenin-labelled probes for detection and host-range studies of tomato yellow leaf curl geminivirus.

We studied the host range of tomato yellow leaf curl virus (TYLCV) in some agronomically important tomato species. Transmission tests with the natural vector Bemisia tabaci from tomato to sweet pepper, eggplant, cucumber, melon, zucchini and spinach showed that these species did not develop symptoms and did not support viral replication. These species therefore do not constitutive a reservoir of the virus and can be cultivated as alternatives to tomato in the most affected areas. For host-range studies, we used a quick and sensitive dot-blot assay employing non-radioactive DNA probes. This technique, developed for detecting TYLCV in plant extracts, is easily used for diagnosis. The sensitivity of this non-radioactive test was comparable to that of radiolabelled probes.

Animals↗

PubMed1981

A new temperate phage of streptomyces venezuelae: morphology, DNA molecular weight and host range of SV2.

A new, narrow host range temperate phage, SV2, was isolated from soil. It lysogenized and lysed strains of Streptomyces venezuelae and seemed to be specific for this species. In general morphology, the virions were typically lambdoid, but had unusually ringed tails similar to those of some rare phages isolated from hosts belonging to different bacterial genera. The molecular weight of double-stranded linear SV2 DNA, estimated at about 24 X 10(6), was lower than the published values for other Streptomyces phages.

Bacteriophages↗