A 6-basepair insert in the reverse transcriptase gene of human immunodeficiency virus type 1 confers resistance to multiple nucleoside inhibitors. 1998

M A Winters, and K L Coolley, and Y A Girard, and D J Levee, and H Hamdan, and R W Shafer, and D A Katzenstein, and T C Merigan
Center for AIDS Research at Stanford, Stanford University, Stanford, California 94305-5107, USA. winters@stanford.edu

While many point mutations in the HIV-1 reverse transcriptase (RT) confer resistance to antiretroviral drugs, inserts or deletions in this gene have not been previously characterized. In this report, 14 RT inhibitor-treated patients were found to have HIV-1 strains possessing a 6-basepair insert between codons 69 and 70 of the RT gene. Known drug resistance mutations were also observed in these strains, with T215Y appearing in all strains. Genotypic analysis indicated that the inserts had substantial nucleotide variability that resulted in relatively restricted sets of amino acid sequences. Linkage of patients' treatment histories with longitudinal sequencing data showed that insert strains appeared during drug regimens containing ddI or ddC, with prior or concurrent AZT treatment. Drug susceptibility tests of recombinant patient isolates showed reduced susceptibility to nearly all nucleoside RT inhibitors. Site- directed mutagenesis studies confirmed the role of the inserts alone in conferring reduced susceptibility to most RT inhibitors. The addition of AZT-associated drug resistance mutations further increased the range and magnitude of resistance. These results establish that inserts, like point mutations, are selected in vivo during antiretroviral therapy and provide resistance to multiple nucleoside analogs.

UI MeSH Term Description Entries
D009154 Mutation Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations. Mutations
D009705 Nucleosides Purine or pyrimidine bases attached to a ribose or deoxyribose. (From King & Stansfield, A Dictionary of Genetics, 4th ed) Nucleoside,Nucleoside Analog,Nucleoside Analogs,Analog, Nucleoside,Analogs, Nucleoside
D002478 Cells, Cultured Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others. Cultured Cells,Cell, Cultured,Cultured Cell
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000595 Amino Acid Sequence The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION. Protein Structure, Primary,Amino Acid Sequences,Sequence, Amino Acid,Sequences, Amino Acid,Primary Protein Structure,Primary Protein Structures,Protein Structures, Primary,Structure, Primary Protein,Structures, Primary Protein
D001483 Base Sequence The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence. DNA Sequence,Nucleotide Sequence,RNA Sequence,DNA Sequences,Base Sequences,Nucleotide Sequences,RNA Sequences,Sequence, Base,Sequence, DNA,Sequence, Nucleotide,Sequence, RNA,Sequences, Base,Sequences, DNA,Sequences, Nucleotide,Sequences, RNA
D015215 Zidovudine A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by an azido group. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA during reverse transcription. It improves immunologic function, partially reverses the HIV-induced neurological dysfunction, and improves certain other clinical abnormalities associated with AIDS. Its principal toxic effect is dose-dependent suppression of bone marrow, resulting in anemia and leukopenia. AZT (Antiviral),Azidothymidine,3'-Azido-2',3'-Dideoxythymidine,3'-Azido-3'-deoxythymidine,AZT Antiviral,AZT, Antiviral,BW A509U,BWA-509U,Retrovir,3' Azido 2',3' Dideoxythymidine,3' Azido 3' deoxythymidine,Antiviral AZT,BWA 509U,BWA509U
D015497 HIV-1 The type species of LENTIVIRUS and the etiologic agent of AIDS. It is characterized by its cytopathic effect and affinity for the T4-lymphocyte. Human immunodeficiency virus 1,HIV-I,Human Immunodeficiency Virus Type 1,Immunodeficiency Virus Type 1, Human
D015658 HIV Infections Includes the spectrum of human immunodeficiency virus infections that range from asymptomatic seropositivity, thru AIDS-related complex (ARC), to acquired immunodeficiency syndrome (AIDS). HTLV-III Infections,HTLV-III-LAV Infections,T-Lymphotropic Virus Type III Infections, Human,HIV Coinfection,Coinfection, HIV,Coinfections, HIV,HIV Coinfections,HIV Infection,HTLV III Infections,HTLV III LAV Infections,HTLV-III Infection,HTLV-III-LAV Infection,Infection, HIV,Infection, HTLV-III,Infection, HTLV-III-LAV,Infections, HIV,Infections, HTLV-III,Infections, HTLV-III-LAV,T Lymphotropic Virus Type III Infections, Human
D016047 Zalcitabine A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication at low concentrations, acting as a chain-terminator of viral DNA by binding to reverse transcriptase. Its principal toxic side effect is axonal degeneration resulting in peripheral neuropathy. 2',3'-Dideoxycytidine,Dideoxycytidine,ddC (Antiviral),HIVID Roche,Hivid,NSC-606170,2',3' Dideoxycytidine,NSC 606170,NSC606170

Related Publications

M A Winters, and K L Coolley, and Y A Girard, and D J Levee, and H Hamdan, and R W Shafer, and D A Katzenstein, and T C Merigan
January 2007, Antimicrobial agents and chemotherapy,
M A Winters, and K L Coolley, and Y A Girard, and D J Levee, and H Hamdan, and R W Shafer, and D A Katzenstein, and T C Merigan
March 1995, The Journal of infectious diseases,
M A Winters, and K L Coolley, and Y A Girard, and D J Levee, and H Hamdan, and R W Shafer, and D A Katzenstein, and T C Merigan
January 2004, Current topics in medicinal chemistry,
M A Winters, and K L Coolley, and Y A Girard, and D J Levee, and H Hamdan, and R W Shafer, and D A Katzenstein, and T C Merigan
April 2008, Journal of virology,
M A Winters, and K L Coolley, and Y A Girard, and D J Levee, and H Hamdan, and R W Shafer, and D A Katzenstein, and T C Merigan
April 2009, Journal of virology,
M A Winters, and K L Coolley, and Y A Girard, and D J Levee, and H Hamdan, and R W Shafer, and D A Katzenstein, and T C Merigan
October 2001, Journal of virology,
M A Winters, and K L Coolley, and Y A Girard, and D J Levee, and H Hamdan, and R W Shafer, and D A Katzenstein, and T C Merigan
July 2002, Antimicrobial agents and chemotherapy,
M A Winters, and K L Coolley, and Y A Girard, and D J Levee, and H Hamdan, and R W Shafer, and D A Katzenstein, and T C Merigan
June 1995, Biochemical and biophysical research communications,
M A Winters, and K L Coolley, and Y A Girard, and D J Levee, and H Hamdan, and R W Shafer, and D A Katzenstein, and T C Merigan
July 2006, Journal of virology,
M A Winters, and K L Coolley, and Y A Girard, and D J Levee, and H Hamdan, and R W Shafer, and D A Katzenstein, and T C Merigan
January 2004, Molecular pharmacology,
Copied contents to your clipboard!