9SPU

Echovirus 18 particle missing one pentamer in situ, symmetrized reconstruction (C5)

Summary for 9SPU

• Entry DOI: 10.2210/pdb9spu/pdb
• EMDB information: 54764 55096
• Descriptor: Echovirus 18 viral protein 1, Echovirus 18 viral protein 3, Echovirus 18 viral protein 2 (3 entities in total)
• Functional Keywords: virus, in situ structure
• Biological source: Echovirus E18; More
• Total number of polymer chains: 33
• Total formula weight: 962616.12

Authors

Mukhamedova, L.,Plevka, P. (deposition date: 2025-09-18, release date: 2026-06-17, Last modification date: 2026-07-29)

Primary citation

Mukhamedova, L.,Buchta, D.,Trebichalska, Z.,Levdansky, Y.,Moravcova, J.,Potesil, D.,Zdrahal, Z.,Hrebik, D.,Nepovimova, L.,Gjolberg, T.T.,Andersen, J.T.,Novacek, J.,Fuzik, T.,Plevka, P.
Particles of echovirus 18 open to release their genomes in vivo.
Proc.Natl.Acad.Sci.USA, 123:e2601182123-e2601182123, 2026

PubMed Abstract: Enteroviruses cause a broad spectrum of human diseases, ranging from mild respiratory or gastrointestinal infections to severe neurological disorders such as aseptic meningitis and encephalitis. Enterovirus cell entry involves receptor-mediated endocytosis followed by destabilizing rearrangements of the virus capsid that enable genome release. However, the mechanism of enterovirus genome release has not been visualized in infected cells. Here, we used cryoelectron tomography and microscopy to image echovirus 18 (E18) entry into host cells and its interaction with the neonatal Fc receptor (FcRn). 30 min postinfection, endosomes and cytoplasm contained empty capsids missing one or several pentamers of capsid proteins, providing evidence that in vivo E18 releases its genome through capsid opening. In vitro, FcRn binding induced the expulsion of pocket factors from hydrophobic pockets in VP1, priming the virus for uncoating. The cryoelectron microscopy reconstruction of genome-containing particles of E18 inside infected cells did not reveal pocket factors, indicating that receptor binding triggers the same priming process during infection. We did not detect activated particles in infected cells, suggesting that these intermediates are short-lived and rapidly release their genomes in vivo. Our results identify capsid opening as the in vivo mechanism of echovirus 18 genome release, providing structural evidence for a process previously only inferred from in vitro experiments.

PubMed: 42475568
DOI: 10.1073/pnas.2601182123

Experimental method

ELECTRON MICROSCOPY (6.5 Å)