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Eyer, L., Kondo, H., Zouharova, D., Hirano, M., Valdés, J.J., Muto, M., Kastl, T., Kobayashi, S., Haviernik, J., Igarashi, M., Kariwa, H., Vaculovicova, M., Cerny, J., Kizek, R., Kröger, A., Lienenklaus, S., Dejmek, M., Nencka, R., Palus, M., Salat, J., De Clercq, E., Yoshii, K., Ruzek, D.
Original Title
Escape of tick-borne flavivirus from 2'-C-methylated nucleoside antivirals is mediated by a single conservative mutation in NS5 that has a dramatic effect on viral fitness
Type
journal article in Web of Science
Language
English
Original Abstract
Tick-borne encephalitis virus (TBEV) causes a severe and potentially fatal neuroinfection in humans. Despite its high medical relevance, no specific antiviral therapy is currently available. Here we demonstrate that treatment with a nucleoside analog, 7-deaza-2=-C-methyladenosine (7-deaza-2=-CMA), substantially improved disease outcomes, increased survival, and reduced signs of neuroinfection and viral titers in the brains of mice infected with a lethal dose of TBEV. To investigate the mechanism of action of 7-deaza-2=-CMA, two drug-resistant TBEV clones were generated and characterized. The two clones shared a signature amino acid substitution, S603T, in the viral NS5 RNA-dependent RNA polymerase (RdRp) domain. This mutation conferred resistance to various 2=-C-methylated nucleoside derivatives, but no cross-resistance was seen with other nucleoside analogs, such as 4=-C-azidocytidine and 2=-deoxy-2=-beta-hydroxy-4=-azidocytidine (RO-9187). All-atom molecular dynamics simulations revealed that the S603T RdRp mutant repels a water molecule that coordinates the position of a metal ion cofactor as 2=-C-methylated nucleoside analogs approach the active site. To investigate its phenotype, the S603T mutation was introduced into a recombinant TBEV strain (Oshima-IC) generated from an infectious cDNA clone and into a TBEV replicon that expresses a reporter luciferase gene (Oshima- REP-luc2A). The mutants were replication impaired, showing reduced growth and a small plaque size in mammalian cell culture and reduced levels of neuroinvasiveness and neurovirulence in rodent models. These results indicate that TBEV resistance to 2=-C-methylated nucleoside inhibitors is conferred by a single conservative mutation that causes a subtle atomic effect within the active site of the viral NS5 RdRp and is associated with strong attenuation of the virus.
Keywords
antiviral agents; antiviral therapy; escape mutant; tick-borne encephalitis virus; tick-borne pathogens
Authors
Released
1. 11. 2017
ISBN
0022-538X
Periodical
JOURNAL OF VIROLOGY
Year of study
91
Number
21
State
United States of America
Pages from
1
Pages to
20
Pages count
BibTex
@article{BUT141910, author="Markéta {Vaculovičová} and Daniel {Růžek} and Luděk {Eyer} and James Jason {Valdés} and Jiří {Černý} and Martin {Palus} and Jiří {Salát} and Darina {Zouharová} and Tomáš {Kastl} and Jan {Haviernik} and René {Kizek}", title="Escape of tick-borne flavivirus from 2'-C-methylated nucleoside antivirals is mediated by a single conservative mutation in NS5 that has a dramatic effect on viral fitness", journal="JOURNAL OF VIROLOGY", year="2017", volume="91", number="21", pages="1--20", doi="10.1128/JVI.01028-17", issn="0022-538X" }