Host translation

Viruses are usually not considered as hving entities because they are not able to replace their parts or carry out metabohsm on their own. They are very small in size, ranging from tens to hundreds of nanometers. They can be replicated only when they are in association with a living cell (host). The host translates the genetic information present in the virus, which lead to its replication. The consequence of this rephcation to the hving host is either disease or death. The viruses have very simple genetic elements that consist of nucleic acid surrounded by protein and other substances (3,9). 

This section is devoted to several cases of translational control where specific initiation factor(s), if involved, have not yet been identified, or where more than one mechanism of control is activated, as in the case of virus-induced shut-off of host translation. 

Many cytopathogenic viruses induce a decline in the rate of host mRNA translation upon infection. Since this shut-off of host translation is accompanied by extensive synthesis of viral protein, and since the decline in host protein synthesis is not concomitant with degradation or inactivation of host mRNA, it is clear that translational control mechanisms are involved in this phenomenon. A number of explanations have been invoked to explain shut-off by various viruses. Here, a few of these will be examined that are related directly to the material already reviewed above, but for a more extensive treatment, surveys by Koch et al. (1982) and elsewhere in this volume should be consulted. 

Jen, G., and Thach, R. E., 1982, Inhibition of host translation in encephalomy-ocarditis virus-infected L cells A novel mechanism, /. Virol. 43 250. 

Lacal, J. C., and Carrasco, L., 1982, Relationship between membrane integrity and the inhibition of host translation in virus-infected mammalian cells. Ear. J. Biochem. 127 359. 

Chantler, J. K., 1978, The use of hypertonicity to selectively inhibit host translation in murine cytomegalovirus-infected cells. Virology 90 166. 

With respect to cellular RNA synthesis, virtually no inhibition of host transcription has been observed following the infection of L cells with reovirus type 3 (Gomatos and Tamm, 1963 Kudo and Graham, 1965 Sharpe and Fields, 1982). Host mRNAs are present in type 3 reovirus-infected L cells late in the infectious cycle, although they are not translated, indicating host mRNA stability in the infected cell (Skup et ai, 1981). If the mechanism of reovirus inhibition of cellular protein synthesis does indeed involve a shift of the host translational machinery from cap dependence to cap independence, then the inhibition of protein synthesis does not require that reovirus induce an inhibition of host mRNA synthesis since all host mRNAs are capped. 

The basic properties of viral RNA which are used in the life cycle of the bacteriophage are the capabilities to act as template for replication as well as to be recognized as messenger RNA by the host translation system. In this contribution we shall be concerned mainly with replication because this process can be regarded as a simple version of Darwinian evolution. 

R = Repressor gene which is responsible for the shut-off of host translation... 

By cell-free enzyme synthesis, the host shut-off was analysed and two mechanisms distinguished Shut-off of host translation and inhibition of host messenger RNA synthesis. 

ScHWEiGER et al., 1972). And although lysozyme messenger shows almost no decay at all, in vivo lysozyme synthesis stops. Both, translational control of available messenger RNA and a differential change in the messenger decay rates seem to be involved. This control seems different from that responsible for the mechanism of shut-off of host translation. 

---