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PubMed1990

Characterization of the minimum replicon of the broad-host-range plasmid pTF-FC2 and similarity between pTF-FC2 and the IncQ plasmids.

The nucleotide sequence of a 3,202-base-pair fragment which contained the minimum region required for replication of the broad-host-range plasmid, pTF-FC2, has been determined. At least five open reading frames and a region that affected the host range were identified. Proteins corresponding in size and location to four of the five open reading frames were produced in an in vitro transcription-translation system. The predicted amino acid sequences of two of the proteins were aligned with those of the RepA and RepC proteins of the broad-host-range IncQ plasmid RSF1010 and found to be 43 and 60% homologous, respectively. Despite this similarity, neither the RepA nor the RepC protein of the IncQ plasmid was able to complement mutations in the pTF-FC2 repA and repC genes. Although there was a considerable amount of DNA homology between pTF-FC2 and RSF1010 in the oriV region and the region coding for the RepA and RepC proteins, no other homology between the two plasmids at either the DNA or protein level could be detected.

Amino Acid Sequence↗

PubMed1996

Complementation of a vaccinia virus host-range K1L gene deletion by the nonhomologous CP77 gene.

We investigated the host-range restriction of a vaccinia virus (VV) K1L deletion mutant in rabbit kidney RK13 cells and the ability of the nonhomologous cowpox virus CP77 gene to overcome this block. Viral early mRNAs were made by K1L- VV but early protein synthesis was arrested consistent with a translational block. Replication of viral DNA did not occur and neither intermediate nor late mRNAs or proteins were detected. These results indicated that host-range restriction occurs earlier in RK13 cells than in Chinese hamster ovary cells (CHO) cells infected with CP77- VV, where the block occurs at translation of intermediate stage mRNA. We confirmed a report (Perkus et al., Virology 179, 276-286, 1990) that the CP77 gene, which allows VV replication in CHO cells, could replace the K1L gene for plaque formation in RK13 cells. However, the size of the plaques formed by K1L-CP77+ VV was smaller than those formed by K1L+CP77- VV. Single-step growth curves also showed that the CP77 gene could functionally replace the K1L gene, although formation of infectious virus was delayed and did not reach the same level as that of K1L+ VV. Most surprisingly, the dramatic shutoff of viral and host gene expression was similar in RK13 cells infected with K1L-CP77- VV and K1L-CP77+ VV and little difference was noted for the first 6 hr. Subsequently, in cells infected with the K1L-CP77+ VV, viral early protein synthesis was spontaneously resurrected and the replication cycle proceeded. Despite the absence of homology, K1L and CP77 gene products appear to be acting in a common virus/cell interaction pathway.

Animals↗

PubMed1993

Evidence that the structural conformation of envelope gp120 affects human immunodeficiency virus type 1 infectivity, host range, and syncytium-forming ability.

We investigated how amino acid changes within and outside the V3 loop of the envelope glycoprotein of human immunodeficiency virus type 1 influence the infectivity, host range, and syncytium-forming ability of the virus. Our studies show that on the genomic backgrounds of the human immunodeficiency virus type 1 strains SF2 and SF13, a reciprocal exchange of full-loop sequences does not alter the syncytium-forming ability of the viruses, indicating that a determinant(s) for this biological property maps outside the loop. However, specific amino acid substitutions, both within and outside the V3 loop, resulted in loss of infectivity, host range, and syncytium-forming potential of the virus. Furthermore, it appears that a functional interaction of the V3 loop with regions in the C2 domain of envelope gp120 plays a role in determining these biological properties. Structural studies of mutant glycoproteins show that the mutations introduced affect the proper association of gp120 with the transmembrane glycoprotein gp41. Our results suggest that mutations that alter the structure of the V3 loop can affect the overall conformation of gp120 and that, reciprocally, the structure of the V3 loop is influenced by the conformation of other regions of gp120. Since the changes in the replicative potential, host range, and fusogenic ability of the mutant viruses correlate well with the changes in gp120 conformation, as monitored by the association of gp120 with gp41, our results support a close relationship between envelope gp120 structural conformation and the biological phenotype of the virus.

Amino Acid Sequence↗

PubMed1984

Host range mutants of bacteriophage Ox2 can use two different outer membrane proteins of Escherichia coli K-12 as receptors.

The Escherichia coli K-12 outer membrane protein OmpA functions as the receptor for bacteriophage Ox2. We isolated a host range mutant of this phage which was able to grow on an Ox2-resistant ompA mutant producing an altered OmpA protein. From this mutant, Ox2h5, a second-step host range mutant was recovered which formed turbid plaques on a strain completely lacking the OmpA protein. From one of these mutants, Ox2h10, a third-step host range mutant, Ox2h12, was isolated which formed clear plaques on a strain missing the OmpA protein. Ox2h10 and Ox2h12 apparently were able to use both outer membrane proteins OmpA and OmpC as receptors. Whereas there two proteins are very different with respect to primary structures and functions, the OmpC protein is very closely related to another outer membrane protein, OmpF, which was not recognized by Ox2h10 or Ox2h12. An examination of the OmpC amino acid sequence, in the regions where it differs from that of OmpF, revealed that one region shares considerable homology with a region of the OmpA protein which most likely is required for phage Ox2 receptor activity.

Alleles↗

PubMed2000

Relationships between polydnavirus gene expression and host range of the parasitoid wasp Campoletis sonorensis.

To evaluate the relationship between immune suppression and host range six lepidopteran species were parasitized by the ichneumonid parasitoid Campoletis sonorensis. Parasitism inhibited the growth of permissive hosts (Heliothis virescens, Helicoverpa zea, and Trichoplusia ni), whereas growth of semi-permissive (Spodoptera exigua, Agrotis ipsilon) and non-permissive hosts (Manduca sexta) was not significantly affected. The 29-36 kDa ovarian protein (OP), responsible for transient immunosuppression in the permissive host H. virescens, bound to and was endocytosed by hemocytes of permissive and non-permissive hosts. Expression of the cysteine-rich polydnavirus gene, VHv1.4, was detected in all the hosts, but declined only in semi- and non-permissive hosts at later times after parasitization. The VHv1.4 protein bound to hemocytes of permissive and semi-permissive hosts, but did not bind to hemocytes of the non-permissive host, M. sexta. Melanization of larval hemolymph was severely inhibited by parasitism in permissive hosts, but was unaffected in M. sexta. In the semi-permissive host, A. ipsilon, hemolymph melanization was transiently inhibited while viral genes were expressed. In conclusion, C. sonorensis OP transiently inhibits encapsulation in all hosts that were tested. The host range of C. sonorensis seems to be determined by whether or not the C. sonorensis ichnovirus (CsIV) is able to establish persistent infections of parasitized larvae to provide long-term suppression of host immunity.

Journal Article↗

PubMed1991

Broad host-range vector for efficient expression of foreign genes in gram-negative bacteria.

A broad host-range expression plasmid was constructed comprising the incQ replicon, the recA promoter from Escherichia coli and the g10-L ribosome binding site (RBS) derived from bacteriophage T7. The structural genes for porcine somatotropin (pst) and E. coli beta-galactosidase (lacZ) were used to monitor gene expression in a diverse collection of Gram-negative bacterial hosts: Escherichia coli, Pseudomonas aeruginosa, Pseudomonas syringae, Pseudomonas putida, Pseudomonas fluorescens, Pseudomonas testosteroni, Serratia marcescens and Erwinia herbicola. The E. coli recA promoter was functional in this wide range of hosts and was inducible by the addition of nalidixic acid. Moreover, the level of lacZ expression was often at least as high as that observed in E. coli. Previous studies had shown that the g10-L RBS was superior to a simple "consensus" RBS sequence for expression of foreign genes in E. coli. Here we demonstrate a 38 to 70 fold increase in expression in two Pseudomonas hosts using the g10-L RBS, indicating that the translational enhancer present in the g10-L RBS is also functional in other bacteria. The juxtaposition of these transcriptional and translational elements in a broad host-range vector provides a simple way to evaluate alternate hosts for recombinant protein production.

Cloning, Molecular↗

PubMed1998

The host range and interference properties of two closely related feline leukemia variants suggest that they use distinct receptors.

The proviral clones 61E and 61C represent two closely related variants of feline leukemia virus (FeLV) that exhibit significant differences in their biological and pathogenic properties. The major pathogenic determinant has been mapped to the extracellular envelope glycoprotein (Env-SU), but the mechanism by which envelope differences influence pathogenesis is not well understood. Moreover, it is unclear whether these viruses infect the same target cells and/or enter cells using the same receptor. In the present study, we exploited a recently developed single cycle infection assay to examine the host range and interference properties of 61E and 61C FeLVs and found that these two FeLV variants differ significantly in their host ranges and receptor usages. FeLV-61C was found to be an ecotropic virus; the entry of viruses bearing a 61C envelope protein (Env-SU) into cell lines was limited to feline T-cells and feline fibroblasts. In contrast, the host range of 61E includes, in addition to all feline cells examined, some canine, murine, and human cell lines. Feline fibroblast and feline T-cells that expressed 61E envelope were resistant to infection with a virus bearing a 61E Env-SU, whereas these same cells were susceptible to infection by an otherwise similar virus pseudotyped with the 61C Env-SU. This pattern of interference was observed in cells expressing 61E envelope alone, in the absence of other FeLV gene products, demonstrating that interference was mediated specifically by Env-SU. Fibroblast cells chronically infected with a 61C virus were partially resistant to infection with a virus having a 61C Env-SU, but were not resistant to infection by a virus having a 61E Env-SU. On the basis of the current understanding of virus-receptor interactions, the lack of interference between 61E and 61C under conditions where there is significant homologous interference, combined with the differences in their host cell range, leads us to conclude that 61E and 61C use two distinct primary cellular receptors for entry.

3T3 Cells↗

PubMed2006

Mutational analysis of aminopeptidase N, a receptor for several group 1 coronaviruses, identifies key determinants of viral host range.

Feline coronavirus (FCoV), porcine transmissible gastroenteritis coronavirus (TGEV), canine coronavirus (CCoV), and human coronavirus HCoV-229E, which belong to the group 1 coronavirus, use aminopeptidase N (APN) of their natural host and feline APN (fAPN) as receptors. Using mouse-feline APN chimeras, we identified three small, discontinuous regions, amino acids (aa) 288 to 290, aa 732 to 746 (called R1), and aa 764 to 788 (called R2) in fAPN that determined the host ranges of these coronaviruses. Blockade of infection with anti-fAPN monoclonal antibody RG4 suggested that these three regions lie close together on the fAPN surface. Different residues in fAPN were required for infection with each coronavirus. HCoV-229E infection was blocked by an N-glycosylation sequon present between aa 288 to 290 in murine APN. TGEV required R1 of fAPN, while FCoV and CCoV required both R1 and R2 for entry. N740 and T742 in fAPN and the homologous R741 in human APN (hAPN) were key determinants of host range for FCoV, TGEV, and CCoV. Residue N740 in fAPN was essential only for CCoV receptor activity. A conservative T742V substitution or a T742R substitution in fAPN destroyed receptor activity for the pig, dog, and cat coronaviruses, while a T742S substitution retained these receptor activities. Thus, the hydroxyl on T742 is required for the coronavirus receptor activity of fAPN. In hAPN an R741T substitution caused a gain of receptor activity for TGEV but not for FCoV or CCoV. Therefore, entry and host range of these group 1 coronaviruses depend on the ability of the viral spike glycoproteins to recognize small, species-specific amino acid differences in the APN proteins of different species.

Amino Acid Substitution↗

PubMedDate not supplied

[Host range of drosophila melanogaster C virus among diptera and lepidoptera (author's transl)].

The host range of the C picornavirus of Drosophila melanogaster was studied, using numerous strains of Drosophila together with four other genera of diptera and two species of lepidoptera. C virus was injected into the different hosts and serially passaged in them. The extracts from each passage were biologically assayed on virus free D. melanogaster. Four different situations were found. 1) A high level of multiplication leading, in 45 strains of Drosophilidae, to the early death of the hosts. This phenomenon was particularly related to the subgroup melanogaster and in the dipteron Ceratitis capitata. The titre of the virus in this latter insect was high as in D. melanogaster, but its cellular tropism was wider. 2) An active viral multiplication but without symptoms, in two strains of D. immigrans and in the lepidopteron Galleria mellonella. In these two insects, the viral titre was clearly inferior to that observed in D. melanogaster. 3) Maintenance of the virus, without multiplication in the dipteron Calliphora erythrocephala and the lepidopteron Arctia caja. In these insects, the decrease in virus titre was directly related to the dilution factor at each passage. 4) Rapid disappearance of the virus, in the mosquitoes Culex pipiens and Aedes aegypti. The host range of C virus is compared to that of Sigma virus of Drosophila and of two other picornaviruses of insects.

Animals↗

PubMed1982

Broad host range plasmid RK2 encodes multiple kil genes potentially lethal to Escherichia coli host cells.

Cloning of specific regions of RK2, a broad host range incompatibility group P plasmid, has revealed three genes: kilA, kilB, and kilC. Each of these genes can cause loss of viability of an Escherichia coli host. This effect on the host is normally prevented by the functions of three additional RK2 genes: korA, korB, and korC. Each kor gene is specific for a particular kil gene. The kil and kor genes are located in four distinct regions of the RK2 genome. The three kil genes are not clustered and, with the possible exception of kilA, they are also well separated from their corresponding kor genes. We have found that the korA and korB determinants are not peculiar to RK2 but instead are highly conserved throughout the incompatibility group P plasmids.

Cell Survival↗

PubMed1983

Characterization of an influenza A host range mutant.

A mixed infection of primary chick kidney cells at 38 degrees with A/Ann Arbor/6/60 cold adapted virus and A/Alaska/6/77 wt virus yielded a cold-reassortant virus, CR43-clone 3, which had a host range different from that of either parent. It does not produce detectable virus when grown in Madin-Darby canine kidney cells, while growing normally in primary chick kidney cells at 33 degrees. Both parents, however, grow well in either cell type at 33 degrees C. Genotypic analysis of viral RNA electrophoresed in polyacrylamide gels has shown that CR43-clone 3 virus has an aberrant NS gene different from the NS gene of either parent virus. Reassortant viruses made between CR43-clone 3 virus and A/California/10/78 (H1N1) virus in primary chick kidney cells at 33 degrees showed the same host range restriction only if the NS gene was derived from the CR43-clone 3 virus. A mixed infection with these same parents, but in Madin-Darby canine kidney cells at 33 degrees C, produced reassortants that always contained the A/California/10/78 NS gene instead of the CR43-clone 3 NS gene. Ferrets inoculated intranasally with the CR43-clone 3 reassortant do not become sick or infected, based on the lack of symptoms: no rhinitis, coryza, or fever; and no detectable virus recovered from nasopharyngeal swabs, turbinate, or lung tissues at 48 hr after infection. Thus, CR43-clone 3 virus contains an aberrant NS gene and manifests a restricted host range phenotype in Madin-Darby canine kidney cells and ferrets.

Animals↗

PubMed1987

DNA sequence of genes 38 encoding a receptor-recognizing protein of bacteriophages T2, K3 and of K3 host range mutants.

Genes 38, which code for a receptor-recognizing protein present at the tip of the long tail fibers, have been sequenced from phages T2, the T-even-type phage K3 and its host range mutants K3hx, K3h1 and K3h1h. The genes from phages T2 and K3 code for proteins consisting of 262 and 260 amino acid residues, respectively. Fifty amino-terminal and 25 carboxy-terminal residues are highly conserved. The amino-terminal amino acids are most likely involved in binding to the neighboring protein 37. Between residues 116 and 226 of the T2 protein and residues 116 and 223 of the K3 protein, sequences exist that are similar to sequences present in Escherichia coli outer membrane proteins and which serve as phage receptors. Most likely, all of these regions in the latter proteins are exposed on the cell surface and are part of their phage receptor areas. In the phage proteins, these sequences are flanked by stretches rich in glycine, perhaps providing an increased flexibility for the polypeptide at these sites; some "wobble" may be required during the protein 38-receptor interaction. The mutational alterations in the host range mutants were found in gene 38. In the K3hx protein, a duplication of six base-pairs caused the wild-type sequence -Gly163-Lys-Leu-Ile- to be changed to -Gly163-Lys-Leu-Lys-Leu-Ile-. In the K3h1 protein, a glutamic acid residue at position 203 was substituted by a lysine. Both alterations occurred within areas similar to outer membrane proteins. Mutant K3h1h, derived from K3h1, exhibits an extended host range as compared to K3h1. No mutational alteration, in addition to that found in K3h1, was found in g38 nor was the part of gene 37 that encodes the carboxy-terminal moiety of the protein altered. K3h1h may represent a "trigger-happy" phage. The results of this and other work show that the phage-phage receptor systems under study represent a primitive immune system.

Amino Acid Sequence↗

PubMed1991

Host range and symptoms are determined by specific domains of the maize streak virus genome.

We have cloned two distinct symptomatic variants of the geminivirus streak virus from maize plants infected with the Nigerian strain (MSV-N). Following "agroinoculation" to maize plants MSV-Nm produces narrow, mildly chlorotic discontinuous streaks, whereas MSV-Ns-infected tissue has wide, severely chlorotic streaks. Symptom appearance is delayed following MSV-Nm inoculation. MSV-Nm has a narrow host range within the Gramineae comprising a fraction of that of the wide host range isolate MSV-Ns. The two isolates are highly homologous and have identical restriction enzyme maps. In order to localize the determinants of pathogenicity we constructed, in vitro, hybrid genomes by restriction enzyme fragment exchange. The determinants of host range, severity of chlorosis, streak length, and timing of symptom appearance map to a fragment which includes the large intergenic region and the 5' terminus of the complementary sense C1 gene. Streak width is determined by the virion-sense portion of the genome, which is consistent with the observation that the virion-sense gene products (V1 and V2) are required for spread of the virus.

Cloning, Molecular↗

PubMed1983

Homology in the transfer origins of broad host range IncP plasmids: definition of two subgroups of P plasmids.

The transfer systems of broad host range IncP plasmids are increasingly used in the genetic analysis and manipulation of many gram-negative bacteria. We have examined the structural and functional relatedness of the transfer origins of ten different broad host range plasmids which belong to the IncP incompatibility group. The data reported here, together with our results on relatedness of the replication segments of these plasmids, demonstrate that the genomes of all IncP plasmids share extensive sequence homology in the regions specifying the transfer origin and replication functions. The homology results reveal the existence of two subclasses among IncP plasmids, designated here as IncP alpha and IncP beta. Furthermore, a functional analysis of the transfer origins of IncP plasmids suggests strongly that the DNA-nicking relaxation complex (Guiney and Helinski 1979) is required for plasmid transfer during conjugation.

Base Sequence↗

PubMed1985

Regulation of replication and maintenance functions of broad host-range plasmid RK2.

Replication of broad host-range plasmid RK2 depends on a cisacting vegatative replication origin oriVRK2 and the polypeptide product(s) of the trans-acting gene trfA as well as on host-specified products. The trfA gene is the second cistron in a polycistronic unit whose first cistron may be kilD, one of 4 known RK2-specified kil loci (kilA, B, C, and D) which are inhibitory for bacterial host or plasmid vector in the absence of kor functions which suppress in trans the effect of their respective kil genes. Transcription of the operon containing trfA is negatively regulated by the products of both the trfB locus (alias korD and korA) and korB. The loci, trfB and korB, are expressed from a single transcriptional unit which we propose to be negatively autoregulated by the products of both loci, although an additional, weaker and unregulated transcript may also express korB. While deletions in the oriVRK2 region have indicated the presence of copy number control elements adjacent to and possibly overlapping with the minimal oriVRK2 segment, the overriding control of copy number seems to reside in the trfB and korB loci which in conjunction appear to reduce expression of the trfA gene to levels limiting for replication. Coregulation of trfA with kil genes may indicate that kil genes play a role in plasmid maintenance other than replication.

Bacterial Proteins↗

PubMed1994

Extension of Autographa californica nuclear polyhedrosis virus host range by interspecific replacement of a short DNA sequence in the p143 helicase gene.

Recombinant baculoviruses obtained by coinfection of insect cells with Autographa californica and Bombyx mori nuclear polyhedrosis viruses (AcNPV and BmNPV, respectively) possess a wider in vitro host range than either parent virus. To localize the DNA sequences responsible for this species specificity, we used a two-step method of production and selection of recombinant viruses with altered specificity. Sf9 cells, which are permissive for AcNPV, were first cotransfected with genomic AcNPV DNA and a complete or incomplete set of BmNPV restriction fragments. AcNPV-BmNPV recombinants from the Sf9 supernatant were then selected on the basis of ability to replicate in B. mori Bm5 cells, which are not permissive for AcNPV. Cotransfection of AcNPV DNA with the 7.6-kbp BmNPV Sma I-C fragment was sufficient to produce recombinants able to infect both Sf9 and Bm5 cells. A series of cotransfections with subclones of this fragment defined a 79-nt sequence within the p143 helicase gene capable of extending AcNPV host range in vitro. In this 79-nt region, BmNPV and AcNPV differ at six positions, corresponding to four amino acid substitutions. The involvement of the 79-nt region in species specificity control was confirmed by cotransfecting AcNPV DNA and gel-purified polymerase chain reaction products derived from the BmNPV p143 gene. Replacement in the AcNPV genome of three AcNPV-specific amino acids by the three corresponding BmNPV-specific amino acids at positions 556, 564, and 577 of the p143 protein extends AcNPV host range to B. mori larvae.

Amino Acid Sequence↗

PubMed1970

Host-range restrictions of murine leukemia viruses in mouse embryo cell cultures.

Murine leukemia virus strains fall into three categories with respect to their ability to propagate in cells of National Institutes of Health (NIH) Swiss and BALB/c mouse embryos. Cultures of NIH cells are 100- to 1,000-fold more sensitive to "N-tropic" strains than BALB/c cell cultures, but are 30- to 100-fold less sensitive to "B-tropic" strains. Some virus strains (dually tropic or "NB-tropic") propagate equally well in both cells. M-MSV pseudotypes show the host-range characteristics of the virus supplying the envelope, both in vitro and in vivo. The host-range characteristics appear to be genetically determined and could not be explained by host-induced modification or virus mixtures. There was no correlation between host range and Gross-AKR or FMR serotype.

Animals↗

PubMed2003

Host range of chlamydiaphages phiCPAR39 and Chp3.

The host range of phiCPAR39 is limited to four Chlamydophila species: C. abortus, C. caviae, C. pecorum, and C. pneumoniae. Chp3 (a newly discovered bacteriophage isolated from C. pecorum) shares three of these hosts (C. abortus, C. caviae, and C. pecorum) but can additionally infect Chlamydophila felis. The ability to support replication was directly correlated with the binding properties of the respective bacteriophages with their host species. Binding studies also show that phiCPAR39 and Chp3 use different host receptors to infect the same host cells: cell binding is sensitive to proteinase K treatment, confirming that the chlamydiaphage receptors are proteinaceous in nature.

Bacteriophages↗