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PubMed2007

The Rta/Orf50 transactivator proteins of the gamma-herpesviridae.

The replication and transcription activator protein, Rta, is encoded by Orf50 in Kaposi's sarcoma-associated herpesvirus (KSHV) and other known gammaherpesviruses including Epstein-Barr virus (EBV), rhesus rhadinovirus (RRV), herpesvirus saimiri (HVS), and murine herpesvirus 68 (MHV-68). Each Rta/Orf50 homologue of each gammaherpesvirus plays a pivotal role in the initiation of viral lytic gene expression and lytic reactivation from latency. Here we discuss the Rta/Orf50 of KSHV in comparison to the Rta/Orf50s of other gammaherpesviruses in an effort to identify structural motifs, mechanisms of action, and modulating host factors.

Animals↗
PubMed1995

The Escherichia coli heat shock response and bacteriophage lambda development.

The Escherichia coli/bacteriophage lambda genetic interaction system has been used to uncover the existence of various biological machines. The starting point of all these studies was the isolation and characterization of E. coli mutants that blocked lambda growth, and the corresponding lambda compensatory mutations. In this manner, the lambda N-promoted transcriptional anti-termination machine was discovered composed of the NusA/NusB/NusE/NusG host proteins. In addition, the DnaK and GroEL chaperone machines were discovered composed of DnaK/DnaJ/GrpE and GroES/GroEL heat shock proteins. The individual members of the DnaK and GroEL chaperone machines have been conserved throughout evolution in both function and structure. Their biological roles include a direct involvement in lambda DNA replication and morphogenesis, the protection of proteins from aggregation, the disaggregation of various protein aggregates, the manipulation of protein structure and function, as well as the autoregulation of the heat shock response. The evolution of lambda to extensively rely on the status of the heat shock response of E. coli is likely linked to its lytic versus lysogenic choice of lifestyle. The bacteriophage T4 gp31 protein has been purified and shown to substitute for many of GroES' co-chaperonin activities.

Bacteriophage lambda↗
PubMed1986

Effect of interferon on Vero cells persistently infected with SSPE virus and lytically infected with measles virus.

The effect of lymphoblastoid interferon (IFN) on viral polypeptides synthesized in a Vero cell culture persistently infected with subacute sclerosing panencephalitis virus (SSPE-Vero) was compared to that of Vero cells infected with exogenous measles virus. After IFN treatment there was no significant decrease in the synthesis of SSPE viral proteins, but inhibition of synthesis of measles polypeptides was readily seen. In Vero and SSPE-Vero cells IFN was able to inhibit replication of Sindbis virus although the effect in Vero cells was significantly more sensitive. In both cell lines IFN was able to stimulate 2'--5' oligoadenylate synthetase (E enzyme) but not the protein kinase system. The SSPE-Vero cells showed a lower basal level of E enzyme activity than the Vero cells.

2',5'-Oligoadenylate Synthetase↗
PubMed2003

Synergistic autoactivation of the Epstein-Barr virus immediate-early BRLF1 promoter by Rta and Zta.

Expression of two Epstein-Barr virus (EBV) immediate-early gene products, Zta (encoded by the BZLF1 gene) and Rta (encoded by the BRLF1 gene), are required for the switch from latent infection to virus replication. We have analyzed the regions of the BRLF1 gene promoter (Rp) that are required for Rta and Zta transactivation of Rp. Notably, significant synergy between the actions of Rta and Zta on Rp was observed in both a B cell line (DG75) and an epithelial cell line (293), suggesting that during induction of the viral lytic cycle low levels of these viral transactivators are likely sufficient to initiate the entire lytic cascade. However, while two Zta binding sites (ZREs) have been identified in Rp, the proximal ZRE was the dominant site for mediating Zta transactivation. Rta activation of Rp was diminished by mutation of the proximal Sp1 binding site, as previously reported (J. Virol. 75 (2001), 5240), but mutation of this site only had a modest impact on transactivation of Rp by Rta in the presence of Zta. Further deletion analyses of Rp failed to identify a critical site for Rta transactivation of Rp in the presence of Zta, with the exception of deleting the TATAA box of Rp, suggesting that a non-DNA binding mechanism may be involved in the observed activation of Rp by Rta. We also observed promiscuous activation of several reporter constructs by Rta, suggesting that Rta activation of gene expression may involve a general non-DNA binding mechanism. Decreasing the amount of transfected Rta expression vector reduced background Rta activation, while retaining specific activation of Rp.

Base Sequence↗
PubMed1977

[The action of selected herbicides on bacteriophages and Escherichia coli (author's transl)].

The effect of eight herbicides on the multiplication of bacteria and bacteriophages was tested with Escherichia coli, strains W1665F+ and C600, and with the RNA-phage M12 and the DNA-phage lambda in turbidimetric investigations and one-step growth experiments. E. coli is inhibited by seven of the herbicides investigated in concentrations of 10(-3)M, partly of 10(-4)M, too, and is promoted by some compounds in weaker concentrations. Naphthylacetic acid, (NES) largely independent of its concentration, causes increased density of bacteria in fluid culture. The multiplication of the M12 phage is inhibited in sometimes wide ranges of concentration by 2,4-D, MCPA, 2,4-DP, and CMPP but it is stimulated by NES and amitrole. The lambda-phage multiplication is inhibited only by CMPP, MCPA, MCPB, and phenylacetic acid interfere with the lysogenization of the bacteria and increase the lytic activity of the lambda-phages as 2,4-DP and NES do. 2,4-D strongly inhibits the plaque-forming ability of M12 phages already prior to their contact with the host cells, whereas MCPA and CMPP are inhibitory in the first phases and 2,4-DP in all phases of the phage replication. In the lambda-phage replication, too, CMPP is effective only in the first phases. Aspects of the mode of action of the herbicides in the procaryoute virus system are discussed.

Cell Division↗
PubMed1999

Maintenance of episomal SV40 genomes in GM637 human fibroblasts.

Episomal SV40 (SV40: simian virus 40, Polyomavirus maccacae) has been reported in SV40-transformed human fibroblast cell lines the integrated SV40 sequences of which are unlikely to give rise to episomal copies by recombinational mechanisms. The levels of episomal viral DNA in these lines are high, being easily visualized by ethidium staining of agarose gels after electrophoresis. We find that the episomal mutant gmSV40 in GM637 cells represents a persistent lytic infection that can be cured by treatment with neutralizing antibody, leaving only the chromosomally integrated viral genomes. The finding that maintenance of the gmSV40 in GM637 cells is due to persistent infection raises a note of caution for SV40-transformed lines with episomal SV40 genomes because these lines often are used in studies of DNA replication and repair. An infective center assay that does not depend on plaque formation shows that gmSV40 is a host range mutant, with poor infectivity for CV-1 monkey kidney cells and greatly increased infectivity for human cells. Passage of gmSV40 through monkey kidney cells selects for variants with greatly increased infectivity for monkey cells and, independently, for cytopathic variants that produce plaques. Thus plaque assays can give very unreliable infective center values in studies of host range mutants.

Animals↗
PubMed2003

Immunity profiles of wild-type and recombinant shiga-like toxin-encoding bacteriophages and characterization of novel double lysogens.

The pathogenicity of Shiga-like toxin (stx)-producing Escherichia coli (STEC), notably serotype O157, the causative agent of hemorrhagic colitis, hemolytic-uremic syndrome, and thrombotic thrombocytopenic purpura, is based partly on the presence of genes (stx(1) and/or stx(2)) that are known to be carried on temperate lambdoid bacteriophages. Stx phages were isolated from different STEC strains and found to have genome sizes in the range of 48 to 62 kb and to carry either stx(1) or stx(2) genes. Restriction fragment length polymorphism patterns and sodium dodecyl sulfate-polyacrylamide gel electrophoresis protein profiles were relatively uninformative, but the phages could be differentiated according to their immunity profiles. Furthermore, these were sufficiently sensitive to enable the identification and differentiation of two different phages, both carrying the genes for Stx2 and originating from the same STEC host strain. The immunity profiles of the different Stx phages did not conform to the model established for bacteriophage lambda, in that the pattern of individual Stx phage infection of various lysogens was neither expected nor predicted. Unexpected differences were also observed among Stx phages in their relative lytic productivity within a single host. Two antibiotic resistance markers were used to tag a recombinant phage in which the stx genes were inactivated, enabling the first reported observation of the simultaneous infection of a single host with two genetically identical Stx phages. The data demonstrate that, although Stx phages are members of the lambdoid family, their replication and infection control strategies are not necessarily identical to the archetypical bacteriophage lambda, and this could be responsible for the widespread occurrence of stx genes across a diverse range of E. coli serotypes.

Coliphages↗
PubMed1985

[Search for the systems of DNA host specificity in Salmonella typhi].

Seventeen pure lines of S. typhi bacteriophages have been obtained from mother races O and Vi; of these, three were used to study 152 S. typhi strains with a view of detecting their DNA host specificity systems. 10 S. typhi strains having the DNA host specificity system have been detected by the rough determination of the lytic spectrum and the cross titration of phage Vi IX.

Adsorption↗
PubMed2000

Homologous recombination between a lactococcal bacteriophage and the chromosome of its host strain.

Genetic exchanges constitute a significant means by which bacteriophages acquire novel characteristics. Phages of Lactococcus lactis occupy a particular niche, the dairy factory environment, where their populations are subjected to constant changes. Little is known about the mechanisms of evolution that lead to the genetic diversity of lactococcal phages. In this study, we described two DNA exchanges involving the lytic phage ul36, a member of the P335 species, and its L. lactis host. They occurred by homologous recombination with phage-related sequences present in the host chromosome. Both mutants generated by these recombination events are insensitive to the phage resistance mechanism AbiK and one has a reduced burst size as well as a new origin of replication. We propose that this type of DNA exchange with prophages or remnants of prophages occurs frequently within the P335 species as supported by DNA-DNA comparisons between P335-like phages.

Bacterial Proteins↗
PubMed2002

Searching for clues: tracking the pathogenesis of human immunodeficiency virus central nervous system disease by use of an accelerated, consistent simian immunodeficiency virus macaque model.

An accelerated model of human immunodeficiency virus central nervous system disease was developed in which more than 90% of infected macaques develop typical simian immunodeficiency virus (SIV) encephalitis with neuronal dysfunction by postinoculation (pi) day 84. Infected macaques had replicating virus and microglial activation in the brain 10 days after inoculation; viral replication and microglial activation were suppressed at pi day 21. By pi day 56, viral recrudescence in the brain was detected in 2 of 6 infected macaques. CD4 cells were the predominant lymphocytes in the brain during acute and asymptomatic infection; cytotoxic T lymphocytes and NK cells predominated in macaques with encephalitis. Low levels of peripheral blood NK lytic activity at pi day 10, elevated cerebrospinal fluid (CSF) monocyte chemoattractant protein-1 after 28 days, and high CSF viral RNA after 42 days predicted SIV encephalitis. This model is ideal to track the viral, cellular, and immunologic changes in the brain during acute and asymptomatic infection and during viral recrudescence and SIV encephalitis.

AIDS Dementia Complex↗
PubMed2002

Genomic analysis of Clostridium perfringens bacteriophage phi3626, which integrates into guaA and possibly affects sporulation.

Two temperate viruses, phi3626 and phi8533, have been isolated from lysogenic Clostridium perfringens strains. Phage phi3626 was chosen for detailed analysis and was inspected by electron microscopy, protein profiling, and host range determination. For the first time, the nucleotide sequence of a bacteriophage infecting Clostridium species was determined. The virus belongs to the Siphoviridae family of the tailed phages, the order Caudovirales. Its genome consists of a linear double-stranded DNA molecule of 33,507 nucleotides, with invariable 3'-protruding cohesive ends of nine residues. Fifty open reading frames were identified, which are organized in three major life cycle-specific gene clusters. The genes required for lytic development show an opposite orientation and arrangement compared to the lysogeny control region. A function could be assigned to 19 gene products, based upon bioinformatic analyses, N-terminal amino acid sequencing, or experimental evidence. These include DNA-packaging proteins, structural components, a dual lysis system, a putative lysogeny switch, and proteins that are involved in replication, recombination, and modification of phage DNA. The presence of genes encoding a putative sigma factor related to sporulation-dependent sigma factors and a putative sporulation-dependent transcription regulator suggests a possible interaction of phi3626 with onset of sporulation in C. perfringens. We found that the phi3626 attachment site attP lies in a noncoding region immediately downstream of int. Integration of the viral genome occurs into the bacterial attachment site attB, which is located within the 3' end of a guaA homologue. This essential housekeeping gene is functionally independent of the integration status, due to reconstitution of its terminal codons by phage sequence.

Attachment Sites, Microbiological↗
PubMed1997

Derepression of prophage P2 by satellite phage P4: cloning of the P4 epsilon gene and identification of its product.

Escherichia coli phage P4 lacks all of the genetic information necessary for capsid, tail, and lysis functions. P4 is therefore dependent on a helper phage, such as P2, for lytic propagation. During P4 superinfection of a P2 lysogen, the P2 prophage is derepressed by the action of the P4-encoded epsilon gene. We have cloned the epsilon gene and identified the 10-kDa E protein. The epsilon gene product is the only P4 protein required to derepress prophage P2, which leads to in situ P2 DNA replication. A two-plasmid derepression assay system has been developed to examine the derepression activity of E. The reporter plasmid contains the two face-to-face promoters, Pe and Pc, involved in the lysis-lysogeny transcriptional switch of phage P2 and the immunity repressor C. The Pe promoter is coupled to a cat reporter gene. In the construct, the C repressor is transcribed from the Pc promoter and represses the Pe promoter, which mimics the in situ-repressed P2 prophage. The E protein is supplied in trans from a compatible plasmid in which the epsilon gene is under the control of the T7 promoter. We show here that in the two-plasmid assay system, induction of the E protein derepresses the Pe promoter. The ash9 mutation, which is located upstream of the epsilon gene, enhances the E-mediated derepression of the Pe promoter. The purified E protein shows no specific DNA binding activity, and the implications of this are discussed.

Bacteriophage P2↗
PubMed1995

Therapy of experimental human brain tumors using a neuroattenuated herpes simplex virus mutant.

BACKGROUND: Engineered herpes simplex virus (HSV) strains previously have been shown to offer a potential therapeutic alternative to conventional treatment modalities for brain tumors. Because HSV Type 1 strain 1716 has a deletion in the gamma 34.5 neurovirulence gene that renders it avirulent in the mouse central nervous system, we have assessed its potential to induce selective lysis of tumor cells versus neurons in vitro and in vivo. EXPERIMENTAL DESIGN: To do this, we studied parental HSV-1 strain 17+ and strain 1716 using human embryonal carcinoma cells (NT2 cells). These cells resemble neuronal progenitor cells and can be induced to differentiate into neurons (NT2N) with retinoic acid. Intracerebral grafts of NT2 cells into the brains of nude mice resulted in lethal brain tumors, and grafts of NT2N cells resulted in the integration of NT2N cells. RESULTS: In vitro studies showed that strain 1716 replicates in and spreads on monolayers of NT2 cells but not in NT2N cells. In vivo, strain 1716 replicated preferentially in NT2 tumors as evidenced by immunohistochemical staining for viral antigens, by in situ hybridization for HSV-specific transcripts, and by titration of virus from brains with tumor after intracranial injection of the virus into these mice. The temporal regression of NT2 tumors in mice treated with strain 1716 was demonstrated in vivo by magnetic resonance imaging. Electron microscopy and studies of DNA fragmentation suggested that regression of NT2 brain tumors in strain 1716-treated mice was mainly caused by a nonapoptotic, lytic mode of cell death. Finally, strain 1716-treated NT2 tumor-bearing mice survived more than twice as long as mock-treated tumor-bearing mice, and these differences in survival (25 vs. 9 weeks) were statistically significant (p < 0.03). CONCLUSIONS: We conclude from these studies that strain 1716 induces regression of human neural tumors established in the brains of nude mice, resulting in their prolonged survival.

Animals↗
PubMed2004

Phenotype of a herpes simplex virus type 1 mutant that fails to express immediate-early regulatory protein ICP0.

Herpes simplex virus type 1 (HSV-1) immediate-early (IE) regulatory protein ICP0 is required for efficient progression of infected cells into productive lytic infection, especially in low-multiplicity infections of limited-passage human fibroblasts. We have used single-cell-based assays that allow detailed analysis of the ICP0-null phenotype in low-multiplicity infections of restrictive cell types. The major conclusions are as follows: (i) there is a threshold input multiplicity above which the mutant virus replicates normally; (ii) individual cells infected below the threshold multiplicity have a high probability of establishing a nonproductive infection; (iii) such nonproductively infected cells have a high probability of expressing IE products at 6 h postinfection; (iv) even at 24 h postinfection, IE protein-positive nonproductively infected human fibroblast cells exceed the number of cells that lead to plaque formation by up to 2 orders of magnitude; (v) expression of individual IE proteins in a proportion of the nonproductively infected cells is incompletely coordinated; (vi) the nonproductive cells can also express early gene products at low frequencies and in a stochastic manner; and (vii) significant numbers of human fibroblast cells infected at low multiplicity by an ICP0-deficient virus are lost through cell death. We propose that in the absence of ICP0 expression, HSV-1 infected human fibroblasts can undergo a great variety of fates, including quiescence, stalled infection at a variety of different stages, cell death, and, for a minor population, initiation of formation of a plaque.

Animals↗
PubMed2005

Induction and utilization of an ATM signaling pathway by polyomavirus.

Progression from G(1) to S is essential for polyomavirus DNA replication and depends on the interaction of large T with the retinoblastoma gene product pRb. This virus-induced replication pathway is accompanied by p53 activation resembling a DNA damage response (12). We sought to determine whether this pathway depends in part on activation of the ATM (ataxia telangiectasia mutated) kinase and whether the virus gains advantages from this pathway beyond that of entry into S. We show that polyomavirus infection activates the S- and G(2)-phase checkpoints in primary as well as established mouse cells. Infected cells undergo a prolonged S phase compared to uninfected serum-stimulated cells and show no evidence of a G(2)-->M transition before lytic death ensues. Infection is accompanied by increases in ATM activity in vitro and in the level of ATM-S1981-P in vivo. The incubation of infected cells with caffeine, a known ATM inhibitor, did not block entry into S but reduced the rate of viral compared to cellular DNA synthesis. Importantly, caffeine lowered the yields of viral DNA an average of 3- to 6-fold and those of infectious virus by as much as 10-fold. Virus yields were 10-fold lower in ATM (-/-) p53(-/-) than in ATM(+/+) p53(-/-) mouse embryo fibroblasts, indicating a p53-independent role of ATM in productive infection. Replacement of the normal SMC1 (structural maintenance of chromosomes, or cohesin) protein, a critical ATM substrate in the DNA repair pathway, with its phosphorylation mutant SMC1(S957AS966A) also lowered virus yields by roughly 90%. We suggest that polyomavirus activates and utilizes a component(s) of an ATM pathway of DNA repair to prolong S phase and aid its own replication.

Animals↗
PubMed1981

In vivo transcription of Bacillus subtilis bacteriophage SPP1.

The temporal program of SPP1 transcription was examined by hybridizing RNA extracted from infected B. subtilis cells, pulse-labelled at various times after infection, to restriction fragments of SPP1 DNA. RNA made early after infection hybridises to contiguous fragments in the left part of the SPP1 molecule, whereas hybridization to fragments in the right part of the chromosome is found late in infection. Viral gene transcription proceeds from right to left on the H-strand throughout the lytic cycle. At late times transcription occurs also from left to right using the L-strand as template. These assignments follow from the established 5'--3' polarity of the complementary (H- and L-) strains of SPP1 DNA and the determination of strand specificity in SPP1 transcription. Early and late transcriptions are also defined physiologically: protein synthesis and phage DNA replication must precede late transcription.

Bacillus subtilis↗
PubMed2005

The use of bacteriophages in eliminating polyresistant strains of Staphylococcus aureus and Streptococcus agalactiae.

Temperate bacteriophages were induced in and released from isolates of Staphylococcus aureus and Streptococcus agalactiae using mitomycin C. Various specific indicator cultures were tested for providing clear plaques after phage infection. Specific lytic mixture of bacteriophages was prepared using the induced, modified and laboratory variants of phages. Under laboratory conditions, the mixture eliminated all isolates from the tested collection of microorganisms. The restriction barrier of some bacterial isolates to bacteriophage infection was overcome either by UV irradiation or in vitro modification of bacteriophage DNA with specific methyltransferases. Conjugative R plasmids, capable of replication in G+ and G- bacteria, were detected and isolated from S. aureus and S. agalactiae antibiotic-resistant strains.

Animals↗
PubMed2006

Functional role of phosphatidylinositol 3-kinase/Akt pathway on cell growth and lytic cycle of Epstein-Barr virus in the Burkitt's lymphoma cell line, P3HR-1.

The phosphatidylinositol 3-kinase (PI3-K)/Akt pathway is involved in various malignancies, but the role of PI3-K/Akt pathway in Epstein-Barr virus (EBV) infected Burkitt's lymphoma (BL) cells remains unclear. To elucidate therapeutic targets for BL, this study investigates the effect of PI3-K/Akt pathway in: EBV-positive BL cell lines Raji, P3HR-1, Akata and Daudi; and EBV-negative BL cell lines Ramos and BJAB. Results of analyses indicate that Akt was constitutively phosphorylated in BJAB, P3HR-1, Akata, and Daudi but not in Ramos and Raji cells. We characterized Akt phosphorylation on cell growth and EBV lytic cycle in P3HR-1 cells, which were phosphorylated most intensively. The Akt was equally phosphorylated in cells cultured with and without fetal bovine serum for a few days. Akt phosphorylation and cell growth were inhibited by PI3-K specific inhibitor LY294002 in a dose-dependent manner. LY294002 markedly down regulated expression of EBV lytic gene BRLF1 protein Rta, BMRF1 protein EA-D, but not BZLF1 protein ZEBRA. The inhibitor reduced viral capsid antigen (VCA) positive cells. Down regulation of Rta by LY294002 occurred at the transcriptional level. These results demonstrate that PI3-K/Akt pathway is activated constitutively in P3HR-1 cells; it promotes cell growth and the lytic cycle cascade downstream of ZEBRA.

B-Lymphocytes↗