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At least 433 records · Page 24Linked to original sources
PubMed1985

The isolation and characterization of the Blym-1 transforming gene.

There are a number of similarities between chicken bursal lymphomas and human Burkitt's lymphomas. Both lymphomas are associated with viral infection, by LLV in bursal lymphomas and Epstein-Barr virus in Burkitt's lymphoma. Avian lymphoid leukosis virus integration is associated with enhanced c-myc expression, while the role EBV plays in tumorigenesis remains unclear. In Burkitt's lymphoma, however, c-myc activation does occur as a result of specific chromosomal translocations involving the human c-myc locus. Furthermore, the activated transforming genes detected by transfection of both bursal lymphoma and Burkitt's lymphoma DNAs are homologous members of the Blym family of genes. These similarities between chicken and human lymphomas provide evidence that viral involvement and oncogene activation are significant in tumor development and suggest they are involved in the multi-step progression to the neoplastic phenotype. The function of the Blym genes remains to be determined. Although the chicken and human Blym genes are only distantly related, they have maintained their homology to the amino-terminal regions of transferrins. This fact may reflect some functional constraint on the evolution of these genes. It is therefore possible that transforming genes such as Blym may function via a transferrin-related mechanism.

Animals↗
PubMed2003

Intracellular trafficking of HIV-1 cores: journey to the center of the cell.

After entry into the cytoplasm, many diverse viruses, including both RNA and DNA viruses, require import into the nucleus and access to the cellular nuclear machinery for productive replication to proceed. Because diffusion through the crowded cytoplasmic environment is greatly restricted, most (if not all) of these viruses must first be actively transported from the site of cytoplasmic entry to the nuclear periphery (Luby-Phelps 2000; Lukacs et al. 2000; Sodeik 2000). Having reached the nucleus, viruses have evolved assorted methods to overcome the formidable physical barrier that is presented by the nuclear envelope. This review examines how these issues relate to human immunodeficiency virus type-1 (HIV-1) infection. Specifically, HIV-1 uncoating, cytoplasmic transport, and nuclear entry are addressed.

Cell Nucleus↗
PubMed1982

Effects of sodium butyrate, a new pharmacological agent, on cells in culture.

Sodium butyrate, at millimolar concentrations, when added to cell cultures produces many morphological and biochemical modifications in a reversible manner. Some of them occur in all cell lines. They concern regulatory mechanisms of gene expression and cell growth: an hyperacetylation of histone resulting from an inhibition of histone deacetylase and an arrest of cell proliferation are almost constantly observed. Some other modifications vary from one cell type to another: induction of proteins, including enzymes, hormones, hemoglobin, inhibition of cell differentiation, reversion of transformed characteristics of cells to normal morphological and biochemical pattern, increase in interferon antiviral efficiency and induction of integrated viruses. Most if not all these effects of butyrate could result from histone hyperacetylation, from changes in chromatin structures as measured by accessibility to DNases and from modifications in cytoskeleton assembly. We do not know at the present time whether butyrate acts on a very specific target site in cell or if it acts on several cell components.

Acetylation↗
PubMed1987

Sequences which flank an 11p deletion observed in an hepatocellular carcinoma map to 11p13.

There is considerable interest in the 11p13 region because of its involvement in Wilms tumor, sporadic aniridia, and other congenital abnormalities. Cloned DNA sequences from this region might be useful in understanding the chromosomal abnormalities which lead to such disorders. However, few such markers exist. Using somatic cell hybrids which contain defined 11p deletions, two cloned DNA sequences which flank a deletion generated in an hepatocellular carcinoma (as a consequence of hepatitis B virus integration) were mapped to 11p13. Thus both ends of the deletion observed in an hepatocellular carcinoma are within 11p13.

Animals↗
PubMed1993

Transactivation of a plasmid-borne bacteriophage T4 late gene.

We examined how a plasmid-borne T4 late gene is activated by infecting T4 phage (transactivation). A gene fusion system was developed where expression of a late gene promoter fused to the lacZ gene may easily be followed by measuring beta-galactosidase activity. Considerable transactivation can occur, provided that the infecting phage contains a mutation which abolishes the denB-encoded endonuclease, and that the gene 46-encoded exonuclease is functional. The level of transactivation was correlated with the formation of high molecular weight DNA composed of tandem repeats of plasmid DNA. The formation of these molecules and subsequent transactivation depended on DNA replication and homology between phage and plasmid DNAs. Also the capacity of bacteriophage T4, grown on cells containing a plasmid-borne T4 gene, to transduce the plasmid provided indirect evidence of the formation of these tandem-repeat molecules. A good correlation was established between the ability to transduce and the presence of sequence homology between the phage and the plasmid. However, the requirement for phage/plasmid homology is no longer prerequisite if transcription from the plasmid is permitted by introducing an alc mutation into the infecting phage, presumably because this allows DNA replication to start through RNA priming.

Bacteriophage T4↗
PubMed1994

HIV-1 integrase blocks infection of bacteria by single-stranded DNA and RNA bacteriophages.

Expression of human immunodeficiency virus-1 integrase in Escherichia coli, at levels that had no effect on bacterial cell growth, blocked plaque formation by bacteriophages having single-stranded genomic DNA (M13) or RNA (R17, Q beta, PRR1). Plaque formation by phages having double-stranded genomic DNA (T4, PR4) was unaffected. Integrase also inhibited infection by the phagemid M13KO7, but it had no effect on production of phage once infection by M13KO7 was established. This result indicated that integrase affects an early stage in infection. Integrase also inhibited phage production following transfection by either single-stranded or double-stranded (replicative form) M13 DNA, it blocked M13 DNA replication, as assayed by incorporation of radioactive nucleotides into DNA, and it failed to affect bacterial pilus function. These data suggest that integrase interacts in vivo with phage nucleic acid, a conclusion supported by studies in which integrase was shown to have a DNA-binding activity in its C-terminal portion. This portion of integrase was both necessary and sufficient for interference of plaque formation by M13 in the present study. Expression of the N-terminal portion of integrase at the same level as intact integrase had little effect on phage growth, indicating that expression of foreign protein in general was not responsible for the inhibitory effect. The simple bacteriophage assay described is potentially useful for identifying integrase mutants that lack single-stranded DNA binding activity.

Antiviral Agents↗
PubMed1981

The influence of divalent cations on the stability of human rotavirus.

The influence of divalent cations on the stability of human rotavirus was investigated using the indirect immunofluorescence (FA) technique in LLC-MK2 cells to titrate infectivity. Rotavirus infectivity was stabilized by calcium and strontium ions in solution but not by magnesium ions. Rotavirus isolates were found to be much less stable at 37 degrees C than at + 4 degrees C or 20 degrees. A study of virus morphology at intervals during the course of the experiment and treatment with the chelating agents EDTA and EGTA suggests that loss of infectivity coincides with the removal of the outer capsid layer and that calcium may be required to maintain virus integrity.

Animals↗
PubMed1997

Biosynthetic retrovectoring systems for gene therapy.

Chemical and physical methods of introducing genes into cells (transfection) are being combined with viral transduction as one possible approach toward overcoming the shortcomings of current gene transfer methods. Although several different strategies are being developed worldwide, this article focuses on modification of retroviral vectoring systems. One goal of this work is to combine the safety and ease of transfection methods with the permanency that is presently achieved only by integrating viruses. Work with retrotransposon pseudotypes, synthetic retrovectors, and liposomal delivery of retrovirus vectors is discussed.

Animals↗
PubMed1988

Role of endogenous retroviruses as mutagens: the hairless mutation of mice.

We have developed an experimental approach to distinguish the 40-60 endogenous C-type proviruses of mice and to determine their association with well characterized developmental and physiological mutations. The hairless (hr) mutation causes a variety of pleiotropic effects. Using oligonucleotide probes specific for different classes of murine leukemia virus, we have identified and cloned a provirus present in HRS/J hr/hr animals but absent in HRS/J +/+. Genetic analyses showed perfect concordance between the hr phenotype and the presence of the provirus in a number of inbred and congenic strains of mice. Molecular analysis of a haired revertant established the causal relationship since it revealed the excision of most of the proviral genome leaving behind one long terminal repeat. These findings show that virus integration caused the hairless mutation and point to the utility of naturally occurring retroviral integrations for accessing the genome of the mouse.

Alleles↗
PubMed1993

Establishment of HTLV-I-infected cell lines from French, Guianese and West Indian patients and isolation of a proviral clone producing viral particles.

Human T-cell leukemia virus (HTLV-I) induces adult T cell leukemia/lymphoma (ATL) and a chronic neurological disease named either tropical spastic paraparesis (TSP) or HTLV-I associated myelopathy (HAM). We report here the establishment and characterization of eight HTLV-I-infected lymphoid cell lines derived either from patients with TSP (5) or from asymptomatic carriers (1). Southern blot analysis of T cell beta chain gene rearrangements indicates that all cell lines are composed of clonal populations. The same type of analysis performed with HTLV-I-specific probes showed that they harbor 1 to 5 copies of full length proviruses often associated with deleted proviruses with a restriction map for BamHI, HindIII, PstI and SacI restriction enzymes resembling those of HTLV-I previously isolated from Japan and Caribbean area. One of the cell lines, 2060, derived from a TSP patient was shown to express a relative large amount of virus easily transmissible to fresh peripheral and cord blood lymphocytes. The full length proviral genome contained in this cell line was cloned and used in transient expression experiments. We showed that the cloned provirus was able to direct the synthesis of the major structural viral proteins, the protease and the tax and rex regulatory proteins. The structural viral proteins could be assembled into free particles detected in the culture medium of transfected cells. Although the infectivity of these viral particles remains to be determined, this new clone can be employed to examine the cell types in which this TSP-derived provirus directs viral protein synthesis and eventually replicates. It should also prove of value in studies on the early cellular events induced by viral products.

Animals↗
PubMed1994

Accumulation of unintegrated viral DNA in rat glial cells infected with neurotropic Friend murine leukemia virus.

FrC6 virus isolated from Friend murine leukemia virus (FLV) as a neurotropic virus clone induced a high-degree of accumulation of unintegrated viral DNA during infection of rat glial cells by 72 h post-infection. When anti-FLV neutralizing antibody, dextran sulfate, or 3'-azido-3'-deoxythymidine (AZT) was added to the culture within 24 h after infection, the accumulation of unintegrated viral DNA was inhibited. However, after 30-36 h post-infection, addition of anti-FLV antibody or dextran sulfate scarcely inhibited the accumulation of the unintegrated viral DNA, while addition of AZT at 30-36 h post-infection still reduced the amount of unintegrated viral DNA. Our results demonstrate that after 30-36 h post-infection, when second-round infection had already taken place, further superinfection with cell-free virus to glial cells was not required for the accumulation of unintegrated viral DNA. Possible mechanisms are discussed.

Animals↗
PubMed1994

A qualitative process theory based model of the HIV-1 virus-cell interaction.

We present a qualitative model of the interaction between the HIV-1 virus and the human cell, based on qualitative process theory. This model takes into account a previous qualitative model of the cell growth. The model presented here can be regarded as a first step for setting up a comprehensive model of the HIV-1 virus-cell interaction in which the possible points where a drug can attack the virus are evident. The first simulation trials indicate that the presented model reproduces (even though in a simplified way) the features of the real behaviour that have been considered in the modelling phase. Although our simulation is limited in the knowledge it expresses, it still gives a stimulating opportunity for the evaluation of the criteria chosen as discriminant in the interaction between virus and cell.

Antiviral Agents↗
PubMed1993

Benign monoclonal T cell proliferation in HTLV-I infection.

A spectrum of carrier states in human T lymphotropic virus type-I (HTLV-I) infection is proposed. The suspected process of clonal selection of HTLV-I infected cells results in the spectrum of nonfatal states from polyclonal to monoclonal virus integration. This idea is based on the discovery that monoclonal proviral HTLV-I DNA was detected in the fresh peripheral blood lymphocytes from some patients with HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP), a nonfatal chronic neurological disorder.

Carrier State↗
PubMed1990

Localization of the gene for the trans-acting transcription factor Sp1 to the distal end of mouse chromosome 15.

The mouse chromosomal location for the gene (Sp1-1) encoding the trans-acting transcription factor Sp1 has been determined. Analysis of restriction fragment length polymorphisms in recombinant inbred, congenic, and interspecific backcross mice using human and mouse cDNA probes demonstrated that Sp1-1 is a single gene closely linked to the mammary tumor virus integration site-1 (Int-1) on the distal end of chromosome 15. Sp1 is a zinc finger protein, but Sp1-1 is not closely linked to any of the other zinc finger protein genes that have been mapped in mouse. Int-1 and other markers flanking the Sp1-1 locus are part of a conserved linkage group represented on human chromosome 12q.

Animals↗