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Results for “Virus Integration”

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At least 559 records · Page 31Linked to original sources
PubMed1976

[The interaction between cells and fibrous dusts (author's transl)].

The shape of fibrous dust particles is an important factor for the biological effects in cell cultures. The fibres elicit a special mechanism of incorporation which is dependent on their length and diameter but independent of their chemical composition. Fibres with a length less than 5 mum are phagocytized rapidly and completely by the cells, comparable to granular dust particles or milled fibres. Phagocytosis of long inorganic fibers is delayed and/or remains incomplete. Incomplete incorporation of the fiber causes a localized discontinuity in the cell membrane. There results continuous liberation of intra-cellular enzymes, which is compensated by an increasing glycolytic metabolism. The interaction between cell and fibre means a chronic irritation which is discussed as a factor in tumour induction. Fibrous dusts, e.g. asbestos and glass fibers, induce the formation of polykaryotic giant cells by way of fusion; asbestos possibly also causes the interspecific fusion of cells. There are indications that in the process of asbestos-induced cell fusion integrated virus genomes are activated and infectious viruses are released. There seems to be a causal relationship between the fibrogenic and carcinogenic effects of inorganic dusts and their shape, i.e. their length and diameter, regardless of their chemical composition. Thus the fibrogenic and carcinogenic effect is limited by a minimal length and a maximal diameter. The findings are discussed with regard to the air burden of fibrous dusts and their implications for human health.

Animals↗
PubMed1999

[In vitro study of the interactions between bovine herpesvirus 4 and the bovine host cells].

This work was devoted to the study of the interactions between bovine herpesvirus 4 (BHV-4) and bovine cells in vitro. It led to the discovery of two interesting properties of BVH-4 replication cycle: first, the cellular receptor heparan sulfate was proven to mediate BVH-4 binding to target cells. This is the first description of the implication of heparan sulfate in the binding process of a gammaherpesvirus. Second, using synchronised cells, the replication of BVH-4 DNA was proven to be dependent on the S phase of the cell cycle. This dependence could explain some properties of BVH-4 infection in vitro and could play an important role in the biology of the infection in vivo. Finally, in order to produce monoclonal antibodies against BVH-4 IE1 and IE2 proteins, the genes coding for these proteins were cloned and expressed in prokaryotic cells.

Animals↗
PubMed1999

[Comparison of intracellular and extracellular particles of the vaccinia virus].

The construction of recombinant vaccinia viruses (VV) is definitely a promising approach to develop vaccines for pets. To produce safer VV recombinant vaccines, it is necessary to understand the pathogenesis of VV infection. The goal of this study was to compare the biological properties of the extracellular and intracellular infectious particles of VV. Four biological properties were investigated: (i) the binding into cellular receptor(s); (ii) the mechanism of entry; (iii) the resistance to neutralisation by antibodies; (iv) the resistance to complement lysis. The results obtained in this study emphasize the differences existing between the two infectious forms of VV and demonstrate the adaptation of the extracellular particle to its role of virus dissemination in vivo. The results of this study implicate that VV strains used as expression vector in vaccinology should be deleted for genes required for EEV morphogenesis.

Animals↗
PubMed2000

[From gene to disease; the APC gene and familial adenomatous polyposis coli].

Familial adenomatous polyposis coli is an autosomal dominant hereditary form of colorectal cancer associated with mutations in the adenomatous polyposis coli (APC) gene on chromosome 5. The APC protein is thought to mediate the stability of beta-catenin in the WNT signaling transduction pathway ('wingless-type mouse mammary tumor virus integration site family member') in normal colonic epithelial cells, thereby indirectly regulating the expression of WNT target genes such as the c-myc-oncogene. APC gene mutations cause the development of multiple adenomatous polyps in the colorectum, which strongly predisposes gene carriers to colorectal cancer. Extracolonic manifestations, including gastric and duodenal polyps, osteomas, desmoids, epidermoid cysts, and retinal lesions, are commonly observed in patients with familial adenomatous polyposis. Detection of mutations in the APC gene allows genetic counselling and reliable identification of at-risk individuals.

Adenomatous Polyposis Coli↗
PubMedDate not supplied

[HIV infection].

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B-Lymphocytes↗
PubMed1999

Gene therapy clinical trials for HIV.

Despite advances in drug treatment for human immunodeficiency virus (HIV), new therapeutics are needed for sustained treatment of this infection. Gene therapy has great potential for HIV due to its specificity for viral targets and prolonged expression of therapeutics. In this review, the various approaches that current gene therapy clinical trials are using to treat HIV disease are described. Results reported from these trials indicate that the approaches tested appear to be safe and confer some benefit to the genetically-modified cell. However, technical improvements must be made in order for gene therapy to realize its true potential.

Adoptive Transfer↗
PubMed2002

Expression analysis of pediatric solid tumor cell lines using oligonucleotide microarrays.

We identified patterns of differentially-expressed genes in cell lines derived from several pediatric solid tumors. Affymetrix Human Cancer G110 Arrays, carrying 1,700 cancer-associated genes, were applied to a panel of 11 cell lines originating from Ewing tumors (ETs), neuroblastomas, and malignant melanoma of soft parts. Hierarchical clustering clearly differentiated these 3 entities and revealed groups of 75, 102, and 36 gene probe-sets exhibiting tumor-type specific up-regulation in these cell lines, respectively. Whereas ET lines demonstrated increased expression of microtubule-associated protein tau (MAPT), protein phosphatase 1 regulatory subunit 1A (PPP1R1A), NIMA (never in mitosis gene a)-related kinase 2 (NEK2), and cyclin D1 (CCND1), neuroblastoma samples exhibited high expression of wingless-type mouse mammary tumor virus integration site family member 11 (WNT11), Drosophila frizzled homolog 2 (FZD2), and adenomatous polyposis coli (APC) which are involved in regulating free beta-catenin levels. These genes likely maintain tumor-specific characteristics and participate in key downstream regulatory mechanisms. We also correlated the expression levels of up-regulated genes in ETs with their chromosomal localization and compared these data to the comparative genomic hybridization profiles of the cell lines. We demonstrate that gains of genetic material contribute essentially to differential gene expression.

Child↗
PubMed2002

[Recent advances in molecular pathogenesis of HIV infection].

Highly active anti-retroviral therapy (HAART) dramatically improves the prognosis of individuals infected with HIV, and changes the pathophysiology of HIV infection. However, the eradication of HIV has not been achieved by HAART due to presence of reservoir cells. More potent strategy of therapy against HIV is needed for further suppression of the replication and eradication of reservoirs. The recent advances about molecular pathogenesis of HIV infection are reviewed in this paper, that leads to discovery of the new molecular targets of anti-HIV drugs.

Antiretroviral Therapy, Highly Active↗
PubMed2002

Anti-herpes simplex virus effect of an aqueous extract of propolis.

BACKGROUND: Propolis, a natural product from beehives, comprises a complex of chemicals, the most important group being flavinoids, which play a role in antiviral protection. OBJECTIVES: To test the inhibitory effect of propolis extract against herpes simplex viruses in vitro and in vivo. METHODS: In vitro: propolis was added to Vero cells at various times and concentrations before, at or after infection with HSV-1. In vivo: the effect of propolis was tested in newborn rats infected s.c. or i.p. and on rabbit come as infected with HSV-1. RESULTS: In vitro: 0.5% propolis extract caused 50% inhibition of HSV infection. There was indirect evidence for a strong interaction between the propolis extract and the surface of the Vero cells, but there was no direct interaction with HSV-1 particles. Administration of propolis before or at the time of infection yielded the most significant inhibitory effect, but even when 10% propolis extract was added 2 hours post-infection it gave 80-85% protection. In vivo: as little as 5% propolis prevented the appearance and development of symptoms of local and i.p. HSV-1 infection in rats and of corneal HSV-1 infection in rabbits. There were no cytotoxic effects at a concentration of 10% in vitro or 20% in vivo. CONCLUSIONS: The potent antiviral activity of propolis against HSV-1 infection in vitro and In vivo is probably due to prevention of virus absorption into the host cells and/or inhibition of an internal step(s) during the viral replication cycle.

Animals↗
PubMed2002

[HIV and CD4 cells].

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CD4-Positive T-Lymphocytes↗
PubMed2003

Adenovirus with insertion-mutated E1A selectively propagates in liver cancer cells and destroys tumors in vivo.

The adenovirus E1A proteins are involved in the transcriptional activation of viral and cellular genes needed for controlling cell cycle and virus replication. Undifferentiated embryonic carcinoma cells have the ability to produce an E1A-like activity that can induce the expression of E1A-targeted adenoviral and cellular genes in the absence of the E1A products. Differentiated embryonic carcinoma cells lose the ability to produce the E1A-like activity. In this study, we investigated the E1A-like activity in cancer cells with an adenovirus having a mutated E1a gene. The mutation is generated by the insertion of a large DNA fragment in the E1a gene and interrupts the COOH-terminal region of both the E1A 12S and 13S proteins. The E1a-mutated virus can efficiently replicate in HepG2 and Hep3B liver cancer cells and produce high titers of virus. Replication of the E1a-mutated virus inhibits tumor formation and destroys tumors in vivo. The results obtained in this study imply that cancer cells may produce an E1A-like activity to support the selective replication of mutated virus in cancer cells. In addition, we found that although the E1a-mutated virus could not replicate in Huh1.cl2 liver cells, the viral DNA could amplify in the cells. This result suggests that replication of adenoviral DNA is necessary, but not sufficient, for generating infectious viral progeny and destroying tumor cells.

Adenovirus E1A Proteins↗
PubMed1992

[Chemotherapy for human immunodeficiency virus infection. Current status and perspectives].

The role of drugs inhibiting viral replication in patients infected with HIV has been confirmed. Until now only dideoxynucleosides, which are reverse transcriptase inhibitors, have demonstrated antiviral activity in humans. A number of compounds acting on other steps of the viral cycle are currently being evaluated and clinical trials are being performed. Some investigators are attempting to inhibit the binding of viral particles to target cells and their penetration into these by acting on the interaction between HIV ant the CD4 molecule. Another approach consists in the characterization of enzymatic activities which are specific of HIV, other than reverse transcriptase, such as ribonuclease H, integrase or protease, in order to prepare specific inhibitors. Attempts are made to inhibit retroviral gene expression and production of viral particles in infected cells. The development of new nucleoside analogues and drugs with mechanisms of action and toxicities different from those of zidovudine should allow in the near future combination chemotherapy of HIV infection.

Dideoxynucleosides↗
PubMed2006

Meaning of DNA detection during the follow-up of HIV-1 infected patients: a brief review.

A growing body of evidence indicates that proviral DNA load quantitation is an important parameter in establishing the dynamics of HIV infection. Proviral DNA load can be determined during the follow-up of infected individuals to evaluate reservoir status in addition to viral replication. Hence, the study of viral reservoirs, represented by HIV-1 latently infected cells, including resting memory CD4+ T cells, monocytes and macrophages, by which HIV-1 can be reactivated, opens new perspectives in the assessment and the comprehension of HIV-1 infection. However, the identification of viral reservoirs, that can store both wild and drug resistance viruses, is one of the most important steps in developing treatment strategies because it is now clear that viral reservoirs not only prevent sterilizing immunity but also represent a major obstacle to curing the infection with the potent antiretroviral drugs currently in use. Even if only careful evaluation of virological and immunological markers is necessary to fully characterize the course of HIV-1 infection and to provide a more complete laboratory-based assessment of disease progression, the availability of a new standardized assay such as DNA proviral load will be important to assess the true extent of virological suppression in treated patients and to verify the efficacy of new immune-based therapies aimed at purging HIV-1 DNA reservoirs. Several studies demonstrate, in fact, that HIV-1 cellular DNA load may be an indicator of spread of infection whereas the plasma RNA load is indicates active infection. This article will review the importance of monitoring HIV-1 proviral load DNA during the follow-up of HIV-1 infected subjects, suggesting that additional information complementing HIV RNA load could provide crucial information to monitor viral replication and the effectiveness of HAART therapy.

DNA, Viral↗
PubMed1985

Tumorigenicity and transcriptional modulation of c-myc and N-ras oncogenes in a human hepatoma cell line.

Tumorigenicity and oncogene expression were examined in HepG2 derived cells, a human hepatoma cell line. HepG2 cells and a single cell clonal HepG2 line, HLD2-6, were equally tumorigenic when injected s.c. into athymic nude mice. Cyclophosphamide pretreatment of both cell lines (500 micrograms cyclophosphamide/ml/two cell cycles) had no effect on tumor incidence or latency (P greater than 0.05). Tumors were nonencapsulated, highly invasive adenocarcinomas and were positive for gamma-glutamyltranspeptidase activity and bile production. Plasma from tumor-bearing mice was positive for human alpha-fetoprotein and negative for hepatitis B virus surface antigen as measured by radioimmunoassay. Two cell lines reestablished into tissue culture from HLD2-6 derived tumors had unaltered cell cycle times. Detailed in vitro translation analysis of RNA isolated from HLD2-6 derived cells and tumors were extremely similar to the translation products of RNA isolated from a normal human liver sample except for a Mr 53,000 polypeptide with an apparent charge shift. c-myc specific transcripts, when compared to a normal human liver sample, were increased in all HLD2-6 cell lines and tumors derived from HLD2-6 cells. This increase in c-myc expression could not be explained by gene amplification or hepatitis B virus integration. N-ras specific transcripts were not elevated in HLD2-6 cells grown in tissue culture but there was a selective increase of the 5.5-kilobase N-ras transcript in HLD2-6 derived tumors grown in nude mice. This increased 5.5-kilobase transcript did not remain elevated if the tumors were reestablished into tissue culture, suggesting some interaction with the host animal. c-Ha-ras expression could not be detected in any HLD2-6 derived tumor or cell line.

Animals↗