The sindbis virus 6K protein can be detected in virions and is acylated with fatty acids

Gaedigk-Nitschko, Kerstin; Schlesinger, Milton J.

doi:10.1016/0042-6822(90)90209-a

Cited by 101 publications

(99 citation statements)

References 12 publications

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“…6K and TF are viral accessory proteins that share an N-terminus but have disparate C-termini, resulting from ribosomal frameshifting, and are hypothesized to form ion channels (67). Although 6K and TF are found at low levels in virion particles (68,85,86) and appear to contribute to viral budding (68,87) and pathogenesis (88), their precise roles in glycoprotein processing, assembly, budding, and particle stability remain to be clarified (67,68,88).…”

Section: Disease Mechanisms and Host Immune Responsesmentioning

confidence: 99%

Chikungunya virus: epidemiology, replication, disease mechanisms, and prospective intervention strategies

Silva¹,

Dermody²

2017

Journal of Clinical Investigation

324

338

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Section: Disease Mechanisms and Host Immune Responsesmentioning

confidence: 99%

Chikungunya virus: epidemiology, replication, disease mechanisms, and prospective intervention strategies

Silva¹,

Dermody²

2017

Journal of Clinical Investigation

324

338

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“…The nucleocapsid contains the single-stranded plus-sense RNA genome of approximately 11.8 kb complexed with multiple copies of a single species of capsid protein (C) of about 30 kDa. The virion envelope consists of a lipid bilayer, derived from the plasma membrane of the host cell, in which are embedded multiple copies of two major virus encoded glycoproteins El and E2 [15] as well as another small peptide, 6K, that is associated with virus particles only at a very low level [16,17]. E1 and E2 proteins both have a molecular mass of about 50 kDa and are anchored in the membrane by conventional membrane-spanning anchors located in their C-terminal regions.…”

Section: Viral Structure Genome Organization and Transmission Cycle mentioning

confidence: 99%

Chikungunya: an emerging and spreading arthropod-borne viral disease.

Cavrini

Gaibani

Pierro

et al. 2009

J Infect Dev Ctries

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The virus causing Chikungunya disease was identified over 50 years ago; however, because the disease appeared only in developing countries, little research on it has been done. Research interest in the disease increased after an important epidemiological outbreak occurred in 2005 on the French metropolitan island of La Reunion located in the south-eastern part of the Indian Ocean. In 2007, a smaller outbreak of Chikungunya developed in the north-eastern part of Italy made possible by immigration of a viremic patient from the Indian Ocean area and the enormous population of Aedes albopictus in Italy. Currently, Chikungunya is spreading in Southeast Asian aspects, clinical pictures, diagnosis and treatment of the disease caused by Chikungunya virus.

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“…SINV has an external diameter of 700 Å and contains 240 copies each of the E2 (423 amino acid residues), E1 (439 amino acid residues), and capsid protein (CP; 64 amino acid residues), all of which are arranged with icosahedral Tϭ4 quasisymmetry (2). A small protein referred to as 6K (55 amino acid residues) is found in substoichiometric amounts in the particle (10,25). The 11,703-nucleotide (nt) positive-sense viral RNA genome is encapsidated by CPs in the cytoplasm of infected cells to form a nucleocapsid core (NC).…”

mentioning

confidence: 99%

Interactions of the Cytoplasmic Domain of Sindbis Virus E2 with Nucleocapsid Cores Promote Alphavirus Budding

Jose¹,

Przybyla²,

Edwards³

et al. 2012

J Virol

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Alphavirus budding from the plasma membrane occurs through the specific interaction of the nucleocapsid core with the cytoplasmic domain of the E2 glycoprotein (cdE2). Structural studies of the Sindbis virus capsid protein (CP) have suggested that these critical interactions are mediated by the binding of cdE2 into a hydrophobic pocket in the CP. Several molecular genetic studies have implicated amino acids Y400 and L402 in cdE2 as important for the budding of alphaviruses. In this study, we characterized the role of cdE2 residues in structural polyprotein processing, glycoprotein transport, and capsid interactions. Along with hydrophobic residues, charged residues in the N terminus of cdE2 were critical for the effective interaction of cores with cdE2, a process required for virus budding. Mutations in the C-terminal signal sequence region of cdE2 affected E2 protein transport to the plasma membrane, while nonbudding mutants that were defective in cdE2-CP interaction accumulated E2 on the plasma membrane. The interaction of cdE2 with cytoplasmic cores purified from infected cells and in vitro-assembled corelike particles suggests that cdE2 interacts with assembled cores to mediate budding. We hypothesize that these cdE2 interactions induce a change in the organization of the nucleocapsid core upon binding leading to particle budding and priming of the nucleocapsid cores for disassembly that is required for virus infection.

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The sindbis virus 6K protein can be detected in virions and is acylated with fatty acids

Cited by 101 publications

References 12 publications

Chikungunya virus: epidemiology, replication, disease mechanisms, and prospective intervention strategies

Chikungunya virus: epidemiology, replication, disease mechanisms, and prospective intervention strategies

Chikungunya: an emerging and spreading arthropod-borne viral disease.

Interactions of the Cytoplasmic Domain of Sindbis Virus E2 with Nucleocapsid Cores Promote Alphavirus Budding

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