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Host range of A/Chicken/Pennsylvania/83 (H5N2) influenza virus.

The highly pathogenic A/Chicken/Penn./1370/83 (H5N2) avian influenza virus, which caused 80% mortality in chickens in Pennsylvania, produced only mild transient illness in experimentally infected pheasants, little or no clinical signs in ring-billed gulls and pigs, and no clinical signs in pekin ducks. Virus could be recovered from only the upper respiratory tract of gulls and pigs for 1-2 days. Infection in ducks resulted in intestinal replication of virus in only 1 out of 12 ducks. By contrast, pheasants shed virus in feces (10(4.7) EID50) for at least 15 days. These studies reinforce wildlife surveillance findings indicating that gulls and ducks are unlikely to have transmitted virus between chicken farms during the 1983 outbreak. Although experimental data suggest that wild gallinaceous birds such as pheasants are potentially capable of virus transmission, there has been no evidence of this from wildlife surveillance in Pennsylvania. Experimental infection of chickens with H5N2 virus isolated from wild ducks one year before the Pennsylvania outbreak or a gull virus (H5N1) isolated in the quarantine area in 1983 resulted in asymptomatic infections and virus replication occurring only in the upper respiratory tract. These studies suggest that if the first H5N2 virus infecting chickens in Pennsylvania originated from waterbirds, changes in host specificity and pathogenicity for chickens and other gallinaceous birds probably occurred during emergence of the Chicken/Penn./83 virus. It is recommended that attention be given in the future to the isolation of domestic poultry from contact with wild aquatic birds.

Animals↗
PubMed2003

Host-range restriction of chimeric yellow fever-West Nile vaccine in fish crows (Corvus ossifragus).

We evaluated a recombinant virus chimera, ChimeriVax-WN, in which the West Nile virus (WNV) surface protein genes (pre-membrane [prM] and envelope [E]) are substituted into the genome of the 17D vaccine strain yellow fever virus (YF-17D), as a vaccine candidate for protection of birds from WNV disease. Using fish crows (Corvus ossifragus) as a model, we found that none of eight crows that received two high doses of vaccine (approximately 100,000 plaque-forming units [PFU]) developed viremia and only one developed WNV-neutralizing antibodies. When challenged with subcutaneous injection of 2,000 PFU of WNV (NY99 strain), all eight developed viremia levels similar to unvaccinated control birds (n = 4). Two of the vaccinated birds died of the infection, compared with no mortality in the four controls. To further investigate the failure of the vaccine, we inoculated chickens with both the vaccine and YF-17D and found no evidence of replication with either of these viruses. These data indicate that this vaccine candidate failed to protect birds from the morbidity and mortality attributed to WNV infections. However, if used in mammals, this recombinant viral vaccine is unlikely to inadvertently enter a natural transmission cycle with birds as amplifying hosts.

Animals↗
PubMed1991

The degree of esterification and points of substitution by O-acetyl and O-(3-hydroxybutanoyl) groups in the acidic extracellular polysaccharides secreted by Rhizobium leguminosarum biovars viciae, trifolii, and phaseoli are not related to host range.

Rhizobium leguminosarum biovars viciae, trifolii, and phaseoli have been grown in the presence and absence of 4',5,7-trihydroxyflavonone (naringenin) or 4',5,7-trihydroxyflavone (apigenin), which induce the expression of nodulation genes of the bacteria. The acidic polysaccharides secreted by the Rhizobium were isolated from the culture media and purified. The polysaccharides were cleaved with a bacteriophage enzyme and the octasaccharide repeating units formed were isolated. The glycosyl sequence and type of nonglycosyl substituents of the repeating units derived from a number of these Rhizobium biovars were shown by fast atom bombardment-mass spectroscopy and proton nuclear magnetic resonance spectroscopy (1H NMR) to be identical. Minor variations in the degree of esterification of the repeating units by O-acetyl and O-(3-hydroxybutanoyl) substituents were observed when the Rhizobium were grown in the presence or absence of the flavonoids. The variation in content and the points of attachment of the O-acetyl and O-(3-hydroxybutanoyl) substituents were as great within each Rhizobium biovar as between different Rhizobium biovars and, contrary to two recent reports (Philip-Hollingsworth, S., Hollingsworth, R. I., and Dazzo, F. B. (1989) J. Biol. Chem. 264, 1461-1466; Philip-Hollingsworth, S., Hollingsworth, R. I., Dazzo, F. B., Djordjevic, M. A., and Rolfe, B. G. (1989) J. Biol. Chem. 264, 5710-5714), the O-acylation patterns were not correlated with the host specificity of the bacteria.

Acetylation↗
PubMed1995

Deletions in one domain of the Friend virus-encoded membrane glycoprotein overcome host range restrictions for erythroleukemia.

Although the Friend virus-encoded membrane glycoprotein (gp55) activates erythropoietin receptors (EpoR) to cause erythroblastosis only in certain inbred strains of mice but not in other species, mutant viruses can overcome aspects of mouse resistance. Thus, mice homozygous for the resistance allele of the Fv-2 gene are unaffected by gp55 but are susceptible to mutant glycoproteins that have partial deletions in their ecotropic domains. These and other results have suggested that proteins coded for by polymorphic Fv-2 alleles might directly or indirectly interact with EpoR and that changes in gp55 can overcome this defense. A new viral mutant with an exceptionally large deletion in its ecotropic domain is now also shown to overcome Fv-2rr resistance. In all cases, the glycoproteins that activate EpoR are processed to cell surfaces as disulfide-bonded dimers. To initiate analysis of nonmurine resistances, we expressed human EpoR and mouse EpoR in the interleukin 3-dependent mouse cell line BaF3 and compared the abilities of Friend virus-encoded glycoproteins to convert these cells to growth factor independence. Human EpoR was activated in these cells by erythropoietin but was resistant to gp55. However, human EpoR was efficiently activated in these cells by the same viral mutants that overcome Fv-2rr resistance in mice. By construction and analysis of human-mouse EpoR chimeras, we obtained evidence that the cytosolic domain of human EpoR contributes to its resistance to gp55 and that this resistance is mediated by accessory cellular factors. Aspects of host resistance in both murine and nonmurine species are targeted specifically against the ecotropic domain of gp55.

Animals↗
PubMed1991

[Plasmid pBS195 with a wide range of hosts, isolated from lactobacilli].

The nonconjugative 4.4 kb plasmid pBS195 has been found in Lactobacillus sp. 195 strain resistant to kanamycin and streptomycin. The plasmid pBS195 determining the resistance to kanamycin has a broad host range. It is inherited by the Gram-positive microorganisms (Bacillus subtilis) as well as by Escherichia coli cells, has the cleavage sites for the restriction endonucleases BamHI, EcoRI, HindIII, PstI, KpnI. The restriction map of the plasmid for these enzymes is constructed. The broad host range, efficiently expressed marker, the presence of the unique restriction sites, small size make the plasmid pBS195 promising for the genetic engineering research.

DNA, Viral↗
PubMed2005

Flexibility in repression and cooperativity by KorB of broad host range IncP-1 plasmid RK2.

KorB, encoded by plasmid RK2, belongs to the ParB family of active partitioning proteins. It binds to 12 operators on the RK2 genome and was previously known to repress promoters immediately adjacent to operators O(B)1, O(B)10 and O(B)12 (proximal) or up to 154 bp away (distal) from O(B)2, O(B)9 and O(B)11. To achieve strong repression, KorB requires a cooperative interaction with one of two other plasmid-encoded repressors, KorA or TrbA. Reporter gene assays were used in this study to test whether the additional KorB operators may influence transcription and to test how KorB acts at a distance. The distance between O(B)9 and trbBp could be increased to 1.6kb with little reduction in repression or cooperativity with TrbA. KorB was also able to repress the promoter and cooperate with TrbA when the O(B) site was placed downstream of trbBp. This suggested a potential regulatory role for O(B) sites located a long way from any known promoter on RK2. O(B)4, 1.9kb upstream of traGp, was shown to mediate TrbA-potentiated KorB repression of this promoter, but no effect on traJp upstream of O(B)4 was observed, which may be due to the roadblocking or topological influence of the nucleoprotein complex formed at the adjacent transfer origin, oriT. Repression and cooperativity were alleviated significantly when a lac operator was inserted between O(B)9 and trbBp in the context of a LacI+ host, a standard test for spreading of a DNA-binding protein. On the other hand, a standard test for DNA looping, movement of the operator to the opposite face of the DNA helix from the natural binding site, did not significantly affect KorB repression or cooperativity with TrbA and KorA over relatively short distances. While these results are more consistent with spreading as the mechanism by which KorB reaches its target, previous estimates of KorB molecules per cell are not consistent with there being enough to spread up to 1kb from each O(B). A plausible model is therefore that KorB can do both, spreading over relatively short distances and looping over longer distances.

Bacterial Proteins↗
PubMed1992

Host range of Clostridium bifermentans serovar. malaysia, a mosquitocidal anaerobic bacterium.

Clostridium bifermentans serovar. malaysia (C.b.m.) is toxic to mosquito larvae. In this study, we quantified its toxicity to the mosquitoes, Aedes aegypti, Ae. albopictus, Ae. caspius, Ae. detritus, Anopheles stephensi, An. gambiae, Culex pipiens and Cx. quinquefasciatus. Anopheles larvae are the most susceptible, followed by Ae. detritus and Ae. caspius, then Culex and other Aedes larvae. According to mosquito species, the LC50 varies from 7 x 10(3) to 1.3 x 10(6) cells/ml. Three concentrations (10(7), 10(6) and 10(5) cells/ml) of C.b.m., Bacillus thuringiensis var. israelensis (B.t.i.) and Bacillus sphaericus were tested on Ae. aegypti, An. stephensi and Cx. pipiens larvae in order to determine the time necessary for each concentration to kill 50 and 90% of the population. Ninety percent of the 3 mosquito populations are killed within 4-15 h by the C.b.m. concentrations. Whatever the concentrations, C.b.m. kills at least 10 times less rapidly than B.t.i. but always quicker than B. sphaericus. Bioassays of C.b.m. bacterial cells or final whole culture were not toxic to Musca domestica and Drosophila melanogaster (Diptera) as well as to Phaedon cochleariae (Coleoptera) and Spodoptera littoralis (Lepidoptera).

Animals↗
PubMed1983

[Homology of plasmids with a wide range of hosts].

According to blotting hybridization and heteroduplex analysis, plasmids R751, R906 and RP4 of Inc Pi group have continuous regions of homology. These homologous regions were mapped on the R751 and RP4-derived pRP401 deletion mutant DNAs. The plasmid pRP401 (m.w. 21.9 kg) retains the broad host range property and has two regions of intensive homology with other Inc P-1 plasmid DNAs. These regions are localized at 8.2-12.0 kb and 13.9-21.9 kb of the physical map of pRP401 plasmid. Homologous regions of pRP401 DNA include at least the replication genes (oriV, trfA, trfB) as well as genes kilB, korA, korB and probably kilC. The data strongly point out that the broad host range plasmids have the same principle of structural and functional organization.

Autoradiography↗
PubMed1989

[A new plasmid pBS1001 with broad range of hosts].

A new broad host-range plasmid capable of conjugative transfer has been isolated and characterized. The plasmid has the high frequency of conjugation transfer, is capable of conjugative transfer mobilization of nonconjugative plasmids, carries no known phenotypic markers. The plasmid demonstrates the specific interaction with the plasmids of P incompatibility group. The comparatively small size of the plasmid permits one to use it efficiently for comparative study of organization of the broad host range plasmids.

Caprolactam↗
PubMed2006

Broad host range vectors for stable genomic library construction.

We describe the construction of 36 stable vectors for genomic library construction in gram-negative species. These vectors contain the pBBR1 replicon that has been shown to stably replicate in every gram-negative species tested. The plasmids also contain bidirectional, rho-independent transcriptional terminators flanking the multiple cloning site, which allows for greater insert stability, and thus, greater genomic representation. Each vector varies in its antibiotic resistance cassette, mobilization function, and promoter used to express insert sequences. These vectors should prove useful in the screening of highly representational genomic libraries in a broad variety of gram-negative species.

Cloning, Molecular↗
PubMed2004

Unexpected host range of hepatitis C virus replicons.

The hepatitis C virus (HCV) pandemic affects the health of more than 170 million people and is the major indication for orthotopic liver transplantations. Although the human liver is the primary site for HCV replication, it is not known if extrahepatic tissues are also infected by the virus nor if nonprimate cells are permissive for RNA replication. Because HCV exists as a quasispecies, it is conceivable that a viral population may include variants that can replicate in different cell types and other species. We have tested this hypothesis and found that subgenomic HCV RNA can replicate in mouse hepatoma and nonhepatic human epithelial cells. Replicons isolated from these cell lines carry new mutations that could be involved in the control of tropism of the virus. Our results demonstrated that translation and RNA-directed RNA replication of HCV do not depend on hepatocyte or primate-specific factors. Moreover, our results could open the path for the development of animal models for HCV infection.

Comment↗
PubMed2005

Characterization of host-range and cell entry properties of the major genotypes and subtypes of hepatitis C virus.

Because of the lack of a robust cell culture system, relatively little is known about the molecular details of the cell entry mechanism for hepatitis C virus (HCV). Recently, we described infectious HCV pseudo-particles (HCVpp) that were generated by incorporating unmodified HCV E1E2 glycoproteins into the membrane of retroviral core particles. These initial studies, performed with E1E2 glycoproteins of genotype 1, noted that HCVpp closely mimic the cell entry and neutralization properties of parental HCV. Because sequence variations in E1 and E2 may account for differences in tropism, replication properties, neutralization, and response to treatment in patients infected with different genotypes, we investigated the functional properties of HCV envelope glycoproteins from different genotypes/subtypes. Our studies indicate that hepatocytes were preferential targets of infection in vitro, although HCV replication in extrahepatic sites has been reported in vivo. Receptor competition assays using antibodies against the CD81 ectodomain as well as ectopic expression of CD81 in CD81-deficient HepG2 cells indicated that CD81 is used by all the different genotypes/subtypes analyzed to enter the cells. However, by silencing RNA (siRNA) interference assays, our results show that the level of Scavenger Receptor Class-B Type-I (SR-BI) needed for efficient infection varies between genotypes and subtypes. Finally, sera from chronic HCV carriers were found to exhibit broadly reactive activities that inhibited HCVpp cell entry, but failed to neutralize all the different genotypes. In conclusion, we characterize common steps in the cell entry pathways of the major HCV genotypes that should provide clues for the development of cell entry inhibitors and vaccines.

Animals↗
PubMed1981

Host range and oncogenicity studies of the murine myeloma MOPC-315 type-C retrovirus.

The biological features of an endogenous type-C RNA tumor virus released by the murine plasmacytoma MOPC-315 were determined. The virus was found to be pure ecotropic and, according to its capability to infect both NIH/3T3 and BALB/3T3 cells, it was established as an NB tropic virus. This tropism became more pronounced as a consequence of multiple passage in balb/3T3 cells. In view of the ability of myeloma viruses to efficiently infect BALB/c cells, their possible role in myeloma induction is considered.

Animals↗
PubMed1984

The korB gene of broad host range plasmid RK2 is a major copy number control element which may act together with trfB by limiting trfA expression.

For replication, plasmid RK2 encodes a vegetative replication origin, oriV RK2, and a gene, trfA, whose polypeptide product(s) is essential for oriV RK2 activity. The trfA gene is transcribed as part of a polycistronic operon which also includes kilD. Transcription of this operon is negatively regulated by the products of the trfB/korD/korA and korB loci. Mini replicons previously studied in detail lack the korB locus and have copy numbers significantly higher than RK2 itself. Here we report that korB in trans expresses incompatibility towards RK2 replicons either when the korB gene dosage is high or when it is expressed from a strong foreign promoter. This incompatibility can be largely overcome if a trfA gene which is expressed from a foreign promoter, and is therefore not regulated by korB, is supplied in trans. When korB is introduced in cis to mini RK2 replicons the copy number is reduced to within the range estimated for parental RK2. Deletions in the oriV RK2 region which otherwise cause quite large increases in plasmid copy number have only a small effect when korB is present in cis. These results suggest that korB in combination with trfB may be the overriding copy number control element in RK2 reducing trfA expression to levels limiting for replication.

Bacterial Proteins↗
PubMed1991

Experimental infection of suckling mice with a host range mutant of Junin virus.

Experimental infection of three mouse strains with a non-pathogenic mutant of Junin virus named Cl67 was compared with respect to the parental XJCl3 strain. After intracerebral (ic) or intraperitoneal inoculation, XJCl3 was highly virulent for 2 day-old C3H/HeJ, OF1, and BALB/cJ mouse strains, whereas its derivative Cl67 was attenuated. Survival of the Cl67-infected mouse was associated with a restricted replication at the site of inoculation which would impair spread of virus. Thus, the reduced virulence of Cl67 for suckling mice is independent of the mouse strain and the route of viral entry. When Cl67 was preinoculated ic 10 days before the challenge inoculation with XJCl3 by the same route, mice were partially protected from lethal infection. Since neutralizing antibodies were first detected at 30 days post-infection, an interference mechanism is postulated as a mechanism of protection of the mice.

Animals↗
PubMed1976

Chromosomally depleted interspecific hybrid cell clones selected with cytotoxic antisera: utilization in the study of control of murine leukemia virus host-range.

A chromosomally stable mouse-Chinese hamster hybrid cell line was subjected to five rounds of selection with cytotoxic antisera raised in rabbits against either the parental mouse 3T3 cells or the parental Chinese hamster Wg-1 cells. Routine karyological analysis of clones isolated at each stage of serum selection revealed that treatment with either serum resulted in a limited loss of chromosomes (compared to the untreated hybrid cell cultured in parallel) and that the pattern of chromosome loss could not be correlated with the particular antiserum used for selection. However, more detailed analysis with the SSC-formamide C-banding technique, which identifies chromosomes containing a mouse centromere region, demonstrated that while large-scale chromosome loss was not achieved as a result of antiserum selection, the limited loss of chromosomes did, in fact, reflect a specific depletion of chromosomes in response to treatment with cytotoxic antiserum. Specific chromosomal elimination was shown to occur as early as the first round of antiserum treatment. Antigenic analysis of the serum-selected clones revealed a quantitative decrease in the expression of the species-specific surface antigens selected against, but no qualitative loss of antigens was detected. The results suggest that treatment with cytotoxic antiserum may select for clones that have lost specific chromosomes bearing genes regulating the expression of species-specific surface antigens, rather than for those demonstrating large-scale depletion of chromosomes bearing the corresponding structural genes. Some of these chromosomally depleted hybrid cell clones have been used (along with pseudotype viruses containing the genome of vesicular stomatitis virus within the envelope of murine leukemia virus, VSV [MuLV]), to study the mechanisms regulating MuLV replication in Chinese hamster cells. The results indicate that the restriction of MuLV replication in Chinese hamster cells operates at two levels: (a) an inability to adsorb to or penetrate Chinese hamster cells; and (b) an additional intracellular block which is dominant in the mouse-Chinese hamster hybrid cell clones examined. This latter block is presently under study.

Antigens↗