Efficacy of an isoxazole-3-carboxamide analog of pleconaril in mouse models of Enterovirus-D68 and Coxsackie B5

Lane, Thomas R.; Fu, Jianing; Sherry, Barbara; Tarbet, E. Bart; Hurst, Brett L.; Riabova, Olga; Kazakova, Elena; Egorova, Anna; Clarke, Penny; Leser, J. Smith; Frost, Joshua; Rudy, Michael J.; Tyler, Ken; Klose, Thomas; Volobueva, Alexandrina S.; Belyaevskaya, Svetlana V.; Zarubaev, Vladimir V.; Kühn, Richard; Makarov, Vadim; Ekins, Sean

doi:10.1016/j.antiviral.2023.105654

Cited by 3 publications

(1 citation statement)

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“…Given that these viruses use distinct repertoires of cellular attachment factors and receptors, it was somewhat unexpected to see parallel evolutionary patterns in the capsid. However, mapping these substitutions on the structure of the EV-D68 capsid ( 16 ) revealed that they either directly overlap with (T208A, VP2.T139) or are located nearby to escape variants identified in a study of neutralizing antigenic sites (K834R and Q835E, near the antigenic site at VP1.285). The T208 site in VP2 represents a shared antigenic site between the EV-D68 capsid and those of EV-A71 (at T210) and CV-A10 ( 17 ).…”

Section: Resultsmentioning

confidence: 99%

Structure and dynamics of enterovirus genotype networks

Dábilla,

Dolan

2024

Sci. Adv.

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Like all biological populations, viral populations exist as networks of genotypes connected through mutation. Mapping the topology of these networks and quantifying population dynamics across them is crucial to understanding how populations adapt to changes in their selective environment. The influence of mutational networks is especially profound in viral populations that rapidly explore their mutational neighborhoods via high mutation rates. Using a single-cell sequencing method, scRNA-seq–enabled acquisition of mRNA and consensus haplotypes linking individual genotypes and host transcriptomes (SEARCHLIGHT), we captured and assembled viral haplotypes from hundreds of individual infected cells, revealing the complexity of viral population structures. We obtained these genotypes in parallel with host cell transcriptome information, enabling us to link host cell transcriptional phenotypes to the genetic structures underlying virus adaptation. Our examination of these structures reveals the common evolutionary dynamics of enterovirus populations and illustrates how viral populations reach through mutational “tunnels” to span evolutionary landscapes and maintain connection with multiple adaptive genotypes simultaneously.

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Section: Resultsmentioning

confidence: 99%