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Structural and Thermodynamic Analysis of the Resistance Development to Pimodivir (VX-787), the Clinical Inhibitor of Cap Binding to PB2 Subunit of Influenza A Polymerase

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    SYSNO ASEP0541489
    Document TypeJ - Journal Article
    R&D Document TypeJournal Article
    Subsidiary JČlánek ve WOS
    TitleStructural and Thermodynamic Analysis of the Resistance Development to Pimodivir (VX-787), the Clinical Inhibitor of Cap Binding to PB2 Subunit of Influenza A Polymerase
    Author(s) Gregor, Jiří (UOCHB-X)
    Radilová, Kateřina (UOCHB-X) ORCID
    Brynda, Jiří (UOCHB-X) RID, ORCID
    Fanfrlík, Jindřich (UOCHB-X) RID, ORCID
    Konvalinka, Jan (UOCHB-X) RID, ORCID
    Kožíšek, Milan (UOCHB-X) RID, ORCID
    Article number1007
    Source TitleMolecules. - : MDPI
    Roč. 26, č. 4 (2021)
    Number of pages13 s.
    Languageeng - English
    CountryCH - Switzerland
    Keywordsinfluenza A polymerase ; antivirals ; pimodivir ; VX-787 ; resistance
    OECD categoryBiochemistry and molecular biology
    R&D ProjectsEF16_019/0000729 GA MŠMT - Ministry of Education, Youth and Sports (MEYS)
    Research Infrastructuree-INFRA CZ - 90140 - CESNET, zájmové sdružení právnických osob
    Method of publishingOpen access
    Institutional supportUOCHB-X - RVO:61388963
    UT WOS000624159600001
    EID SCOPUS85102604093
    DOI10.3390/molecules26041007
    AnnotationInfluenza A virus (IAV) encodes a polymerase composed of three subunits: PA, with endonuclease activity, PB1 with polymerase activity and PB2 with host RNA five-prime cap binding site. Their cooperation and stepwise activation include a process called cap-snatching, which is a crucial step in the IAV life cycle. Reproduction of IAV can be blocked by disrupting the interaction between the PB2 domain and the five-prime cap. An inhibitor of this interaction called pimodivir (VX-787) recently entered the third phase of clinical trial, however, several mutations in PB2 that cause resistance to pimodivir were observed. First major mutation, F404Y, causing resistance was identified during preclinical testing, next the mutation M431I was identified in patients during the second phase of clinical trials. The mutation H357N was identified during testing of IAV strains at Centers for Disease Control and Prevention. We set out to provide a structural and thermodynamic analysis of the interactions between cap-binding domain of PB2 wild-type and PB2 variants bearing these mutations and pimodivir. Here we present four crystal structures of PB2-WT, PB2-F404Y, PB2-M431I and PB2-H357N in complex with pimodivir. We have thermodynamically analysed all PB2 variants and proposed the effect of these mutations on thermodynamic parameters of these interactions and pimodivir resistance development. These data will contribute to understanding the effect of these missense mutations to the resistance development and help to design next generation inhibitors.
    WorkplaceInstitute of Organic Chemistry and Biochemistry
    Contactasep@uochb.cas.cz ; Kateřina Šperková, Tel.: 232 002 584 ; Jana Procházková, Tel.: 220 183 418
    Year of Publishing2022
    Electronic addresshttps://doi.org/10.3390/molecules26041007
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