Elizabeth J Tanner, Hong-mei Liu ... Karla Kirkegaard
When antiviral compounds target oligomeric assemblages, the formation of chimeric oligomers within cells can negate selection for naturally occurring drug-resistant variants.
High-throughput and ultra-stable magnetic tweezers reveal that Remdesivir induces a long-lived backtrack pause upon incorporation by the coronavirus polymerase, and SARS-CoV-2 is able to evade interferon-induced antiviral ddhCTP.
Nicholas van Buuren, Timothy L Tellinghuisen ... Karla Kirkegaard
Interactions between viral genomes within the same cells can impact the selection of drug-resistant variants and this has been finessed by hepatitis C virus.
Studies of the substrate selectivity of concentrative nucleoside transporters provide proof of principle for structure-based improvement of drug delivery by these transporters.
Shortened hepatitis C therapy, with retreatment if needed, can reduce antiviral drug use in patients with mild liver disease, but day 2 viral load is not an adequate predictor of outcome.
Exploiting virus-encoded ion channels as drug targets drove a multi-faceted approach to deriving potent small molecules targeting HCV p7, simultaneously providing new insights into its fundamental biology.
High-resolution structures of HIV-1 RT in complex with two newly developed non-nucleoside inhibitors explain how they retain antiviral activities against drug-resistant RT mutants with considerably reduced susceptibility to rilpivirine.