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Alphavirus virion

STRUCTURE AND REPLICATION OF ALPHAVIRUSES Virion Structure Replication... [Pg.561]

An additional virus that has more recently gained some attention as a possible vector is that of the sindbis virus. A member of the alphavirus family, this ssRNA virus can infect a broad range of both insect and vertebrate cells. The mature virion particles consist of the RNA genome com-plexed with a capsid protein C. This, in turn, is enveloped by a lipid bilayer in which two additional viral proteins (El and E2) are embedded. The E2 polypeptide appears to mediate viral binding to the surface receptors of susceptible cells. The major mammalian cell surface receptor it targets appears to be the highly conserved, widely distributed laminin receptor. [Pg.430]

Genomic RNA. The viral genome is a positive-stranded RNA of approximately 11,700 nucleotides and has the structural features of messenger RNA (ie, mRNA, a 5 methylated cap [m7GpppA] and a poly-A tract at the 3 end).77 As a complete and functional mRNA, genomic RNA purified from virions is fully infectious when artificially introduced (ie, transfected) into susceptible cells. Similarly, RNA transcribed from a full-length complementary DNA (cDNA) clone of an alphavirus is also infectious,... [Pg.569]

Fig. 28-3. Structure of an alphavirus. Shown is the three-dimensional reconstruction of Sindbis virus at 28 A resolution from computer-processed images taken by electron cryomicroscopy, (a) The original electron micrograph shows virus particles in vitreous ice. (b) The surface view of the virus shows details of the 80 trimeric spikes, which are arranged in a T=4 icosahedron. Each spike protrudes 50 A from the virion surface and is believed to be composed of three E1-E2 glycoprotein heterodimers, (c) The cross-sectional view shows the outer surface spikes (yellow) and the internal nucleocapsid (blue), composed of the capsid and viral RNA. The space between the spikes and the nucleocapsid would be occupied by the lipid envelope. The green arrows mark visible points of interaction between the nucleocapsid and trans-membranal tails of the glycoprotein spikes, (d) The reconstructed capsid also exhibits a T=4 icosahedral symmetry. Computer models Courtesy of Angel M. Paredes, Cell Research Institute and Department of Microbiology, The University of Texas at Austin, Austin, Tex. Similar but not identical versions of these computer models were published in Paredes AM, Brown DT, Rothnagel R, et al. Three-dimensional structure of a membrane-containing virus. Proc Natl Acad Sci USA. 1993 90 9095-9099. Fig. 28-3. Structure of an alphavirus. Shown is the three-dimensional reconstruction of Sindbis virus at 28 A resolution from computer-processed images taken by electron cryomicroscopy, (a) The original electron micrograph shows virus particles in vitreous ice. (b) The surface view of the virus shows details of the 80 trimeric spikes, which are arranged in a T=4 icosahedron. Each spike protrudes 50 A from the virion surface and is believed to be composed of three E1-E2 glycoprotein heterodimers, (c) The cross-sectional view shows the outer surface spikes (yellow) and the internal nucleocapsid (blue), composed of the capsid and viral RNA. The space between the spikes and the nucleocapsid would be occupied by the lipid envelope. The green arrows mark visible points of interaction between the nucleocapsid and trans-membranal tails of the glycoprotein spikes, (d) The reconstructed capsid also exhibits a T=4 icosahedral symmetry. Computer models Courtesy of Angel M. Paredes, Cell Research Institute and Department of Microbiology, The University of Texas at Austin, Austin, Tex. Similar but not identical versions of these computer models were published in Paredes AM, Brown DT, Rothnagel R, et al. Three-dimensional structure of a membrane-containing virus. Proc Natl Acad Sci USA. 1993 90 9095-9099.
It is important to know whether viral-specified proteins are involved in the inhibition of host protein synthesis and ts mutants have been used to try to answer this question. RNA t mutants did not inhibit cellular protein synthesis at the restrictive temperature (Atkins, 1976). Under these conditions, RNA / mutants of alphaviruses make neither viral encoded proteins nor viral RNAs (Keranen and Kaariainen, 1975 Hashimoto and Simizu, 1978). From these findings, we can conclude that initiation of viral RNA replication is necessary for inhibition of host protein synthesis and also that viral components introduced into cells by the infecting virions are not directly responsible for this inhibition. [Pg.472]


See other pages where Alphavirus virion is mentioned: [Pg.365]    [Pg.569]    [Pg.365]    [Pg.569]    [Pg.20]    [Pg.61]    [Pg.63]    [Pg.283]    [Pg.294]    [Pg.337]    [Pg.354]    [Pg.364]    [Pg.368]    [Pg.368]    [Pg.370]    [Pg.374]    [Pg.587]    [Pg.476]   
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