Chapter IV 



Chemistry of Virus Receptors 



Alfred Gottschalk 



Walter and Eliza Hall Institute of Medical Research, 



Melbourne, Australia 



Infection of a host cell by a virus particle is initiated by the entry of the 

 virus into the cell. Several mechanisms are known providing such an entry. 

 Phages of the T system infecting Escherichia coli B, a bacterium surrounded 

 by a multi-layer membrane consisting mainly of rigid, structural polysac- 

 charides and lipopolysaccharides, have evolved an elaborate mechanism of 

 invasion. Specific adsorption (chemisorption) of the phage to the surface of 

 the susceptible coli strain is followed by enzyme action on membrane 

 constituents. By these events a passage is formed through which the genetic 

 material (DNA) of the phage is introduced into the interior of the host cell. 

 Plant viruses enter their hosts through vector or other lesions of the surface 

 cells of leaves, etc. For most animal viruses it seems to be characteristic that 

 their host cells are endowed with phagocytic powers. Thus, the epithelial 

 cells of the respiratory and alimentary mucous membranes, the alveolar cells 

 of the lung, the vascular endothelial cells, the endothelial Kupffer cehs, and 

 mesenchymal cells are known to have phagocytic properties and to be host 

 cells for various viruses, the intake of the virus by the host cell being termed 

 "viropexis" (Fazekas de St. Groth, 1948b). Animal viruses with a wide range 

 of host cells, like vaccinia virus, ectromelia virus, psittacosis virus, and 

 others, rely for propagation on random collisions with a phagocytic host cell, 

 once having entered the body through a lesion of the skin, the bite of a 

 mosquito, or through an internal surface. Animal viruses with a greatly 

 restricted range of host cells, especially viruses infecting the respiratory tract, 

 have developed a specific mechanism of attachment to their host cells as a 

 preliminary to the intake of the virus into the cell. The specificity of this 

 attachment, like the specificity of an enzyme for its substrate or an antibody 

 for its antigen, resides in the complementariness of molecular structures 

 present at the surfaces of the host cell and of the virus particle. The segment 

 of the host cell surface instrumental in binding the virus is called the cellular 

 receptor. It is only for the myxovirus group, comprising influenza viruses 

 A, B, C and D, Newcastle disease, mumps, and fowl plague viruses, that 

 the chemistry of the cellular receptors has been elucidated, at least to some 

 extent. 



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