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Viruses viral-coat proteins

Very few self-sufficient viruses have only 60 protein chains in their shells. The satellite viruses do not themselves encode all of the functions required for their replication and are therefore not self-sufficient. The first satellite virus to be discovered, satellite tobacco necrosis virus, which is also one of the smallest known with a diameter of 180 A, has a protein shell of 60 subunits. This virus cannot replicate on its own inside a tobacco cell but needs a helper virus, tobacco necrosis virus, to supply the functions it does not encode. The RNA genome of the satellite virus has only 1120 nucleotides, which code for the viral coat protein of 195 amino acids but no other protein. With this minimal genome the satellite viruses are obligate parasites of the viruses that parasitize cells. [Pg.329]

In all jelly roll barrels the polypeptide chain enters and leaves the barrel at the same end, the base of the barrel. In the viral coat proteins a fairly large number of amino acids at the termini of the polypeptide chain usually lie outside the actual barrel structure. These regions vary considerably both in size and conformation between different coat proteins. In addition, there are three loop regions at this end of the barrel that usually are quite long and that also show considerable variation in size in the plant viruses and the... [Pg.335]

Figure 16.14 Schematic diagrams of three different viral coat proteins, viewed in approximately the same direction. Beta strands I through 8 form the common jelly roll barrel core, (a) Satellite tobacco necrosis virus coat protein, (b) Subunit VPl from poliovirus. Figure 16.14 Schematic diagrams of three different viral coat proteins, viewed in approximately the same direction. Beta strands I through 8 form the common jelly roll barrel core, (a) Satellite tobacco necrosis virus coat protein, (b) Subunit VPl from poliovirus.
The cleft where this drug binds is inside the jelly roll barrel of subunit VPl. Most spherical viruses of known structure have the tip of one type of subunit close to the fivefold symmetry axes (Figure 16.15a). In all the picor-naviruses this position is, as we have described, occupied by the VPl subunit. Two of the four loop regions at the tip are considerably longer in VPl than in the other viral coat proteins. These long loops at the tips of VPl subunits protrude from the surface of the virus shell around its 12 fivefold axes (Figure 16.15b). [Pg.337]

Synthetic haptens mimicking some critical epitopic structures on larger macromolecules are often conjugated to carriers to create an immune response to the larger parent molecule. For instance, short peptide segments can be synthesized from the known sequence of a viral coat protein and coupled to a carrier to induce immunogenicity toward the native virus. This type of synthetic approach to immunogen production has become the basis of much of the current research into the creation of vaccines. [Pg.747]

In the second research strategy, plant viruses have been utilized as pliable genetic platforms for protein expression. Three formats have been developed, and the one that has undergone the most extensive evaluation is the display of epitopes on the surface of the virus as fusions with the viral coat protein. This epitope-display system... [Pg.138]

Some attempts have been made to rationally increase the efficiency of endosomal escape. One such avenue entails the incorporation of selected hydrophobic (viral) peptides into the gene delivery systems. Many viruses naturally enter animal cells via receptor-mediated endocytosis. These viruses have evolved efficient means of endosomal escape, usually relying upon membrane-disrupting peptides derived from the viral coat proteins. [Pg.435]

Viral coat proteins, see Southern bean mosaic virus, Tobacco mosaic virus, or Tomato bushy stunt virus... [Pg.283]

Redox Fe-S proteins High-potential iron protein Ferredoxin Viral coat proteins f Tomato bushy stunt virus protein I Southern bean mosaic virus protein Tobacco mosaic virus protein... [Pg.319]

Wei, N., and Morris, T. J. (1991). Interactions between viral coat protein and a specific binding region on turnip crinkle virus RNA. J. Mol. Biol. 222, 437-443. [Pg.258]

Interference with assembly of viral coat proteins and viral RNA into new virus particles. Interferons may induce in the ribosomes of the host cells production of enzymes that inhibit translation of viral proteins. Avarol and avarine are thought to interfere with cytoskeletal assembly of virus particles. PROTEASE inhibitors can prevent the release of reverse transcriptase, and HIV-1 proteinase (e.g. saquinavir) are under development or in trial application. [Pg.38]

A single mechanism will not describe even the "controlled aggregation of proteins in nature. A single viral coat protein, for example, may form several different contacts with itself and other proteins, depending on its final position within the shell structure. Indeed, the original postulate of "quasi-equivalent binding at lattice points in virus capsules was modified to "non-equivalency" when the first structure was solved at atomic dimensions. For example, the coat of Tomato bushy stunt virus consists of 180 identical subunits of a 43 kD protein which self-interact at lattice points in at least three distinct ways k... [Pg.23]

Viral coat proteins gC and gB of herpes simplex virus [11]... [Pg.24]

The outcome of infection by SV40 depends on the organism infected. When simian cells are infected, the virus enters the cell and loses its protein coat. The viral DNA is expressed first as mRNAs and then as proteins. The large-T protein is the first one made (Figure 14.6), triggering the replication of viral DNA, followed by viral coat proteins. The virus takes over the cellular machinery for both replication of DNA and protein synthesis. New virus particles are assembled, and eventually the infected cell bursts, releasing the new virus particles to infect other cells. [Pg.408]

The adeno-associated virus (AAV) is a nonpathogenic, ssDNA virus belonging to the Parvoviridae family of viruses. This virus has two genes The cap gene encodes for three viral coat proteins, and the rep gene encodes for four proteins involved in viral replication and integration. This virus needs additional genes to replicate that are provided by the helper virus, which usually is the adenovirus or herpes virus. Interest in this virus as a vector arose from the... [Pg.245]

Fomivirsen inhibits CMV by at least two mechanisms. The first is a sequence-specific antisense binding to inhibit expression of immediate-early genes, thus preventing viral replication. The second is sequence-independent and involves inhibition of adsorption of CMV to host cells, probably by direct binding to viral coat proteins (20,21). The reduction of immediate-early protein synthesis occurs in a dose-dependent manner. Although it does inhibit viral replication, fomivirsen does not eradicate the virus whose DNA, as for all herpesviruses, is integrated into the human genome. Therefore, treatment will have to continue for the life of the patient. [Pg.337]

When a virus infects a cell, several events occur that are specific for the invader and hence offer opportunities for selective attack. First of all, there is the contact with the cell, then the penetration of the cell s plasma membrane and the (often simultaneous) rejection of the viral coating-protein. If the virus is of the RN A type, reverse transcriptase is soon in manufacture, but in any case the synthesis of nucleic acid polymerases dominates this early stage of invasion. Next follows the synthesis of viral nucleic acids, structural proteins, and yet more enzymes, followed by the assembly of these components to form the complete virus. Finally, some thousands of these virions are liberated from each cell. Apart from the possibilities for finding selective inhibitors for each of these stages, the patient could also be helped by other drugs to control the secondary (non-viral) symptoms, which are often of an inflammatory or anaphylactic character. [Pg.225]

Structure viral-coat proteins Sheath around nucleic acid of viruses... [Pg.304]

Filamentous viruses, which are high-aspect ratio agents that proliferate in the presence of host cells, have regular self-assembled structures, and the viral coat proteins on their surface can be genetically or chemically modified to functionalise the nanovector. The tobacco mosaic virus is one of the most extensively studied ID structure for nanoscale applications, and their properties, functionalisation, and assembly into nanodevices are highlighted in the recent review by Ghodssi and co-workers. Mao and co-workers have recently demonstrated that filamentous bacteriophage can be converted into novel photo-responsive nanowires... [Pg.299]


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