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.
Broader global access to Paxlovid, coupled with appropriately timed treatment, can mitigate the severity and transmission of SARS-Cov-2 as the virus and the landscape of immunity continue to evolve.
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.