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Viral attachment proteins

Other viral targets Attachment proteins Fusion proteins Disassembly/Uncoating... [Pg.3]

Viral and cellular lipid membranes must first fuse to allow entry of the viral core into a host cell. The primary receptor required for the entry of primate lentiviruses, HIV-1, HIV-2, and SIV, into cells is the CD4 molecule (1). The interaction of viral envelope protein with CD4 not only attaches virus particles to the cell surface but also induces conformational changes in the envelope protein. These structural alterations allow a secondary interaction with a coreceptor to occur which triggers the fusion process. [Pg.209]

A virus must attach to a host cell before it can penetrate, which is why so much research is involved in studying the exact mechanisms of viral attachment. A common method of attachment involves the binding of one of the spike proteins on the envelope of the virus to a specific receptor on the host cell. Figure 14.7 shows an example of HIV attachment. A specific spike protein called gpl20 binds to a CD4 receptor on helper T cells. After this happens, a co-receptor complexes with CD4 and gpl20. Another spike protein, gp41, then punctures the cell so that the capsid can enter. [Pg.409]

Figure 7.1-3. The ideal synthetic (nonviral) gene delivery vector. After dense DNA packaging is accomplished (e.g., by protamine sulfate), the surface of synthetic particles (which is usually positively charged) needs to be shielded (e.g., by poly (ethylene-glycol) [PEG]) so that they do not attach to blood elements or to each other and, therefore, have an extended circulating plasma half-life (1) (passive targeting to leaky vessels ). The surface of the particles will contain specific ligands for active targeting to selected cells/ tissues (2). By engineering viral fusion proteins to the particle coat, cell entry is facilitated... Figure 7.1-3. The ideal synthetic (nonviral) gene delivery vector. After dense DNA packaging is accomplished (e.g., by protamine sulfate), the surface of synthetic particles (which is usually positively charged) needs to be shielded (e.g., by poly (ethylene-glycol) [PEG]) so that they do not attach to blood elements or to each other and, therefore, have an extended circulating plasma half-life (1) (passive targeting to leaky vessels ). The surface of the particles will contain specific ligands for active targeting to selected cells/ tissues (2). By engineering viral fusion proteins to the particle coat, cell entry is facilitated...

See other pages where Viral attachment proteins is mentioned: [Pg.286]    [Pg.117]    [Pg.436]    [Pg.456]    [Pg.371]    [Pg.252]    [Pg.196]    [Pg.6392]    [Pg.10]    [Pg.37]    [Pg.196]    [Pg.286]    [Pg.117]    [Pg.436]    [Pg.456]    [Pg.371]    [Pg.252]    [Pg.196]    [Pg.6392]    [Pg.10]    [Pg.37]    [Pg.196]    [Pg.339]    [Pg.196]    [Pg.197]    [Pg.5]    [Pg.12]    [Pg.111]    [Pg.114]    [Pg.184]    [Pg.132]    [Pg.195]    [Pg.247]    [Pg.170]    [Pg.196]    [Pg.197]    [Pg.388]    [Pg.459]    [Pg.476]    [Pg.1619]    [Pg.853]    [Pg.119]    [Pg.387]    [Pg.1475]    [Pg.69]    [Pg.403]    [Pg.221]    [Pg.242]    [Pg.478]    [Pg.489]    [Pg.734]    [Pg.848]    [Pg.585]    [Pg.119]    [Pg.947]    [Pg.1857]   
See also in sourсe #XX -- [ Pg.137 ]

See also in sourсe #XX -- [ Pg.137 ]




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Attachment proteins

Viral proteins

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