Virus synthesis

However, in a systemic host of TMV (P. floridana) the infiltration of tannic acid (0.034%) 24 hours after virus inoculation reduced virus titer about 75% during the first week after infection. After two weeks there was no significant difference in total virus content between tannic acid-treated and water-treated samples. Thus tannic acid does interfere with virus synthesis at an early stage in a temporary way. 

Virus infection obviously upsets the regulatory mechanisms of the host, since there is a marked overproduction of nucleic acid and protein in the infected cell. In some cases, virus infection causes a complete shutdown of host macromolecular synthesis while in other cases host synthesis proceeds concurrently with virus synthesis. In either case, the regulation of virus synthesis is under the control of the virus rather than the host. There are several elements of this control which are similar to the host regulatory mechanisms, but there are also some uniquely viral regulatory mechanisms. We discuss various regulatory mechanisms when we consider the individual viruses later in this chapter. 

Hall, W.W., Lamb, R.A., and Choppin, P.W. 1980. The polypeptides of canine distemper virus Synthesis in infected cells and relatedness to the polypeptides of other morbilliviruses. Virology 100, 433 49. Herden, C., Herzog, S., Richt, J.A., Nesseler, A., Christ, M., Failing, K., and Frese, K. 2000. Distribution of Boma disease virus in the brain of rats infected with an obesity-inducing virus strain. Brain Pathol 10, 39-48. 

As shown above, a shunt does occur in the mode of the utilization of glucose-6-phosphate in the shift from normal growth to virus synthesis. We can exclude two possible mechanisms. First, the change in glucose utilization to the glycolytic pathway is not merely a shift of reversible systems caused by removal of desoxyribose phosphate from the system by virus. In variations of the basic virus-host system, RNA synthesis is completely inhibited even though DNA synthesis may be diminished or even completely repressed. 

Holland, J. J., 1964, Inhibition of host cell macromolecular synthesis by high multiplicities of poliovirus under conditions preventing virus synthesis, J. Mol. Biol. 8 574. 

Keranen, S., and Ruohonen, L., 1983, Nonstructural proteins of Semliki Forest virus Synthesis, processing and stability in infected cells, J. Virol. 47 505. 

Kinetics of Utilization of Host Nucleic Acid in Virus Synthesis.262... 

Increase in enzymic activity of the infected cell. An increase in enzymic activity of the infected cell is contrary to the observations recorded above, and, indeed, with the exception of an enhancement of deoxyribonuclease, the activities of the bacterial enzymes appear to remain constant after infection of E. coli with the T phages (225a,227,227a). Since the enzymes appear to retain activity after infection, this suggests that the virus interferes with the synthesis of new enzymes, as well as RNA and protein, perhaps by diverting energy and metabolites from normal synthetic pathways to pathways of virus synthesis. 

When N -labeled E. coli are infected with T6r+ bacteriophage, about 80% of the viral N is derived from the medium and the other 20% comes from the bacterial cell (Kozloff, Knowlton, Putnam, and Evans, 160,163) the converse holds true when E. coli are infected with T7 (Putnam, Miller, Palm, and Evans, 262). Thus, the assimilation of virus N resembles that for virus P in that relatively more of the inorganic compounds of the medium are channeled into virus synthesis for the large phages than for the small ones. However, several important differences exist between N and P metabolism during phage multiplication (1) Analytically, P occurs almost wholly in the virus nucleic acid, whereas N is about equally divided between the nucleic acid and protein of the phage. Tracer... 

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