Double resistance to ganciclovir and foscarnet of four human cytomegalovirus strains recovered from AIDS patients. 1995

A Sarasini, and F Baldanti, and M Furione, and E Percivalle, and R Brerra, and M Barbi, and G Gerna
Viral Diagnostic Service, University of Pavia, Istituto di Ricovero e Cura a Carattere Scientifico Policlinico S. Matteo, Italy.

Four human cytomegalovirus (HCMV) isolates from four different AIDS patients treated with both ganciclovir and foscarnet and not responding clinically to antiviral treatment, were studied in order to verify the occurrence of double resistance to both drugs, and to define whether single or multiple HCMV strains could be responsible for the double resistance. Peripheral blood leukocytes (PBL), the relevant conventional viral isolates, and plaque-purified strains from all four patients were examined by antiviral drug susceptibility testing by an immediate-early antigen plaque reduction assay and by restriction fragment length polymorphism (RFLP) analysis using polymerase chain reaction (PCR)-amplified multiple genome regions and endonucleases. All four HCMV strains had a high level of resistance to both ganciclovir and foscarnet. A single HCMV strain was shown to be responsible for the dual resistance in each patient. HCMV strain identity and uniqueness were shown for each of the four patients in blood samples, viral isolates, and plaque-purified strains. In addition, in two patients the same single HCMV strain shifted progressively from drug sensitivity to ganciclovir and then to ganciclovir-foscarnet resistance. These findings document that resistance to both ganciclovir and foscarnet of HCMV strains recovered from blood of AIDS patients represents an emerging problem. Although it is known that multiple HCMV strains may cocirculate in the blood of AIDS patients, single strains appear to be responsible for the dual resistance. Molecular mechanisms responsible for the double resistance of the four reported strains are under study.

UI MeSH Term Description Entries
D008297 Male Males
D010948 Viral Plaque Assay Method for measuring viral infectivity and multiplication in CULTURED CELLS. Clear lysed areas or plaques develop as the VIRAL PARTICLES are released from the infected cells during incubation. With some VIRUSES, the cells are killed by a cytopathic effect; with others, the infected cells are not killed but can be detected by their hemadsorptive ability. Sometimes the plaque cells contain VIRAL ANTIGENS which can be measured by IMMUNOFLUORESCENCE. Bacteriophage Plaque Assay,Assay, Bacteriophage Plaque,Assay, Viral Plaque,Assays, Bacteriophage Plaque,Assays, Viral Plaque,Bacteriophage Plaque Assays,Plaque Assay, Bacteriophage,Plaque Assay, Viral,Plaque Assays, Bacteriophage,Plaque Assays, Viral,Viral Plaque Assays
D002460 Cell Line Established cell cultures that have the potential to propagate indefinitely. Cell Lines,Line, Cell,Lines, Cell
D003586 Cytomegalovirus Infections Infection with CYTOMEGALOVIRUS, characterized by enlarged cells bearing intranuclear inclusions. Infection may be in almost any organ, but the salivary glands are the most common site in children, as are the lungs in adults. CMV Inclusion,CMV Inclusions,Congenital CMV Infection,Congenital Cytomegalovirus Infection,Cytomegalic Inclusion Disease,Cytomegalovirus Colitis,Cytomegalovirus Inclusion,Cytomegalovirus Inclusion Disease,Cytomegalovirus Inclusions,Inclusion Disease,Perinatal CMV Infection,Perinatal Cytomegalovirus Infection,Renal Tubular Cytomegalovirus Inclusion,Renal Tubular Cytomegalovirus Inclusions,Salivary Gland Virus Disease,Severe Cytomegalovirus Infection,Severe Cytomegalovirus Infections,Infections, Cytomegalovirus,CMV Infection, Congenital,CMV Infection, Perinatal,Colitis, Cytomegalovirus,Congenital CMV Infections,Congenital Cytomegalovirus Infections,Cytomegalic Inclusion Diseases,Cytomegalovirus Colitides,Cytomegalovirus Inclusion Diseases,Cytomegalovirus Infection,Cytomegalovirus Infection, Congenital,Cytomegalovirus Infection, Perinatal,Cytomegalovirus Infection, Severe,Cytomegalovirus Infections, Severe,Disease, Cytomegalic Inclusion,Disease, Cytomegalovirus Inclusion,Diseases, Cytomegalovirus Inclusion,Inclusion Disease, Cytomegalic,Inclusion Disease, Cytomegalovirus,Inclusion Diseases,Inclusion Diseases, Cytomegalovirus,Inclusion, CMV,Inclusion, Cytomegalovirus,Infection, Congenital CMV,Infection, Congenital Cytomegalovirus,Infection, Cytomegalovirus,Infection, Perinatal CMV,Infection, Perinatal Cytomegalovirus,Infection, Severe Cytomegalovirus,Perinatal CMV Infections,Perinatal Cytomegalovirus Infections
D003587 Cytomegalovirus A genus of the family HERPESVIRIDAE, subfamily BETAHERPESVIRINAE, infecting the salivary glands, liver, spleen, lungs, eyes, and other organs, in which they produce characteristically enlarged cells with intranuclear inclusions. Infection with Cytomegalovirus is also seen as an opportunistic infection in AIDS. Herpesvirus 5, Human,Human Herpesvirus 5,Salivary Gland Viruses,HHV 5,Herpesvirus 5 (beta), Human,Cytomegaloviruses,Salivary Gland Virus,Virus, Salivary Gland,Viruses, Salivary Gland
D004352 Drug Resistance, Microbial The ability of microorganisms, especially bacteria, to resist or to become tolerant to chemotherapeutic agents, antimicrobial agents, or antibiotics. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS). Antibiotic Resistance,Antibiotic Resistance, Microbial,Antimicrobial Resistance, Drug,Antimicrobial Drug Resistance,Antimicrobial Drug Resistances,Antimicrobial Resistances, Drug,Drug Antimicrobial Resistance,Drug Antimicrobial Resistances,Drug Resistances, Microbial,Resistance, Antibiotic,Resistance, Drug Antimicrobial,Resistances, Drug Antimicrobial
D005260 Female Females
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000328 Adult A person having attained full growth or maturity. Adults are of 19 through 44 years of age. For a person between 19 and 24 years of age, YOUNG ADULT is available. Adults
D000998 Antiviral Agents Agents used in the prophylaxis or therapy of VIRUS DISEASES. Some of the ways they may act include preventing viral replication by inhibiting viral DNA polymerase; binding to specific cell-surface receptors and inhibiting viral penetration or uncoating; inhibiting viral protein synthesis; or blocking late stages of virus assembly. Antiviral,Antiviral Agent,Antiviral Drug,Antivirals,Antiviral Drugs,Agent, Antiviral,Agents, Antiviral,Drug, Antiviral,Drugs, Antiviral

Related Publications

A Sarasini, and F Baldanti, and M Furione, and E Percivalle, and R Brerra, and M Barbi, and G Gerna
August 1992, Lancet (London, England),
A Sarasini, and F Baldanti, and M Furione, and E Percivalle, and R Brerra, and M Barbi, and G Gerna
May 1993, The Journal of infectious diseases,
A Sarasini, and F Baldanti, and M Furione, and E Percivalle, and R Brerra, and M Barbi, and G Gerna
June 1991, The Journal of infectious diseases,
A Sarasini, and F Baldanti, and M Furione, and E Percivalle, and R Brerra, and M Barbi, and G Gerna
August 1991, AIDS (London, England),
A Sarasini, and F Baldanti, and M Furione, and E Percivalle, and R Brerra, and M Barbi, and G Gerna
August 1994, The American journal of medicine,
A Sarasini, and F Baldanti, and M Furione, and E Percivalle, and R Brerra, and M Barbi, and G Gerna
November 1991, American journal of hospital pharmacy,
A Sarasini, and F Baldanti, and M Furione, and E Percivalle, and R Brerra, and M Barbi, and G Gerna
October 2020, Mikrobiyoloji bulteni,
A Sarasini, and F Baldanti, and M Furione, and E Percivalle, and R Brerra, and M Barbi, and G Gerna
January 1995, European journal of ophthalmology,
A Sarasini, and F Baldanti, and M Furione, and E Percivalle, and R Brerra, and M Barbi, and G Gerna
May 1991, Lancet (London, England),
A Sarasini, and F Baldanti, and M Furione, and E Percivalle, and R Brerra, and M Barbi, and G Gerna
August 1991, Lancet (London, England),
Copied contents to your clipboard!