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At least 433 records · Page 24Linked to original sources
PubMed1974

Fish rhabdovirus replication in non-piscine cell culture: new system for the study of rhabdovirus-cell interaction in which the virus and cell have different temperature optima.

The replication of three rhabdoviruses associated with diseases of fish has been demonstrated in cells of continuously cultivated non-piscine cell lines. Spring viremia of carp (SVC) virus and the salmonid fish viruses, Egtved and infectious hematopoietic necrosis virus, all replicated in mammalian WI-38 (human diploid cell strain) and BHK/21 cells and in cells of one or more reptilian cell lines at the temperatures commonly used to propagate these viruses in fish cells. The infections were cytopathic: SVC virus plaque assays may be performed in several types of mammalian cell culture. "Autointerference" apparently mediated by abortive "T" particle formation was observed during serial nondiluted passages of SVC virus in BHK/21 and TH1 cells, but not in RTG-2 or WI-38 cells. Optimal temperatures for replication of SVC and Egtved viruses in BHK/21 cells were identical to those determined in poikilothermic vertebrate cell cultures. However, these viruses replicated relatively more efficiently at suboptimal temperatures in "cold-blooded" vertebrate cells than in the hamster cells. Studies of [(3)H]uridine incorporation into uninfected BHK/21 cells incubated at different temperatures revealed that [(3)H]uridine uptake is sharply reduced at temperatures below 24.5 C. Growth curve studies of SVC virus in BHK/21 cells incubated at 23 C revealed that a clear-cut large excess of virus-induced [(3)H]uridine incorporation could be demonstrated in the absence of actinomycin D. Actinomycin D treatment (1 mug/ml) led to efficient inhibition of control cell [(3)H]uridine uptake, but also markedly reduced the total counts per minute of virus-induced [(3)H]uridine uptake, without depressing the yield of released infectious virus. Actinomycin D added to SVC virus-infected BHK/21 cell cultures at concentrations as low as 0.01 mug/ml caused a significant decrease in the level of virus-induced [(3)H]uridine uptake, despite the fact that this concentration is insufficient to efficiently suppress "background" cellular [(3)H]uridine incorporation.

Animals↗
PubMed1982

Susceptibility of bovine macrophages to infectious bovine rhinotracheitis virus infection.

Infectious bovine rhinotracheitis virus replicated in cultured bovine alveolar macrophages (AM). However, yields of infectious virus were low, with maximum titers approximately 100 times that of the residual inoculum. Immunofluorescence and electron microscopic studies indicated that the majority of macrophages produced viral antigen, but after infection at a multiplicity of 0.1, only 4.1% of AM produced infectious centers. Virus-infected AM culture supernatants possessed interfering activity, probably due to interferon. Incubation of fresh AM with these fluids rendered them refractory to infection. Although AM from infectious bovine rhinotracheitis virus-immune and -susceptible donors were equally permissive and their susceptibility was unaltered by incubation with bacterial lipopolysaccharide, bovine mammary macrophages which were elicited with lipopolysaccharide became nonpermissive when further incubated for 48 h with 1 microgram of lipopolysaccharide per ml. Under these conditions, infected mammary macrophages failed to synthesize viral DNA, and there was reduced synthesis of "late" viral polypeptides.

Animals↗
PubMed1973

Attempts to detect homologous autointerference in vivo with influenza virus and vesicular stomatitis virus.

Von Magnus particles of influenza virus and defective interfering T particles of vesicular stomatitis virus were unable to provide significant protection of mice from disease or death when inoculated intranasally or intracerebrally along with moderate or high doses of homologous infectious challenge virus. However, yields of infectious virus from the affected organs were reduced as compared to controls inoculated with infectious virus alone. Serial intracerebral passage of vesicular stomatitis virus in mouse brain at high doses failed to produce T particles detectable by in vitro autointerference assays on BHK(21) cells, whether or not T particles were introduced along with B virions at the first passage. When very low challenge doses of infectious B virions were inoculated intracerebrally along with high doses of homologous defective particles, there was significant prolongation of life, although most mice died eventually of slowly progressing disease. Also, the virus yields in the brains of these mice were significantly reduced, and virus was no longer detectable in the brains of "protected" mice surviving for 10 days or more. Our results suggest that although homologous autointerference does occur in vivo, it is a more complex phenomenon than in vitro cell culture experiments might indicate.

Animals↗
PubMed1973

Mycoplasma-associated induction of interferon in ovine leukocytes.

A mycoplasmal species, Acholeplasma laidlawii, isolated as a contaminant from a fetal lamb kidney cell line, was shown to be associated with the induction of interferon in cultures of ovine peripheral blood leukocytes. Broth cultures of the mycoplasma induced between 20 and 230 U of interferon per ml in leukocytes from two adult ewes. The amount of interferon produced correlated with the inoculum size of mycoplasma. Interferon production was associated with replication of the mycoplasma in the leukocyte cultures. Interferon was not induced by sterile mycoplasmal broth, a cell-free filtrate of the mycoplasmal cultures, or heat-inactivated mycoplasmas. The antiviral substance was characterized as interferon by the usual criteria.

Animals↗
PubMed1999

Site-specific recombination of temperate Myxococcus xanthus phage Mx8: regulation of integrase activity by reversible, covalent modification.

Temperate Myxococcus xanthus phage Mx8 integrates into the attB locus of the M. xanthus genome. The phage attachment site, attP, is required in cis for integration and lies within the int (integrase) coding sequence. Site-specific integration of Mx8 alters the 3' end of int to generate the modified intX gene, which encodes a less active form of integrase with a different C terminus. The phage-encoded (Int) form of integrase promotes attP x attB recombination more efficiently than attR x attB, attL x attB, or attB x attB recombination. The attP and attB sites share a common core. Sequences flanking both sides of the attP core within the int gene are necessary for attP function. This information shows that the directionality of the integration reaction depends on arm sequences flanking both sides of the attP core. Expression of the uoi gene immediately upstream of int inhibits integrative (attP x attB) recombination, supporting the idea that uoi encodes the Mx8 excisionase. Integrase catalyzes a reaction that alters the primary sequence of its gene; the change in the primary amino acid sequence of Mx8 integrase resulting from the reaction that it catalyzes is a novel mechanism by which the reversible, covalent modification of an enzyme is used to regulate its specific activity. The lower specific activity of the prophage-encoded IntX integrase acts to limit excisive site-specific recombination in lysogens carrying a single Mx8 prophage, which are less immune to superinfection than lysogens carrying multiple, tandem prophages. Thus, this mechanism serves to regulate Mx8 site-specific recombination and superinfection immunity coordinately and thereby to preserve the integrity of the lysogenic state.

Bacteriophages↗
PubMed1999

Characterization of the major control region of Vibrio cholerae bacteriophage K139: immunity, exclusion, and integration.

The temperate bacteriophage K139 is highly associated with pathogenic O1 Vibrio cholerae strains. The nucleotide sequence of the major control region of K139 was determined. The sequences of four (cox, cII, cI, and int) of the six deduced open reading frames and their gene order indicated that K139 is related to the P2 bacteriophage family. Two genes of the lysogenic transcript from the mapped promoter PL encode homologs to the proteins CI and Int, with deduced functions in prophage formation and maintenance. Between the cI and int genes, two additional genes were identified: orf2, which has no significant similarity to any other gene, and the formerly characterized gene glo. Further analysis revealed that Orf2 is involved in preventing superinfection. In a previous report, we described that mutations in glo cause an attenuation effect in the cholera mouse model (J. Reidl and J. J. Mekalanos, Mol. Microbiol. 18:685-701, 1995). In this report, we present strong evidence that Glo participates in phage exclusion. Glo was characterized to encode a 13.6-kDa periplasmic protein which inhibits phage infection at an early step, hence preventing reinfection of vibriophage K139 into K139 lysogenic cells. Immediately downstream of gene int, the attP site was identified. Upon analysis of the corresponding attB site within the V. cholerae chromosome, it became evident that phage K139 is integrated between the flagellin genes flaA and flaC of O1 El Tor and O139 V. cholerae lysogenic strains.

Amino Acid Sequence↗
PubMed2004

The vir gene of bacteriophage MAV1 confers resistance to phage infection on Mycoplasma arthritidis.

Lysogenization of Mycoplasma arthritidis with the MAV1 bacteriophage increases the virulence of the mycoplasma in rats. The MAV1 vir gene is one of only two constitutively transcribed phage genes in the lysogen. We show here that Vir is a lipoprotein and is located on the outer surface of the cell membrane. To investigate whether Vir is a virulence factor, the vir gene was cloned into the transposon vector Tn4001T and inserted in the genome of the nonlysogen strain 158. The virulence of the resulting transformants was no different from that of the parent strain. Interestingly, all vir-containing transformants were resistant to infection by MAV1. Vir had no effect on MAV1 adsorption. We conclude that Vir is not a virulence factor but functions to exclude superinfecting phage, possibly by blocking the injection of phage DNA into the bacterial cytoplasm.

Animals↗
PubMed1973

Superinfection exclusion by incomplete genomes of bacteriophage T4.

The genetic basis of superinfection exclusion by bacteriophage T4 was investigated by using incomplete genomes derived from the gene 66 mutant E920g. Incomplete genomes, which included a region of T4 between genes 42 and 44, were able to exclude superinfecting phage with an efficiency similar to that of complete genomes. Those genomes which did not include this region were unable to exclude superinfecting phage. A mutant with reduced ability to exclude super-infecting phage was isolated after mutagenesis with hydroxylamine. The mutation maps midway between amN122 in gene 42 and amB22 in gene 43. The efficiency of exclusion of superinfecting phage (as measured by the percentage of superinfected cells which failed to release any phage carrying selected markers of the superinfecting phage) by this mutant was 50 to 60%, whereas for wild type it was 85 to 95%. Uptake of (3)H-leucine by cells infected with the mutant was inhibited by superinfection with ghosts and it has therefore been designated imm1, for lack of immunity to superinfecting phage and ghosts. The formation of infective centers by cells infected with imm1 or another imm(-) mutant (imm2) was not inhibited by superinfection with ghosts.

Alleles↗
PubMed1973

Defective interfering particles of poliovirus. IV. Mechanisms of enrichment.

Infection of HeLa cells by mixtures of standard poliovirus and defective, interfering (DI) poliovirus particles leads to a higher ratio of DI particles in the progeny than in the inoculum. The extent of this enrichment could be varied by various manipulations of the co-infected cells. At any time during the infection cycle, virions made within short times after addition of radioactive uridine were hyperenriched in DI particles; this transient hyperenrichment fell to the equilibrium enrichment level within 45 min after uridine addition. A shift of the temperature of infection from 37 to 31 C also led to a hyperenrichment of DI particles and pulse-labeling revealed a superimposed transient hyperenrichment. By contrast, cells continuously infected at 31 C showed a severe decrement in DI particles apparently because poliovirus DI particles behave as cold-sensitive mutants for RNA synthesis. Cycloheximide treatment early in the infection cycle also led to hyperenrichment. Study of the cycloheximide effect showed that the drug acted as if to change the input ratio of standard to DI particles. These effects on enrichment can be explained as aspects of two different phenomena: enrichment due to preferential DI RNA synthesis and enrichment due to preferential encapsidation of DI RNA. Both mechanisms probably play a role in the normal level of enrichment.

Carbon Radioisotopes↗
PubMed1974

Spackle and immunity functions of bacteriophage T4.

Cells of Escherichia coli B infected with the immunity-negative (imm2) mutant of bacteriophage T4 are able to develop a substantial level of immunity to superinfecting phage ghosts if the ghost challenge is made late in infection. This background immunity is not seen in infections with phage carrying the spackle (s) mutation in addition to the imm2 lesion. The level of immunity in s(-) infections is intermediate between that of imm(-) and wild-type infections under standard assay conditions. With respect to genetic exclusion of superinfecting phage, cells infected with imm(-) phage are completely deficient, whereas infections with the s(-) phage are only partially deficient compared to wild-type infections. Whereas s(-)-infected cells are unable to resist lysis from without by a high multiplicity of infection (MOI) of superinfecting phage, cells infected with imm(-) phage show less than wild-type levels of resistance and the majority of cells remaining intact are unable to incorporate leucine or form infective centers. Under conditions of superinfection by low MOI of homologous phage, imm(-)-infected cells are lysis inhibited, whereas s(-)-infected cells do not show this property. Superinfecting phage inject their DNA into imm(-)-infected cells with the same efficiency as seen in wild-type infections, but this efficiency is reduced when the cells are first infected with s(-) phage. The s function of T4 appears not only to affect the host cell wall as previously postulated by Emrich, but may also affect the junctures of cell wall and membrane with consequences similar to those of the imm function.

Bacterial Proteins↗
PubMed1974

Defective interfering passages of Sindbis virus: nature of the intracellular defective viral RNA.

BHK cells infected with defective-interfering passages of Sindbis virus accumulate a species of RNA (20S) that is about half the molecular weight of the major viral mRNA (26S). We have performed competitive hybridization experiments with these species of RNA and have established that 20S RNA contains approximately 50% of the nucleotide sequences present in 26S RNA. Our further studies, however, demonstrate that 20S RNA is unable to carry out the messenger function of 26S RNA. We found very little of the defective RNA associated with polysomes in vivo. In addition, it was unable to stimulate protein synthesis in vitro under conditions in which 26S RNA was translated. We have also examined viral RNA synthesis in BHK cells infected with standard or defective-interfering passages of Sindbis virus. This comparison suggests that defective partioles do not synthesize a functional replicase.

Animals↗
PubMed1975

Bacteriophage P22 virion protein which performs an essential early function. II. Characterization of the gene 16 function.

P16 is a virion protein and, as such, is incorporated into the phage head as a step in morphogenesis. The role of P16 in assembly is not essential since particles are formed without this protein which appear normal by electron microscopy. P16 is essential when the particle infects a cell in the following cycle of infection. In the absence of functional P16, the infection does not appear to proceed beyond release of phage DNA from the capsid. No known genes are expressed, no DNA is transcribed, and the host cell survives the infection, continuing to grow and divide normally. The P16 function is required only during infection for the expression of phage functions. Induction in the absence of P16 proceeds with the expression of early and late genes and results in particle formation. P16 must be incorporated during morphogenesis into progeny particles after both infection and induction for the progeny to be infectious. The P16 function is necessary for transduction as well as for infection. Its activity is independent of new protein synthesis and it is not under immunity control. P16 can act in trans, but appears to act preferentially on the phage or phage DNA with which it is packaged. The data from complementation studies are compatible with P16 release from the capsid with the phage DNA. In the absence of P16 the infection is blocked, but the phage genome is not degraded. The various roles which have been ruled out for P16 are: (i) an early regulatory function, (ii) an enzymatic activity necessary for phage production, (iii) protection of phage DNA from host degradation enzymes, (iv) any generalized alteration of the host cell, (v) binding parental DNA to the replication complex, and (vi) any direct involvement in the replication of P22 DNA. P16 can be responsible for: (i) complete release of the DNA and disengagement from the capsid, (ii) bringing the released DNA to some necessary cell site or compartment such as the cytoplasm, (iii) removal of other virion proteins from the injected DNA, and (iv) alterations of the structure of the injected DNA.

Adsorption↗
PubMed1968

Replication of mengovirus in HeLa cells preinfected with nonreplicating poliovirus.

The replication of mengovirus in HeLa cells preinfected with poliovirus in the presence of 10(-3) M guanidine was investigated. Although host cell protein synthesis is inhibited by the presence of nonreplicating poliovirus, it is found that mengovirus ribonucleic acid (RNA) and protein synthesis proceed normally under the same conditions. Furthermore, no effects on mengovirus growth by poliovirus can be detected either when Mengo protein synthesis is interrupted by Acti-Dione or when its RNA synthesis is reduced by incubation at 28 C. It is suggested that the poliovirus inhibitory factor may be able to distinguish between an RNA element required in the protein-synthesizing apparatus of the host cell and a comparable element in that of the heterologous virus.

Carbon Isotopes↗
PubMed1977

Characterization of a temperature-sensitive mutant of human adenovirus type 7.

The properties of a naturally occurring temperature-sensitive (ts) mutant of human adenovirus type 7 (Ad7) were studied. Mutant Ad7 (19), or E46-, was the nonhybrid adenovirus component derived from the defective simian virus 40 (SV40)-Ad7 hybrid (PARA). Growth of the mutant was restricted at 40.5 degrees C, and the ratios of virus yields in KB cells at 40.5 and 33 degrees C were 10(-2) to 10(-3). Viral DNA synthesis and the synthesis of adenovirus-specific antigens (tumor, capsid, hexon, and penton antigens) appeared normal at the restrictive temperature. The assembly of virus particles was aberrant, as determined by thin-section of infected cells. The infectivity of mutant virions was heat labile at 50 degrees C, suggesting a ts defect in a structural component of the viron. Analysis by polyacrylamide gel electrophoresis of [35S]methionine-labeled polypeptides synthesized in mutant-infected cells suggested that at least the major virion polypeptides were synthesized at the restrictive temperature. A lack of inhibition of host protein synthesis late in mutant infections, as compared with wild-type (WT) infections at both the permissive and nonpermissive temperatures, made quantitation of infected-cell polypeptides difficult. Analysis of the assembly of capsomeres from cytoplasmic extracts of infected cells on sucrose gradients and by non-dissociating polyacrylamide gel electrophoresis suggested that hexon capsomeres were made at 40.5 degrees C. The hexon capsomeres made by the mutant at either 33 or 40.5 degrees C displayed a decreased migration in the non-dissociating gels compared with the WT hexon capsomeres. The molecular weights of the mutant and WT hexon polypeptides were identical. These results suggest that the ts lesion of this group B human Ad7 mutant may be reflected in altered hexons. The mutant Ad7 interfered with the replication of adenovirus types 2 and 21 at the elevated temperature.

Adenoviruses, Human↗
PubMed1977

Formation of reticuloendotheliosis virus pseudotypes of Rous sarcoma virus.

Superinfection of chicken embryo fibroblasts transformed by the defective Bryan strain of Rous sarcoma virus (BH-RSV) with two different reticuloendotheliosis viruses (REVs), REV strain T (REV-T) or spleen necrosis virus (SNV), resulted in the production of infectious sarcoma virus pseudotypes. These pseudotypes were neutralized by antiserum prepared against SNV and were unable to infect chicken cells preinfected with either REV-T or SNV. These results suggest that defective BH-RSV is able to use the glycoprotein from REV to form infectious pseudotypes. On the other hand, neither REV-T nor SNV was able to supply a functional reverse transcriptase to the polymerase-negative mutant BH-RSValpha, nor was REV-T or SNV able to complement the defect in the internal protein gene of the temperature-sensitive avian sarcoma virus mutant NY45.

Animals↗
PubMed1977

Pseudotypes of vesicular stomatitis virus with the envelope properties of mammalian and primate retroviruses.

By employing improved techniques it has been possible to produce and characterize a representative spectrum of mammalian and primate retrovirus pseudotypes of vesicular stomatitis virus (VSV). Selection of appropriate cell lines for both the production and subsequent detection of the VSV pseudotypes has been the most important factor in permitting their demonstration. The host range for penetration of these retrovirus pseudotypes of VSV has been defined and found to differ from that reported for the replication of the corresponding retroviruses. Additionally, retroviruses having an identical host range for replication were distinguishable by differences in their host range for penetration, implying that restriction of replication may be occurring by different mechanisms. Studies of the plaque-forming efficiency of retrovirus pseudotypes of VSV in cell lines nonpermissive for replication of the corresponding retroviruses permitted a distinction to be made between the restriction of replication occurring as a consequence of postpenetration events and that occurring as a consequence of a block of penetration itself. The demonstration of primate retrovirus pseudotypes of VSV permits the use of VSV as a probe for the detection of this group of viruses.

Animals↗
PubMed1978

Replication process of the parvovirus H-1. X. Isolation of a mutant defective in replicative-form DNA replication.

A temperature-sensitive mutant of H-1, ts14, that is partially defective in replicative-form (RF) DNA synthesis has been isolated. ts14 H-1 is characterized by a decrease in plaque-forming ability and production of infectious virus at the restrictive temperature of 39.5 degrees C. RF DNA synthesis of ts14 is reduced to 3 to 7% of that of wild-type H-1 at either the restrictive or the permissive temperature. A complementation analysis of RF synthesis of ts14 and a viable defective H-1 virus, DI-1, or wild-type H-3 indicates that the defective RF DNA synthesis of ts14 is cis-acting. ts14, unlike wild-type H-1, causes a multiplicity-dependent inhibition of DI-1 or H-3, but not LuIII, RF DNA synthesis. Mixed infections of cells with two parvoviruses also exhibited a cross-interference for viral protein synthesis that was multiplicity dependent, ts14 inhibited infectious virus production of H-1 or H-3, but not LuIII. LuIII-or H-3-pseudotype particles were produced by coinfection with H-1. H-3 and H-1 showed similar interactions with ts14, and H-3 DNA was more homologous to H-1 than was LuIII by comparative physical mapping studies. The results suggest that ts14 is a mutant with a defect in a regulatory sequence of its DNA that influence RF DNA replication.

DNA Replication↗