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Virus binding to cells

The virus is small, fragile and of relatively simple construction. The virus binds to cells that have a particular surface antigen called CD4. CD4 is found on T helper cells, monocytes and macrophages. [Pg.164]

Fomivirsen is a phosphorothioate antisense oligionucleotide complementary to the mRNA sequence for the major immediate-early region of CMV and inhibits CMV replication through sequence-specific and nonspecific mechaiusms, including inhibition of virus binding to cells. Fomivirsen is active against CMV strains resistant to ganciclovir, foscamet, and cidofovir. [Pg.821]

Such sugar-dendrimer complexes ( sugar balls ) have been used to inhibit the interactions of viruses with cell surfaces. Many viruses bind to particular carbohydrate residues on cell surfaces, which in turn facilitate their entry into cells and the resultant infection process. A virus particle presents a multi-dentate surface consisting of many carbohydrate-binding proteins able to interact with multiple cell-surface carbohydrates. The surface of a dendrimer that is modified with... [Pg.366]

Analysis of SFV entry has thus shown that the virus binds to receptors on the cell surface and moves by lateral diffusion into coated pits to be internalized by coated vesicles. The endocytosed virus is delivered into endosomes. Here presumably, the viral envelope is activated by the low pH prevailing in this compartment to fuse with the vacuolar membrane. This results in the release of the viral nucleocapsid into the cytoplasm. During normal infection, the virus might not enter into lysosomes although SFV particles have been identified in this compartment using the large loads of virus needed to visualize the entry process by electron microscopy. Even if this were to happen normally, the viral nucleocapsid would escape destruction because of the rapidity of the fusion mechanism. [Pg.104]

The mode of action of this drug is not completely clear. It has been shown that virus absorbed to cells in vitro in the presence of 105 was susceptible to antibody inactivation several hours after infection whereas virus in a corresponding system free of 105 was not. This suggested that perhaps the drug did not inactivate the virus itself but prevented the penetration of the virus into the host cell 321 Subsequent studies have supported this conclusion 342 The manner in which cell penetration is prevented is not known. Perhaps 105 selectively binds to or in some way inhibits an enzyme essential for cell penetration or perhaps it acts by selectively binding the virus to areas of the cell wall which are not susceptible to penetration 3421. Other studies have also demonstrated a therapeutic effect of this drug 343). [Pg.84]

This stage consists of the virus binding to the cell. This involves the specific binding of a glycoprotein that appears on the external structure of a virus to a host cell receptor. [Pg.437]

Special interest has been taken in the inhibition of enzymes involved in cleaving the glycosidic bonds of neuraminic acid (a complex C9-carbon sugar acid), because this process is critical to the spread of infection after the influenza virus binds to the host cell. Following the analysis of the structure of complexes of the enzyme and substrate (bound in a distorted conformation), unsaturated compounds, for example 43 (Figure 1.14), were made as mimics of the latter in the reaction transition state and found to be potent neuraminidase inhibitors and anti-influenza compounds [49]. [Pg.38]

Lectins Promote Interaction Between Cells Influenza Virus Binds to Sialic Acid Residues... [Pg.1141]

The ability of the virus to agglutinate erythrocytes has been first reported in 1941. It took more than a decade before it was shown that influenza virus binds to erythrocytes and other cells via 7 -acetylneuraminic acid residues present on the cell surface and that this binding is a prerequisite for initiation of infection [24,25]. Other viruses, such as Sendai, Newcastle disease, polyoma and rotavirus also exhibit an affinity for sialie... [Pg.476]

Vimses are made up of a protein capsule, some with a lipoprotein envelope around it, containing genetic material (either DNA or RNA), with maybe a few enzymes but very little else and hence they are not considered to be cells, but, rather, infectious particles. Viruses are able to bind to cell membranes, penetrate and infect cells of other organisms. Viruses are intracellular parasites they cannot replicate themselves without using the contents of the host cell to synthesize the cellular components necessary for their reproduction. This makes the development of effective antiviral drugs that do not damage healthy host cells very difficult. [Pg.161]


See other pages where Virus binding to cells is mentioned: [Pg.266]    [Pg.479]    [Pg.266]    [Pg.87]    [Pg.266]    [Pg.479]    [Pg.266]    [Pg.87]    [Pg.165]    [Pg.315]    [Pg.367]    [Pg.359]    [Pg.178]    [Pg.230]    [Pg.390]    [Pg.3]    [Pg.578]    [Pg.937]    [Pg.942]    [Pg.359]    [Pg.261]    [Pg.434]    [Pg.451]    [Pg.463]    [Pg.465]    [Pg.1759]    [Pg.11]    [Pg.436]    [Pg.421]    [Pg.113]    [Pg.80]    [Pg.426]    [Pg.294]    [Pg.406]    [Pg.370]    [Pg.605]    [Pg.684]    [Pg.11]    [Pg.256]    [Pg.289]    [Pg.952]    [Pg.250]    [Pg.435]   
See also in sourсe #XX -- [ Pg.186 ]

See also in sourсe #XX -- [ Pg.186 ]

See also in sourсe #XX -- [ Pg.186 ]




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Binding cells

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