Virus binding and entry病毒结合和进入.pptVIP

Virus binding and entry 9/9/2004 + 9/14/2004 General points - virus entry The first event in any virus life-cycle - often limits infection to the “correct” cell Can be primary determinant of tropism Tissue tropism - e.g. measles (skin cells) vs. mumps (salivary gland) Species tropism - e.g. togavirus (both insect/mammalian cells), poliovirus (primate cells), T4 phage - (few strains of E.coli) Binding - initially electrostatic, based on charge ± pH, specific ions - followed by local hydrophobic interactions Initial binding is often low affinity, but high avidity (tight binding) due to multiple binding sites The virus binds to a receptor on the cell surface - can be ubiquitous/specific, with variable density Initial binding is followed by penetration and subsequent uncoating General points II - virus entry Whether or not the virus is enveloped makes a big difference - at least for penetration All viruses must cross a lipid bilayer, plant and bacterial viruses must also cross a cell wall Uncoating means that the stable virus stucture must become unstable -transition from extracellular (chemical) form to intracellular (biological) form There must be some sort of “trigger” or regulated disassembly process T-even (T2) phage structure Entry of T-even bacteriophage - binding Best understood = T4 phage (the virus in the Hershey-Chase experiment) Initial binding is reversible and electrostatic - the outer-most part of the long tail fiber binds to surface lipopolysaccharides (LPS) of the bacterium (binding can occur in vitro, and is competed by specific sugars) - a non-specific receptor Binding is “additive” until all six tail fibers are bound Binding of 3 fibers is needed to initiate infection The virus may “browse” the surface - looking for a suitable site for penetration (possibly sites of cell wall synthesis where the outer and plasma membranes are close together). Note - this is a multi-valent interaction Entry of T-even bacteriophage - binding II The receptor