Early Events of Virus Multiplication

As we have noted, the outcome of a virus infection is the synthesis of viral nucleic acid and viral protein coats. In effect, the virus takes over the biosynthetic machinery of the host and uses it for its own synthesis. A few enzymes needed for virus replication may be present in the virus particle and may be introduced into the cell during the infection process, but the host supplies everything else energy-generating system, ribosomes, amino-acid activating enzymes, transfer RNA (with a few exceptions), and all soluble factors. The virus genome codes for all new proteins. Such proteins would include the coat protein subunits (of which there are generally more than one kind) plus any new virus-specific enzymes. 

Attachment There is a high specificity in the interaction between virus and host. The most common basis for host specificity involves the attachment process. The virus particle itself has one or more proteins on the outside which interact with specific cell surface components called receptors. The receptors on the cell surface are normal surface components of the host, such as proteins, polysaccharides, or lipoprotein-polysaccharide complexes, to which the virus particle attaches. In the absence of the receptor site, the virus cannot adsorb, and hence cannot infect. If the receptor site is altered, the host may become resistant to virus infection. However, mutants of the virus can also arise which are able to adsorb to resistant hosts. 

In general, virus receptors carry out normal functions in the cell. For example, in bacteria some phage receptors are pili or flagella, others are cell-envelope components, and others are transport binding proteins. The receptor for influenza vims is a glycoprotein found on red blood cells and on cells of the mucous membrane of susceptible animals, whereas the receptor site of poliovirus is a lipoprotein. However, many animal and plant viruses do not have specific attachment sites at all and the vims enters passively as a result of phagocytosis or some other endocytotic process. 

Penetration The means by which the vims penetrates into the cell depends on the nature of the host cell, especially on its surface stmctures. Cells with cell walls, such as bacteria, are infected in a different manner from animal cells, which lack a cell wall. The most complicated penetration mechanisms have been found in viruses that infect bacteria. The bacteriophage T4, which infects E. coli, can be used as an example. 

The particle has a head, within which the viral DNA is folded, and a long, fairly complex tail, at the end of which is a series of tail fibers. During the attachment process, the vims particles first attach to the cells by means of the tail fibers. These tail fibers then contract, and the core of the tail makes contact with the cell envelope of the bacterium. The action of a lysozyme-like enzyme results in the formation of a small hole. The tail sheath contracts and the DNA of the vims passes into the cell through a hole in the tip of the tail, the majority of the coat protein remaining outside. The DNA of T4 has a total length of about 50 /xm, whereas the dimensions of the head of the T4 particle are 0.095 Am by 0.065 fim. This means that the DNA must be highly folded and packed very tightly within the head. 

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