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Biomedical subjects

V Calvez

Publications and source records attributed to V Calvez.

At least 91 records · Page 5Linked to original sources
PubMed1998

[Resistance to antiretroviral agents: mechanism and study methods].

FREQUENT MUTATIONS: Associated with the high turnover rate of the HIV, frequent inverse transcriptase errors lead to a wide range of possible mutations. Certain mutations can modify the response to antiretroviral agents. The development of resistant strains is mediated by the selection pressure of antiretroviral agents and occurs at a very variable rate depending on the antiretroviral agent used. TO LOWER THE RISK OF RESISTANCE: Persistent replication, whatever the cause, favors the emergence of resistant mutants. Thus the antiretroviral treatment must be initiated early and with the most powerful protocol possible in order to reduce viral replication as quickly as possible. CONTRIBUTION OF VIROLOGY TESTS: It is not always possible to predict the efficacy of antiviral agents from phenotyping and genotyping results. Their use is currently limited to cases of treatment failure. Their contribution in everyday clinical practice remains to be defined.

Anti-HIV Agents↗
PubMed1998

[Cognitive disorders in AIDS: clinical, virological and neuroradiological features].

HIV-associated neurocognitive disorders are mainly reported during the late stages of the disease, in deeply immunosuppressed patients Clinically, they present as a subcortical cognitive impairment, dominated by reduced psychomotor speed and memory deficit. Encephalic magnetic resonance imaging shows in most cases a diffuse leucoencephalopathy, and there is often a poor correlation between clinical status and neuroradiological findings. The diagnostic and prognostic value of HIV load in blood and cerebrospinal fluid is currently under investigation. Finally, the efficacy of new antiretroviral drugs on HIV dementia remains uncertain.

Acquired Immunodeficiency Syndrome↗
PubMed1997

[What is a virus?].

Viruses are simple biological particles, consisting of a genome, a protein capsid and, in the case of enveloped viruses, an external lipidic envelope. Owing to the presence of envelope, most enveloped viruses are fragile although some exceptions may be observed. Viruses behave as complete intracellular parasites. Their multiplication results from the replication and self-assembly of viral components, this process being directed by the viral genome after it has been released within an infected cell. Virus classification is now essentially based on molecular properties, concerning both the structure and replication strategy of viruses. In virus taxonomy, serial hierarchical levels are family, subfamily, genus and species. Within species, lower hierarchical levels are type, subtype, variant and strain. Knowledge of virus structure and classification is essential for considering the physiopathology, diagnosis and therapy of viral infections.

Humans↗
PubMed1997

[The future of antiviral drugs].

Despite much recent progress, antiviral chemotherapy has still to meet some major challenges: residual cytotoxicity of much antiviral drugs; emergence of viral strains resisting to the most specific antiviral drugs; inability of the most active antiviral drugs to suppress latent viral infections. Several approaches using gene therapy (e.g. hybridons, ribozymes, or dominant negative mutants) might theoretically provide efficient solutions against viral latency.

Antiviral Agents↗
PubMed1997

Exacerbations of clinical symptoms in human immunodeficiency virus type 1-infected patients with multicentric Castleman's disease are associated with a high increase in Kaposi's sarcoma herpesvirus DNA load in peripheral blood mononuclear cells.

The epidemiologic link between multicentric Castleman's disease (MCD) and Kaposi's sarcoma (KS) and the high frequency of KS herpesvirus (KSHV) detection in both diseases raise the question of a role of this new virus in the pathogenesis of MCD. To explore this hypothesis, the KSHV DNA load was investigated in peripheral blood mononuclear cells of 3 human immunodeficiency virus (HIV)-infected patients with MCD at different points during the clinical course. Clinical parameters, such as fever and the presence of lymphadenopathy, were systematically assessed. Hemogram and C-reactive protein level determinations were performed as standard procedures. KSHV DNA load was investigated by means of semiquantitative polymerase chain reaction assay using peripheral blood mononuclear cells of the patients. A correlation between the variation in clinical and biologic parameters related to MCD and KSHV DNA load was found, suggesting a close relationship between KSHV and MCD in HIV-1-infected patients.

Castleman Disease↗
PubMed1997

Lack of evidence of human herpesvirus 8 DNA sequences in HIV-negative patients with various lymphoproliferative disorders of the skin.

Human herpesvirus 8 (HHV-8) is a new virus which has been reported in Kaposi's sarcoma and some lymphoproliferative disorders such as Castleman's disease and body-cavity-based lymphoma. Because HHV-8 shares homology with Epstein-Barr virus (EBV), we searched for the presence of HHV-8 DNA sequences in various cutaneous T- and B-cell lymphoma by the polymerase chain reaction (PCR). Forty-seven HIV-negative patients with cutaneous lymphoma or large plaque parapsoriasis were enrolled in the study. For the detection of HHV-8 DNA sequences we used PCR followed by a hybridization with a digoxigenin-labelled probe and nested-PCR. HHV-8 DNA sequences could only be detected in a patient with large plaque parapsoriasis. Our study does not suggest any direct implication of HHV-8 in the pathogenesis of most cutaneous lymphoma. Serological studies will be helpful to appreciate if there is an epidemiological link between HHV-8 and cutaneous lymphomas.

DNA, Viral↗
PubMed1996

Direct gene transfer of a plasmid carrying the herpes simplex virus-thymidine kinase gene (HSV-TK) in transplanted murine melanoma: in vivo study.

The aim of the study was to use a virus-free system to transfer the Herpes Simplex Virus-thymidine kinase (HSV-TK) gene in mice bearing melanoma tumours. B16 F1 murine melanoma cells were injected subcutaneously. On days 11 and 14, an intratumoral injection of either naked plasmid containing the HSV-TK gene (pAG0) or pAG0-lipofectamine complexes was given. Ganciclovir (120 mg/kg/day) was given for 5 days starting on day 14. Tumour weight reduction (40-50%) was observed in treated animals versus different control groups. Moreover, histopathological analysis on tumours showed large areas of cavitary necrosis (85%) in treated groups compared to controls (10%). Using a simple and safe method, the results presented here demonstrated that virus-free mediated delivery of the HSV-TK gene is efficient in vivo in murine malignant melanoma.

Animals↗
PubMed1996

Virus-free transfer of the herpes simplex virus thymidine kinase gene followed by ganciclovir treatment induces tumor cell death.

We report virus-free transfer of a "suicide" gene into tumoral cells. The system can be used in vitro or in vivo to induce tumor cell death. A plasmid carrying the herpes simplex virus thymidine kinase (HSV-TK) gene with its 5'- and 3'-flanking regions was used both alone and in liposomes to transduce B16 cells. In vitro, a 5-day treatment with ganciclovir after transfection with the HSV-TK gene in liposomes induced a significant lysis of B16 melanoma cells as assessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide test. The efficacy of transfection was determined using liposomes harboring the beta-galactosidase reporter gene and was around 10%. Thus, the cytotoxicity observed resulted presumably from a large bystander effect. In vivo, direct transfer of the TK DNA into established B16 melanoma tumors in C57B6 mice followed by i.p. ganciclovir treatment induced a 50% reduction of tumor weight after 8 days and an increased necrosis. Despite the use of the nonspecific strong TK promoter, no necrosis was detected in normal tissues surrounding the tumor or elsewhere. Thus, this system of tumor transfection, which does not involve any viral vector, is safe and straightforward and seems to be suitable for testing in clinical trials.

Animals↗
PubMed1995

Cell clones cured of persistent poliovirus infection display selective permissivity to the wild-type poliovirus strain Mahoney and partial resistance to the attenuated Sabin 1 strain and Mahoney mutants.

We report the isolation and characterization of HEp-2c cell clones obtained after two successive persistent poliovirus (PV) infections. Once cured, some of the cell clones displayed selective permissivity toward the wild-type Mahoney strain and partial resistance to particular mutants of this strain, including the Sabin 1 strain. Two cell clones, CI 4 and CI 10, were studied in greater detail. The cytopathic effects of Mahoney infection were comparable in the cell clones and in HEp-2c cells. The cytopathic effects of infection by Sabin 1 or Mahoney mutants were greatly delayed in CI 4 and CI 10. In the genomic region encoding the capsid proteins, determinants involved in the resistance of the cell clones to the Mahoney mutants were localized in the amino-terminal part of VP1 (amino acids 22 and 43), the B-C loop of VP1 (amino acids 94-102), and the loop of VP3 connecting its amino-terminal to beta strand B (amino acid 60). These genomic regions are thought to be involved in the early steps of viral infection. Virus adsorption was slower and less efficient on CI 10 cells than on parental HEp-2c cells. Virus adsorption was faster on CI 4 than on HEp-2c cells, and at least as efficient, but there was less receptor-induced structural modification of the capsid, a step that is required for decapsidation. Furthermore, infection of CI 4 by a Mahoney mutant in which the B-C loop of VP1 has been deleted was affected in the later steps of infection. These results indicate that, in cells cured of persistent PV infection, poliovirus multiplication was restricted at several stages and particularly at two steps of virus entry: adsorption and/or the uncoating transitions following adsorption onto the receptor.

Base Sequence↗
PubMed1995

Herpesvirus-like DNA sequences in patients with Mediterranean Kaposi's sarcoma.

DNA sequences closely related to herpesvirus-like sequences have been found in AIDS-associated Kaposi's sarcoma. Using PCR, we found herpesvirus-like DNA sequences in Kaposi's lesions and normal adjacent skin in five patients with Mediterranean Kaposi's sarcoma. We did not find these sequences in tissues from patients without Kaposi's sarcoma. Semi-quantitative PCR revealed many more herpesvirus-like sequences in Kaposi's lesions than in unaffected skin. Our results reinforce the hypothesis that an infectious agent closely related to gamma-herpesvirus is implicated in the pathogenesis of Mediterranean and AIDS-associated Kaposi's sarcoma.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Substitutions in the capsids of poliovirus mutants selected in human neuroblastoma cells confer on the Mahoney type 1 strain a phenotype neurovirulent in mice.

Poliovirus (PV) type 1 mutants selected in human neuroblastoma cells persistently infected (PVpi) with the wild-type Mahoney strain exhibited a mouse-neurovirulent phenotype. Four of the five substitutions present in the capsid proteins of a PVpi were demonstrated to extend the host range of the Mahoney strain to mice. These new mouse-neurovirulent determinants were located in the three-dimensional structure of the viral capsid; two of them (residues 142 of VP2 and 60 of VP3) were located in loops exposed at the surface of the protein shell, whereas the other two (residues 43 of VP1 and 62 of VP4) were located on the inside of the capsid. VP1 residue 43 and VP2 residue 142 substitutions were also selected in a PVpi derived from the attenuated Sabin strain. We suggest that the selective pressure of human neuroblastoma cell factor(s) involved in early steps of PV multiplication could be responsible for the arising of amino acid substitutions which confer adaptation to the mouse central nervous system to PV.

Amino Acid Sequence↗