Selection and characterization of a mutant of feline immunodeficiency virus resistant to 2',3'-dideoxycytidine | Zendy

Holly Kay Medlin | Zendy; Yanqiu Zhu | Zendy; K M Remington | Zendy; T R Phillips | Zendy; Thomas W. North | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Selection and characterization of a mutant of feline immunodeficiency virus resistant to 2',3'-dideoxycytidine

Author(s) -

Holly Kay Medlin,

Yanqiu Zhu,

K M Remington,

T R Phillips,

Thomas W. North

Publication year - 1996

Publication title -

antimicrobial agents and chemotherapy

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.07

H-Index - 259

eISSN - 1070-6283

pISSN - 0066-4804

DOI - 10.1128/aac.40.4.953

Subject(s) - reverse transcriptase , zalcitabine , mutant , feline immunodeficiency virus , mutagenesis , biology , virology , resistance mutation , mutation , microbiology and biotechnology , rna directed dna polymerase , virus , rna , genetics , lentivirus , gene , viral disease

We have selected and plaque purified a mutant of feline immunodeficiency virus (FIV) that is resistant to 2',3'-dideoxycytidine (ddC). This mutant was selected in cultured cells in the continuous presence of 25 microM ddC. The mutant, designated DCR-5c, was fourfold resistant to ddC, threefold resistant to 2',3'-dideoxyinosine, and more than fourfold resistant to phosphonoformic acid. DCR-5c displayed little or no resistance to (-)-beta-2',3'-dideoxy-3'-thiacytidine, 3'-azido-3'-deoxythymidine, or 9-(2-phosphonylmethoxyethyl) adenine. Reverse transcriptase purified from DCR-5c was less susceptible to inhibition by ddCTP, phosphonoformic acid, ddATP, or azido-dTTP than the wild-type FIV reverse transcriptase. Sequence analysis of DCR-5c revealed a single base change (G to C at nucleotide 2342) in the reverse transcriptase-encoding region of FIV. This mutation results in substitution of His for Asp at codon 3 of FIV reverse transcriptase. The role of this mutation in ddC resistance was confirmed by site-directed mutagenesis.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research