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At least 613 records · Page 34Linked to original sources
PubMed1998

The host range of chronic wasting disease is altered on passage in ferrets.

Chronic wasting disease (CWD), a member of the transmissible spongiform encephalopathies (TSEs), was first identified in captive mule and black-tail deer in 1967. Due to the failure to transmit CWD to rodents, we investigated the use of ferrets (Mustela putorius furo) as a small animal model of CWD. The inoculation of CWD into ferrets resulted in an incubation period of 17-21 months on primary passage that shortened to 5 months by the third ferret passage. The brain tissue of animals inoculated with ferret-passaged CWD exhibited spongiform degeneration and reactive astrocytosis. Western blot analysis of ferret-passaged CWD demonstrated the presence of PrP-res. Unlike mule deer CWD, ferret-passaged CWD was transmissible to Syrian golden hamsters (Mesocricetus auratus). Increasing the passage number of CWD in ferrets increased the pathogenicity of the agent for hamsters. This increase in host range of a field isolate on interspecies transmission emphasizes the need for caution when assessing the potential risk of transmission of TSEs, such as bovine spongiform encephalopathy, to new host species.

Animals↗
PubMed1969

Bacteriophage typing of Salmonella. I. Isolation and host range study of bacteriophages.

A series of bacteriophages, lytic for bacteria belonging to the genera Escherichia and Salmonella, were isolated. The phages were isolated from fecal samples, intestinal contents of turkey poults, and carrier cultures of S. typhimurium, S. typhimurium var copenhagen, S. heidelberg, and E. coli. The feasibility of using different habitats as sources of Salmonella phages was evaluated. The carrier cultures were the most promising source for phages active on the serotypes for which the phages were sought. A host range study of the isolated phages was made. Eight phages were selected to develop a phage typing scheme for S. typhimurium, S. typhimurium var copenhagen, and S. heidelberg.

Animals↗
PubMed2000

Broad-host-range shuttle vectors for screening of regulated promoter activity in viridans group streptococci: isolation of a pH-regulated promoter.

Viridans group streptococci are major constituents of the normal human oral flora and are also identified as the predominant pathogenic bacteria in native valve infective endocarditis. Little information is available regarding the regulation of gene expression in viridans group streptococci, either in response to changes in the oral environment or during development of endocarditis. We therefore constructed a set of broad-host-range vectors for the isolation of promoters from viridans group streptococci that are activated by specific environmental stimuli in vitro or in vivo. A genomic library of Streptococcus gordonii strain CH1 was constructed in one of the new vectors, and this library was introduced into a homologous bacterium by using an optimized electroporation protocol for viridans group streptococci. Because viridans group streptococci entering the bloodstream from the oral cavity encounter an increase in pH, we selected promoters upregulated by this specific stimulus. One of the selected promoter sequences showed homology to the promoter region of the hydA gene from Clostridium acetobutylicum, the expression of which is known to be regulated by the environmental pH. The isolation of this pH-regulated promoter shows that S. gordonii can sense an increase in the environmental pH, which serves as a signal for bacterial gene activation. Furthermore, this demonstrates the usefulness of these new selection vectors in research on adaptive gene expression of viridans group streptococci and possibly also of other gram-positive bacteria.

Base Sequence↗
PubMed1983

Host range mutants of human rhinovirus in which nonstructural proteins are altered.

Human rhinovirus type 2 did not replicate in nonpermissive mouse cells; the restriction was not in adsorption but in the early events of virus replication. Mutants which had been adapted to grow in mouse cells had the following characteristics: (i) no change in the structural protein, (ii) a larger nonstructural protein and its precursor protein, and (iii) an altered viral RNA synthesis. The altered nonstructural proteins correlated with a change in host range of the virus and may be involved in viral RNA synthesis.

Animals↗
PubMed2003

A replication competent adenovirus 5 host range mutant-simian immunodeficiency virus (SIV) recombinant priming/subunit protein boosting vaccine regimen induces broad, persistent SIV-specific cellular immunity to dominant and subdominant epitopes in Mamu-A*01 rhesus macaques.

CTL are important in controlling HIV and SIV infection. To quantify cellular immune responses induced by immunization, CD8(+) T cells specific for the subdominant Env p15m and p54m epitopes and/or the dominant Gag p11C epitope were evaluated by tetramer staining in nine macaques immunized with an adenovirus (Ad) 5 host range mutant (Ad5hr)-SIVenv/rev recombinant and in four of nine which also received an Ad5hr-SIVgag recombinant. Two Ad5hr-SIV recombinant priming immunizations were followed by two boosts with gp120 protein or an envelope polypeptide representing the CD4 binding domain. Two mock-immunized macaques served as controls. IFN-gamma-secreting cells were also assessed by ELISPOT assay using p11C, p15m, and p54m peptide stimuli and overlapping pooled Gag and Env peptides. As shown by tetramer staining, Ad-recombinant priming elicited a high frequency of persistent CD8(+) T cells able to recognize p11C, p15m, and p54m epitopes. The presence of memory cells 38 wk postinitial immunization was confirmed by expansion of tetramer-positive CD8(+) T cells following in vitro stimulation. The SIV-specific CD8(+) T cells elicited were functional and secreted IFN-gamma in response to SIV peptide stimuli. Although the level and frequency of response of peripheral blood CD8(+) T cells to the subdominant Env epitopes were not as great as those to the dominant p11C epitope, elevated responses were observed when lymph node CD8(+) T cells were evaluated. Our data confirm the potency and persistence of functional cellular immune responses elicited by replication competent Ad-recombinant priming. The cellular immunity elicited is broad and extends to subdominant epitopes.

Adenoviruses, Human↗
PubMed1993

Interference with superinfection and with cell killing and determination of host range and growth kinetics mediated by feline leukemia virus surface glycoproteins.

The functions of the surface glycoproteins (SU) of feline leukemia viruses (FeLVs) are of interest since these proteins mediate virus infection and interference and are critical determinants of disease specificity. In this study, we examined the biochemical and genetic determinants of SU important to virus entry and cell killing. In particular, we developed and used vesicular stomatitis virus (VSV)/FeLV pseudotype virus interference assays to determine interference subgroupings and assess mechanisms of host cell restriction. We also assessed roles of SU in virus growth kinetics and in the inhibition of cell killing caused by superinfection with cytopathic virus. Subgroup classification by VSV/FeLV pseudotype assay was in agreement with that defined previously by focus interference assay and was found to be determined by changes near the N terminus of SU for FeLV subgroups A (FeLV-A) and C. Virus host range restriction was found to be mediated at the level of virus entry in most cases, although postentry events mediated restriction in the failure of a subgroup A-like, T-cell cytopathic and immunodeficiency-inducing clone (FeLV-FAIDS-EECC) to replicate in feline fibroblasts. FeLV-FAIDS-EECC-induced cell killing was also inhibited by prior infection with one of two FeLV-A isolates. This inhibition could be conveyed by as few as four amino acid changes near the N terminus of the FeLV-A SU and also appeared to be mediated at a postentry level. Lastly, the SU-coding sequence was also found to determine differences in growth kinetics of viruses within the same subgroup. These studies demonstrate that subtle alterations in the FeLV SU, particularly in the N-terminal region, impart multiple significant functional differences which distinguish virus variants.

Amino Acid Sequence↗
PubMed1996

Disruption of M-T5, a novel myxoma virus gene member of poxvirus host range superfamily, results in dramatic attenuation of myxomatosis in infected European rabbits.

Myxoma virus is a pathogenic poxvirus that induces a lethal myxomatosis disease profile in European rabbits, which is characterized by fulminating lesions at the primary site of inoculation, rapid dissemination to secondary internal organs and peripheral external sites, and supervening gram-negative bacterial infection. Here we describe the role of a novel myxoma virus protein encoded by the M-T5 open reading frame during pathogenesis. The myxoma virus M-T5 protein possesses no significant sequence homology to nonviral proteins but is a member of a larger poxviral superfamily designated host range proteins. An M-T5- mutant virus was constructed by disruption of both copies of the M-T5 gene followed by insertion of the selectable marker p7.5Ecogpt. Although the M-T5- deletion mutant replicated with wild-type kinetics in rabbit fibroblasts, infection of a rabbit CD4+ T-cell line (RL5) with the myxoma virus M-T5- mutant virus resulted in the rapid and complete cessation of both host and viral protein synthesis, accompanied by the manifestation of all the classical features of programmed cell death. Infection of primary rabbit peripheral mononuclear cells with the myxoma virus M-T5-mutant virus resulted in the apoptotic death of nonadherent lymphocytes but not adherent monocytes. Within the European rabbit, disruption of the M-T5 open reading frame caused a dramatic attenuation of the rapidly lethal myxomatosis infection, and none of the infected rabbits displayed any of the characteristic features of myxomatosis. The two most significant histological observations in rabbits infected with the M-T5-mutant virus were (i) the lack of progression of the infection past the primary site of inoculation, coupled with the establishment of a rapid and effective inflammatory reaction, and (ii) the inability of the virus to initiate a cellular reaction within secondary immune organs. We conclude that M-T5 functions as a critical virulence factor by allowing productive infection of immune cells such as peripheral lymphocytes, thus facilitating virus dissemination to secondary tissue sites via the lymphatic channels.

Animals↗
PubMed1996

A broad-host-range in vivo pop-out and amplification system for generating large quantities of 50- to 100-kb genomic fragments for direct DNA sequencing.

A prerequisite for sequencing large genomes is to obtain 30- to 150-kb genomic DNA fragments in adequate quantity. Previously, we developed a system which enables one to excise and amplify in vivo such segments directly from the Escherichia coli genome. This system, which employed the yeast Flp/FRT elements for excision and the plasmid R6K-based replication machinery for DNA amplification, permits one to bypass conventional cloning [Pósfai et al. (1994) Nucleic Acids Res. 22, 2392-2398]. To extend the applicability of such a system to many species, we describe here a broad-host-range (bhr) system in which the amplification of the excised DNA fragment depends on the oriV element and the Rep (TrfA) protein from the promiscuous RK2/RP4 plasmid. We have constructed insertion plasmids which carry the FRT and oriV sites. To introduce such plasmids into the appropriate position in the host genome, a short genomic sequence homologous to this position was cloned into the multiple cloning site (MCS) of the FRT/oriV insertion plasmid and then recombined into this position in the genome by RecA-mediated recombination. In such a manner, many strains with single FRT/oriV insertions at various positions could be generated. Subsequent genetic crosses or phage transduction allow two neighboring FRT/oriV sites (less than 150 kb apart) to be brought into a single genome. In the present report, the lacZ and phoB sites, which are 51 kb apart in the E. coli genome, were used for the introduction of the FRT/oriV sites. To deliver the Flp (excision) and Rep (amplification) functions in trans, the yeast FLP and RK2 plasmid trfA genes were placed under the control of the Ptet promoter/operator which is tightly regulated by the TetR repressor. The addition of heated chlortetracycline (cTc) inactivates TetR, turning on the synthesis of Flp and TrfA, which respectively, execute (i) excision of the 51-kb genomic segment between the two FRT sites (in lacZ and in phoB), and (ii) its amplification.

Chromosome Walking↗
PubMedDate not supplied

Comparison of the host ranges and antigenicity of Cryptosporidium parvum and Cryptosporidium wrairi from guinea pigs.

Oocysts of a Cryptosporidium isolate from guinea pigs were not infectious for adult mice, but were infectious for two of three newborn calves and for suckling mice. However, oocysts isolated from calves or mice infected with guinea pig Cryptosporidium were not infectious for guinea pigs. Four isolates of C. parvum from calves were incapable of infecting weanling guinea pigs. Microscopic examination of tissue from the colon and cecum of suckling guinea pigs inoculated with C. parvum revealed sparse infection of some pups. These host range studies and previously described differences in 125I-labeled oocyst surface protein profiles between Cryptosporidium sp. from guinea pigs and C. parvum suggest they are distinct species. We propose the name Cryptosporidium wrairi be retained. Studies with monoclonal antibodies indicate that C. wrairi and C. parvum are antigenically related.

Animals↗
PubMed1999

Direct selection of IS903 transposon insertions by use of a broad-host-range vector: isolation of catalase-deficient mutants of Actinobacillus actinomycetemcomitans.

Transposon mutagenesis in bacteria generally requires efficient delivery of a transposon suicide vector to allow the selection of relatively infrequent transposition events. We have developed an IS903-based transposon mutagenesis system for diverse gram-negative bacteria that is not limited by transfer efficiency. The transposon, IS903phikan, carries a cryptic kan gene, which can be expressed only after successful transposition. This allows the stable introduction of the transposon delivery vector into the host. Generation of insertion mutants is then limited only by the frequency of transposition. IS903phikan was placed on an IncQ plasmid vector with the transposase gene located outside the transposon and expressed from isopropyl-beta-D-thiogalactopyranoside (IPTG)-inducible promoters. After transposase induction, IS903phikan insertion mutants were readily selected in Escherichia coli by their resistance to kanamycin. We used IS903phikan to isolate three catalase-deficient mutants of the periodontal pathogen Actinobacillus actinomycetemcomitans from a library of random insertions. The mutants display increased sensitivity to hydrogen peroxide, and all have IS903phikan insertions within an open reading frame whose predicted product is closely related to other bacterial catalases. Nucleotide sequence analysis of the catalase gene (designated katA) and flanking intergenic regions also revealed several occurrences of an 11-bp sequence that is closely related to the core DNA uptake signal sequence for natural transformation of Haemophilus influenzae. Our results demonstrate the utility of the IS903phikan mutagenesis system for the study of A. actinomycetemcomitans. Because IS903phikan is carried on a mobilizable, broad-host-range IncQ plasmid, this system is potentially useful in a variety of bacterial species.

Aggregatibacter actinomycetemcomitans↗
PubMed1991

Host range, replicative, and cytopathic properties of human immunodeficiency virus type 1 are determined by very few amino acid changes in tat and gp120.

Human immunodeficiency virus type 1 (HIV-1) isolates display differences in a variety of in vitro biological properties, including the ability to infect different cell types, the kinetics of replication, and cytopathicity in the infected cells. Studies with isolates obtained from the same individual over time have shown that these in vitro properties of the viral isolates correlate with pathogenicity in the host. The later isolates, recovered when disease has developed, display a wider cellular host range, replicate rapidly and to high titers in the infected cells, and induce syncytia in these cells. In the present studies, the genomic determinants of these biological properties were defined with recombinant viruses generated between two HIV-1 isolates recovered sequentially from the same individual. The results show that the rate of HIV-1 replication in the HUT 78 T-cell line is controlled by the first coding exon of tat. Infection of T-cell and monocytic cell lines is determined by two specific regions in the envelope gp120, one of which also confers the ability of an isolate to induce syncytia. Amino acid sequence comparison of the regions identified revealed minor differences between the two viral isolates: 2 amino acids in the tat gene product and 10 and 12 amino acids in the two regions of envelope gp120. These data suggest that small changes in the tat and env proteins can have dramatic effects on the pathogenic potential of HIV-1.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Modifying the host range properties of retroviral vectors.

Gene therapy protocols would be greatly facilitated by the availability of targetable injectable vectors which could deliver genes in vivo to specific target cells or to specific disease sites. Efforts to develop such retroviral vectors are therefore a high priority in gene therapy research. In this review, we describe the current state of our understanding of the structure and function of the retroviral envelope glycoprotein complex. We then discuss the results of the various strategies that have been devised to modify the host range of the retroviral envelope glycoproteins with a view to achieving retroviral vectors capable of delivering their genes in a highly specific manner to selected human target cells. The strengths and limitations of these strategies are examined.

Gene Targeting↗
PubMed1984

Extension of bacteriophage lambda host range: selection, cloning, and characterization of a constitutive lambda receptor gene.

A set of plasmids has been constructed that carry a constitutive lamB gene (LamBc phenotype) from Escherichia coli and that confer functional phage lambda receptors to bacteria other than E. coli. This E. coli LamBc strain has been selected to escape both maltose-inducible and glucose-repressible control. Constitutivity results from an IS-3 insertion, carrying a mobile promoter, proximal to lamB. The LamBc DNA has been cloned into both broad and narrow host-range plasmids, and the resulting pTROY plasmids have been transferred to diverse bacteria. Both Salmonella typhimurium/pTROY and Klebsiella pneumoniae/pTROY strains efficiently adsorb phage lambda; Pseudomonas aeruginosa/pTROY strains do not. Introduction of a functional E. coli LamB protein into foreign bacterial will allow these bacteria carrying pTROY plasmids to be infected by phage lambda recombinant DNA libraries, phage lambda::Tn insertion mutagenesis vectors, and in vivo lambda-packaged cosmids.

Bacterial Outer Membrane Proteins↗
PubMed1970

Host range mutants of polyoma virus.

A line of polyoma-transformed mouse cells has been isolated which is fully susceptible to lytic infection by polyoma virus. This line has been used to select virus mutants which have lost most or all of their ability to grow in the untransformed parental line while retaining the ability to grow in the transformed derivative. These virus mutants are also defective in their ability to transform cells of rat or hamster origin. Since the DNA extracted from the mutants has the same host range as the whole virus, the mutants appear to be blocked at some intracellular step which is required both for the completion of virus development in mouse cells and for transformation in rat or hamster cells.

Animals↗
PubMed2001

Glycoprotein D-independent infectivity of pseudorabies virus results in an alteration of in vivo host range and correlates with mutations in glycoproteins B and H.

Infection of cells by herpesviruses is initiated by the interaction of viral envelope glycoproteins with cellular receptors. In the alphaherpesvirus pseudorabies virus (PrV), the causative agent of Aujeszky's disease in pigs, the essential glycoprotein D (gD) mediates secondary attachment of virions to target cells by binding to newly identified cellular receptors (R. J. Geraghty, C. Krummenacher, G. H. Cohen, R. J. Eisenberg, and P. G. Spear, Science 280:1618-1620, 1998). However, in the presence of compensatory mutations, infection can also occur in the absence of gD, as evidenced by the isolation in cell culture of an infectious gD-negative PrV mutant (PrV-gD(-) Pass) (J. Schmidt, B. G. Klupp, A. Karger, and T. C. Mettenleiter, J. Virol. 71:17-24, 1997). PrV-gD(-) Pass is replication competent with an only moderate reduction in specific infectivity but appears to bind to receptors different from those recognized by wild-type PrV (A. Karger, J. Schmidt, and T. C. Mettenleiter, J. Virol. 72:7341-7348, 1998). To analyze whether this alteration in receptor usage in vitro influences infection in vivo, the model host mouse and the natural host pig were intranasally infected with PrV-gD(-) Pass and were compared to animals infected by wild-type PrV. For mice, a comparable progress of disease was observed, and all animals infected with mutant virus died, although they exhibited a slight delay in the onset of symptoms and, correspondingly, a longer time to death. In contrast, whereas wild-type PrV-infected pigs showed clinical signs and histological and histopathological findings typical of PrV infection, no signs of disease were observed after infection with PrV-gD(-) Pass. Moreover, in these animals, virus-infected cells were not detectable by immunohistochemical staining of different organ samples and no virus could be isolated from nasal swabs. Mutations in glycoproteins B and H were found to correlate with, and probably contribute to, gD-independent infectivity. In conclusion, although PrV-gD(-) Pass is virulent in mice, it is apparently unable to infect the natural host, the pig. This altered host range in vivo correlates with a difference of receptor usage in vitro and demonstrates for the first time the importance of gD receptors in alphaherpesvirus infection of an animal host.

Animals↗
PubMed2006

Evolution of broad host range in retroviruses leads to cell death mediated by highly cytopathic variants.

The ability of many retroviruses to cause disease can be correlated to their cytopathic effect (CPE) in tissue culture characterized by an acute period of cell death and viral DNA accumulation. Here, we show that mutants of a subgroup B avian retrovirus (Alpharetrovirus) cause a very dramatic CPE in certain susceptible avian cells that is coincident with elevated levels of apoptosis, as measured by nuclear morphology, and persistent viral DNA accumulation. These mutants also have a broadly extended host range that includes rodent, cat, dog, monkey, and human cells (31). Previously, we have shown that the mutants exhibit diminished resistance to superinfection. The results presented here have important implications for the process of evolution of retroviruses to use distinct cellular receptors.

Alpharetrovirus↗
PubMed1999

Characterization of a new iridovirus isolated from crickets and investigations on the host range

Typical signs of an iridovirus infection were observed in two species of fatally diseased crickets, Gryllus campestris L. and Acheta domesticus L. (Orthoptera, Gryllidae). The infection was manifested by hypertrophy and bluish iridescence of the affected fat body cells. Electron microscope investigations led to the identification of a new iridovirus, which was termed cricket iridovirus (CrIV). In negatively stained preparations the size of the icosahedral virus particles ranged from 151 nm (side-side) to 167 nm (apex-apex). Assembly of virions occurred in the cytoplasm of hypertrophied fat body cells, where they often accumulated in paracrystalline arrays. Genetic analyses of purified viral DNA using a variety of restriction enzymes revealed that CrIV is distinct from all other known iridoviruses that have been isolated from insects and reported so far. In host range studies it was shown that CrIV can be transmitted perorally to other orthopteran species, causing characteristic symptoms and fatal disease. These species include Gryllus bimaculatus L. (Orthoptera, Gryllidae) and the African migratory locust Locusta migratoria migratorioides (R. & F.) (Orthoptera, Acrididae), which represents one of the most important pest insects in developing countries, as well as the cockroaches Blattella germanica L. and Blatta orientalis L. (both Orthoptera, Blattidae). Consequently, the isolation and characterization of this new cricket iridovirus is of particular interest in view of its possible use in biological or integrated control. Copyright 1999 Academic Press.

Journal Article↗
PubMed1991

Use of a broad-host-range gyrA plasmid for genetic characterization of fluoroquinolone-resistant gram-negative bacteria.

The gyrA genotypes of ciprofloxacin-resistant clinical isolates of Escherichia coli (n = 3), Klebsiella pneumoniae (n = 4), Providencia stuartii (n = 2), Pseudomonas aeruginosa (n = 1), and Acinetobacter calcoaceticus (n = 1) were analyzed in a dominance test. This test is based on the dominance of a wild-type gyrA gene (gyrA+) over the quinolone resistance allele (gyrA) in a heterodiploid strain. Plasmid pBP515, developed to carry the gyrA+ gene of E. coli K-12 on a broad-host-range vector derived from pRSF1010, was used to obtain heterodiploid strains. Plasmid pBP515 encodes kanamycin and gentamicin resistance and is transferable via mobilization by a pRP1-derived helper plasmid (pRP1H) to strains of several gram-negative species. After the introduction of pBP515, single-cell MICs (as measured by reduction of the viable cell count) of ciprofloxacin and nalidixic acid decreased by 4- to greater than 8,000-fold for all strains tested, and 8 of the 11 strains regained ciprofloxacin susceptibilities similar to those of the respective wild types. The results indicate that (i) high-level fluoroquinolone resistance in clinical isolates of E. coli, K. pneumoniae, P. aeruginosa, and A. calcoaceticus can result from mutational alteration of the gyrA gene, and (ii) gyrA mutations are involved in high levels of fluoroquinolone resistance in P. stuartii. Additional mutations outside the gyrA locus may contribute to resistance in K. pneumoniae and P. stuartii.

Acinetobacter↗