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V Calvez

Publications and source records attributed to V Calvez.

96 records · Page 6Linked to original sources
PubMed1993

Precise missense and silent point mutations are fixed in the genomes of poliovirus mutants from persistently infected cells.

Poliovirus mutants selected in persistently infected human neuroblastoma cells have a modified cell tropism and can establish a secondary persistent infection in nonneural cells, such as HEp-2c cells. Nucleotide sequence analysis revealed that the genome of a persistent mutant, S11, differed from that of the parental lytic Sabin 1 poliovirus strain by 31 point mutations. Three mutations occurred in the noncoding regions. The other mutations resulted in 12 amino acid substitutions; 1 substitution occurred in a nonstructural protein (3A), while the other 11 substitutions were clustered in the capsid proteins VP2 and VP1. The same missense mutations, as well as many of the silent mutations that we observed in mutant S11, also accumulated in the genome of two other persistent viruses isolated from independent infections. This finding indicates that both missense and silent mutations are selected during the persistent infection of neuroblastoma cells and suggests that the secondary structure of RNA in the coding region may play a role in viral infection.

Capsid↗
PubMed1993

Identification of a region of the poliovirus genome involved in persistent infection of HEp-2 cells.

Poliovirus mutants were selected during the persistent infection of human neuroblastoma cells. These viruses could establish secondary persistent infections in HEp-2 nonneural cells. We report the identification of a region of the genome of a persistent virus (S11) that was sufficient to confer to a recombinant virus the phenotype that causes persistent infection in HEp-2 cells. This region, between nucleotides 1148 and 3481, contained 11 missense mutations mapping exclusively in the genes of capsid proteins VP1 and VP2. Because recombinant viruses carrying only one of these two mutated genes were not able to cause persistent infection, it seems very probable that two or more mutations in these genes are required for expression of the phenotype that causes persistent infection.

Capsid↗
PubMedDate not supplied

Mutations in the human immunodeficiency virus type 1 reverse transcriptase gene observed in stavudine and didanosine strains obtained by in vitro passages.

We have selected a human immunodeficiency virus type 1 (HIV1) using the technique of in vitro selection to generate variants that are resistant to didanosine and/or stavudine. After serial passages of the Lai strain of HIV1 in MT-2 cells in increased concentrations of didanosine-stavudine association, 2 novel mutations in reverse transcriptase at codon 57 (Asp-->His) and at codon 98 (AIa-->Val) were observed. These mutations were associated with an 11.5-fold increase in the didanosine and a 4.5-fold increase in the stavudine 50% inhibitory concentration.

Anti-HIV Agents↗
PubMedDate not supplied

AIDS-related primary lymphoma of the pleural cavity. A case report.

BACKGROUND: Pleural effusions are common in patients with the acquired immunodeficiency syndrome (AIDS). Their most frequent causes are Kaposi's sarcoma and mycobacterial infections. We report cytologic, immunophenotypic and molecular features of a primary pleural non-Hodgkin's lymphoma (NHL) that represent an uncommon cause of isolated pleural effusion in patients with AIDS. CASE: A 66-year-old, human immunodeficiency virus-positive male presented with chest pain and dyspnea. He had no history of opportunistic infections or Kaposi's sarcoma. A chest radiography displayed a right-sided pleural effusion. Cytology of pleural fluid revealed lymphomatous cells with markedly irregular nuclei. Their immunophenotype was indeterminate. Computed tomography of the thorax and abdomen did not show any tumor mass. Molecular analysis demonstrated that the lymphomatous cells had a B-cell genotype and contained Kaposi's sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV) DNA sequences. CONCLUSION: This case belongs to a new subgroup of AIDS-related NHL that is characterized by unusual morphology, null immunophenotype, B-cell genotype and association with both KSHV and EBV.

Aged↗
PubMedDate not supplied

[The discovery of three novel human viruses, human herpesviruses 6, 7, and 8].

Three novel human herpesviruses have been discovered in the last years: human herpesvirus 6 (HHV-6) in 1986, human herpesvirus 7 (HHV-7) in 1990, human herpesvirus 8 (HHV-8) in 1994. HHV-6 and HHV-7 were identified after their isolation from blood lymphocyte cultures, while HHV-8 was first detected by means of a specific molecular biology approach in the search for the etiologic agent of Kaposi's sarcoma. The three viruses infect lymphocytes, T-cells in the case of HHV-6 and HHV-7, B-cells in the case of HHV-8. Human infection with HHV-6 and HHV-7 is ubiquitous and widespread while HHV-8 infection seems to be more restricted, at least in Western countries. The propagation in cell culture in vitro can be done easily with HHV-6, with more difficulties in the case of HHV-7 and has not been completely obtained in the case of HHV-8. The polymerase chain reaction is the common method for the detection of these three viruses in human samples. The oncogenic role of HHV-6 and HHV-7 which were both classified in Betaherpesvirinae subfamily has not been convincingly demonstrated. HHV-8, classified as a member of Gammaherpesvirinae subfamily, is strongly associated with three lymphoproliferative diseases: Kaposi's sarcoma, Castleman's disease and primary effusion lymphomas.

Herpesviridae Infections↗