ArticleJournal of virology2003
Interactions between the transmembrane segments of the alphavirus E1 and E2 proteins play a role in virus budding and fusion.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- Article
- Article
- Cryogenic electron microscopy and tomography reveal imperfect icosahedral symmetry in alphaviruses.PNAS nexus · 2024Article
- Alphavirus-Induced Membrane Rearrangements during Replication, Assembly, and Budding.Pathogens (Basel, Switzerland) · 2021Review
- A molecular understanding of alphavirus entry.PLoS pathogens · 2020Review
- Chikungunya Virus: An Emergent Arbovirus to the South American Continent and a Continuous Threat to the World.Frontiers in microbiology · 2020Review
- Implication for alphavirus host-cell entry and assembly indicated by a 3.5Å resolution cryo-EM structure.Nature communications · 2018Article
- The Interplay of Viral and Host Factors in Chikungunya Virus Infection: Targets for Antiviral Strategies.Viruses · 2018Review
- Review
- Chikungunya virus: epidemiology, replication, disease mechanisms, and prospective intervention strategies.The Journal of clinical investigation · 2017Review
- Suramin Inhibits Chikungunya Virus Entry and Transmission.PloS one · 2015Article
- Characterization of chikungunya virus-like particles.PloS one · 2014Article
- Crystal structure of aura virus capsid protease and its complex with dioxane: new insights into capsid-glycoprotein molecular contacts.PloS one · 2012Article
- Molecular links between the E2 envelope glycoprotein and nucleocapsid core in Sindbis virus.Journal of molecular biology · 2011Article
- 4.4 Å cryo-EM structure of an enveloped alphavirus Venezuelan equine encephalitis virus.The EMBO journal · 2011Article
- Activation of the alphavirus spike protein is suppressed by bound E3.Journal of virology · 2011Article
- Characterization of the GXXXG motif in the first transmembrane segment of Japanese encephalitis virus precursor membrane (prM) protein.Journal of biomedical science · 2010Article
- Alphavirus Entry and Membrane Fusion.Viruses · 2010Article
- Identification of a broad-spectrum arenavirus entry inhibitor.Journal of virology · 2008Article
- Transmembrane domains of hepatitis C virus envelope glycoproteins: residues involved in E1E2 heterodimerization and involvement of these domains in virus entry.Journal of virology · 2007Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The alphavirus envelope is built by heterodimers of the membrane proteins E1 and E2. The complex is formed as a p62E1 precursor in the endoplasmic reticulum. During transit to the plasma membrane (PM), it is cleaved into mature E1-E2 heterodimers, which are oligomerized into trimeric complexes, so-called spikes that bind both to each other and, at the PM, also to nucleocapsid (NC) structures under the membrane. These interactions drive the budding of new virus particles from the cell surface. The virus enters new cells by a low-pH-induced membrane fusion event where both inter- and intraheterodimer interactions are reorganized to establish a fusion-active membrane protein complex. There are no intact heterodimers left after fusion activation; instead, an E1 homotrimer remains in the cellular (or viral) membrane. We analyzed whether these transitions depend on interactions in the transmembrane (TM) region of the heterodimer. We observed a pattern of conserved glycines in the TM region of E1 and made two mutants where either the glycines only (SFV/E1(4L)) or the whole segment around the glycines (SFV/E1(11L)) was replaced by leucines. We found that both mutations decreased the stability of the heterodimer and increased the formation of the E1 homotrimer at a suboptimal fusion pH, while the fusion activity was decreased. This suggested that TM interactions play a role in virus assembly and entry and that anomalous or uncoordinated protein reorganizations take place in the mutants. In addition, the SFV/E1(11L) mutant was completely deficient in budding, which may reflect an inability to form multivalent NC interactions at the PM.
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