Literature DB >> 10846072

The core of the respiratory syncytial virus fusion protein is a trimeric coiled coil.

J M Matthews1, T F Young, S P Tucker, J P Mackay.   

Abstract

Entry into the host cell by enveloped viruses is mediated by fusion (F) or transmembrane glycoproteins. Many of these proteins share a fold comprising a trimer of antiparallel coiled-coil heterodimers, where the heterodimers are formed by two discontinuous heptad repeat motifs within the proteolytically processed chain. The F protein of human respiratory syncytial virus (RSV; the major cause of lower respiratory tract infections in infants) contains two corresponding regions that are predicted to form coiled coils (HR1 and HR2), together with a third predicted heptad repeat (HR3) located in a nonhomologous position. In order to probe the structures of these three domains and ascertain the nature of the interactions between them, we have studied the isolated HR1, HR2, and HR3 domains of RSV F by using a range of biophysical techniques, including circular dichroism, nuclear magnetic resonance spectroscopy, and sedimentation equilibrium. HR1 forms a symmetrical, trimeric coiled coil in solution (K(3) approximately 2.2 x 10(11) M(-2)) which interacts with HR2 to form a 3:3 hexamer. The HR1-HR2 interaction domains have been mapped using limited proteolysis, reversed-phase high-performance liquid chromatography, and electrospray-mass spectrometry. HR2 in isolation exists as a largely unstructured monomer, although it exhibits a tendency to form aggregates with beta-sheet-like characteristics. Only a small increase in alpha-helical content was observed upon the formation of the hexamer. This suggests that the RSV F glycoprotein contains a domain that closely resembles the core structure of the simian parainfluenza virus 5 fusion protein (K. A. Baker, R. E. Dutch, R. A. Lamb, and T. S. Jardetzky, Mol. Cell 3:309-319, 1999). Finally, HR3 forms weak alpha-helical homodimers that do not appear to interact with HR1, HR2, or the HR1-HR2 complex. The results of these studies support the idea that viral fusion proteins have a common core architecture.

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Year:  2000        PMID: 10846072      PMCID: PMC112087          DOI: 10.1128/jvi.74.13.5911-5920.2000

Source DB:  PubMed          Journal:  J Virol        ISSN: 0022-538X            Impact factor:   5.103


  65 in total

1.  Inhibiting HIV-1 entry: discovery of D-peptide inhibitors that target the gp41 coiled-coil pocket.

Authors:  D M Eckert; V N Malashkevich; L H Hong; P A Carr; P S Kim
Journal:  Cell       Date:  1999-10-01       Impact factor: 41.582

Review 2.  Paramyxovirus fusion: a hypothesis for changes.

Authors:  R A Lamb
Journal:  Virology       Date:  1993-11       Impact factor: 3.616

3.  HIV-1 inhibition by a peptide.

Authors:  S Jiang; K Lin; N Strick; A R Neurath
Journal:  Nature       Date:  1993-09-09       Impact factor: 49.962

4.  Inhibition of HIV-1 infection by a fusion domain binding peptide from the HIV-1 envelope glycoprotein GP41.

Authors:  S Jiang; K Lin; N Strick; A R Neurath
Journal:  Biochem Biophys Res Commun       Date:  1993-09-15       Impact factor: 3.575

5.  Studies with cross-linking reagents on the oligomeric form of the paramyxovirus fusion protein.

Authors:  R Russell; R G Paterson; R A Lamb
Journal:  Virology       Date:  1994-02-15       Impact factor: 3.616

6.  Mutational analysis of the leucine zipper-like motif of the human immunodeficiency virus type 1 envelope transmembrane glycoprotein.

Authors:  S S Chen; C N Lee; W R Lee; K McIntosh; T H Lee
Journal:  J Virol       Date:  1993-06       Impact factor: 5.103

7.  Analysis of respiratory syncytial virus F, G, and SH proteins in cell fusion.

Authors:  B R Heminway; Y Yu; Y Tanaka; K G Perrine; E Gustafson; J M Bernstein; M S Galinski
Journal:  Virology       Date:  1994-05-01       Impact factor: 3.616

8.  Peptides corresponding to a predictive alpha-helical domain of human immunodeficiency virus type 1 gp41 are potent inhibitors of virus infection.

Authors:  C T Wild; D C Shugars; T K Greenwell; C B McDanal; T J Matthews
Journal:  Proc Natl Acad Sci U S A       Date:  1994-10-11       Impact factor: 11.205

9.  Gradient-tailored excitation for single-quantum NMR spectroscopy of aqueous solutions.

Authors:  M Piotto; V Saudek; V Sklenár
Journal:  J Biomol NMR       Date:  1992-11       Impact factor: 2.835

10.  Structure of influenza haemagglutinin at the pH of membrane fusion.

Authors:  P A Bullough; F M Hughson; J J Skehel; D C Wiley
Journal:  Nature       Date:  1994-09-01       Impact factor: 49.962

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  32 in total

1.  Mutations in the fusion peptide and adjacent heptad repeat inhibit folding or activity of the Newcastle disease virus fusion protein.

Authors:  T A Sergel; L W McGinnes; T G Morrison
Journal:  J Virol       Date:  2001-09       Impact factor: 5.103

2.  Cleavage of the human respiratory syncytial virus fusion protein at two distinct sites is required for activation of membrane fusion.

Authors:  L González-Reyes; M B Ruiz-Argüello; B García-Barreno; L Calder; J A López; J P Albar; J J Skehel; D C Wiley; J A Melero
Journal:  Proc Natl Acad Sci U S A       Date:  2001-08-07       Impact factor: 11.205

3.  Neutralization of human respiratory syncytial virus infectivity by antibodies and low-molecular-weight compounds targeted against the fusion glycoprotein.

Authors:  Margarita Magro; David Andreu; Paulino Gómez-Puertas; José A Melero; Concepción Palomo
Journal:  J Virol       Date:  2010-06-09       Impact factor: 5.103

4.  Mutations in the putative HR-C region of the measles virus F2 glycoprotein modulate syncytium formation.

Authors:  Richard K Plemper; Richard W Compans
Journal:  J Virol       Date:  2003-04       Impact factor: 5.103

5.  A capsid protein of nonenveloped Bluetongue virus exhibits membrane fusion activity.

Authors:  Mario Forzan; Christoph Wirblich; Polly Roy
Journal:  Proc Natl Acad Sci U S A       Date:  2004-02-04       Impact factor: 11.205

6.  Targeting a binding pocket within the trimer-of-hairpins: small-molecule inhibition of viral fusion.

Authors:  Christopher Cianci; David R Langley; Douglas D Dischino; Yaxiong Sun; Kuo-Long Yu; Anne Stanley; Julia Roach; Zhufang Li; Richard Dalterio; Richard Colonno; Nicholas A Meanwell; Mark Krystal
Journal:  Proc Natl Acad Sci U S A       Date:  2004-10-06       Impact factor: 11.205

7.  A conserved region between the heptad repeats of paramyxovirus fusion proteins is critical for proper F protein folding.

Authors:  Amanda E Gardner; Kimberly L Martin; Rebecca E Dutch
Journal:  Biochemistry       Date:  2007-04-07       Impact factor: 3.162

8.  Structural characterization of the human respiratory syncytial virus fusion protein core.

Authors:  X Zhao; M Singh; V N Malashkevich; P S Kim
Journal:  Proc Natl Acad Sci U S A       Date:  2000-12-19       Impact factor: 11.205

9.  Coordinate deletion of N-glycans from the heptad repeats of the fusion F protein of Newcastle disease virus yields a hyperfusogenic virus with increased replication, virulence, and immunogenicity.

Authors:  Sweety Samal; Sunil K Khattar; Sachin Kumar; Peter L Collins; Siba K Samal
Journal:  J Virol       Date:  2011-12-28       Impact factor: 5.103

10.  Elevated temperature triggers human respiratory syncytial virus F protein six-helix bundle formation.

Authors:  Abdul S Yunus; Trent P Jackson; Katherine Crisafi; Irina Burimski; Nicole R Kilgore; Dorian Zoumplis; Graham P Allaway; Carl T Wild; Karl Salzwedel
Journal:  Virology       Date:  2009-11-18       Impact factor: 3.616

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