Virus-host systems

J he abundance of organic materials that occur in the plant kingdom offer an opportunity for searching for specific compounds interfering with virus replication in plants. It is hoped that such compounds, if discovered, could be used efficiently for virus control and also serve as tools for our understanding of the complex virus-host system. 

The precise sequence of events resulting from the infection of a cell by a virus will vaiy with different virus-host systems, but they will be variations of four basic themes. 

Controls of gene expression have been observed though not elucidated in several archaeal virus host systems [136,137],... 

Both of these ideas have their attractions, but they seem unable to account for all virus-host systems, particularly those in which the reduction in host cell protein synthesis occurs soon after infection. The increased permeability of the membrane to monovalent cations is generally thought to occur too late in the infection, and the out-competition by viral mRNA can only cause a significant reduction in host cell protein synthesis when viral mRNA has been produced in sufficient amounts to suppress initiation on host mRNA. As a total explanation, the competition hypothesis seems limited to those systems where the overall rate of protein synthesis remains relatively constant after infection, the rate of host protein synthesis declining progressively as the rate of viral protein synthesis increases. It cannot, for instance, explain the rapid reduction in host protein synthesis which occurs shortly after... 

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. 

The phenomenon of protein synthesis inhibition in VSV-infected cells has been well described for various other virus-host systems. The characteristics of inhibition appear to depend in part on the host cell studied and on the multiplicity of infection. From pulse-labeling experiments, Mudd and Summera (1970) reported a 90% inhibition of total protein synthesis at 4 hr postinfection in HeLa cells by the Indiana serotype of VSV. These studies were done on HeLa cells grown in suspension infected at a multiplicity of infection of 85. Only a 40%... 

The design of chimeric viruses to create a functional vector system combining components of different viruses and thus expanding the virus host range was one of the early approaches employed by Yusibov et al. [32]. Antigenic determinants from... 

To date viruses have been isolated and brought into culture for the bloom-forming species P. pouchetii and P. globosa. The genus includes, however, more species of which only one other is known to form a colony bloom (P. antarctica). Given the dependence of viral induced algal mortality on virus and host cell abundance, it would be of special interest to be able to bring into culture virus-host model systems of species that do not form such dense blooms and compare with... 

Influenza virus host resistance model to test the overall health of the immune system ... 

Adsorption of enteric viruses on mineral surfaces in soil and aquatic environments is well recognized as an important mechanism controlling virus dissemination in natural systems. The adsorption of poliovirus type 1, strain LSc2ab, on oxide surfaces was studied from the standpoint of equilibrium thermodynamics. Mass-action free energies are found to agree with potentials evaluated from the DLVO-Lifshitz theory of colloid stability, the sum of electrodynamic van der Waals potentials and electrostatic double-layer interactions. The effects of pH and ionic strength as well as electrokinetic and dielectric properties of system components are developed from the model in the context of virus adsorption in extra-host systems. 

The use of experimental animals in testing the activity of chemical germicides in general against viruses is considered neither necessary nor desirable [21]. Established and well-characterized cell lines are the recommended host system. In some cases, such as when working with adenoviruses [22], it is advisable to carry two cell lines one for the preparation of virus pools and the other to assay for its infectivity. The use of embryonated eggs may be needed in rare cases, such as for the production of high-titered pools for influenza viruses. 

In working with chemical germicides, an accurate measure of the degree of loss in virus infectivity is essential. Therefore, assay systems that detect and/or measure the presence of viral proteins, nucleic acids, or enzymes without determining viral infectivity are considered unsuitable [21]. It must also be remembered here that no matter what host system is used, inability to detect infectious virus particles in it does not necessarily mean the complete absence of infectivity for the natural host. 

Any good test for vimcidal activity must incorporate a measurement of infectivity of the challenge vims. This is essential to determine the level of loss in viral infectivity for the host system used. In many tests for virucidal activity, only very small fractions (often only 1-10%) of the test sample eluates are titrated for infectious vims, and the absence of infectivity in the host system may be taken as evidence of the formulation s effectiveness. The limit of detection for the assay system is rarely quoted, but when no infectious virus is detected, the results should be quoted as less than the theoretical detection limit. For a higher level of confidence in the results, it is desirable to titrate most or all of the test sample eluates. In order to save time and materials, ultrafiltration can be used to reduce the volume of the eluates using filters that allow very little protein binding. 

Both rodent CM Vs provide useful systems to analyse virus-host interactions and hence to discern the role of immune-evasive proteins encoded by their genomes. In the case of MCMV, a wealth of knowledge concerning the importance of host genetic factors and dissection of various compartments of the immune response in... 

In this chapter, we will explore the importance of proteomics in studying virus-host interactions in several viral systems including HCMV, KSHV, EBV, HSV, HIV-1, HTLV-1, and HCV. We will also describe the methods that have been employed to study viral disease progression using several techniques including 2DE, LC-MS/MS, SELDI, and protein microarrays. 

One question that deserves attention is the fact that, at least in the case of some virus-cell systems, viral RNA translation is inhibited preferentially over host mRNA translation, for example, in reovirus-infected L cells (Gupta et al., 1974). An interesting possibility was raised by Nilsen and Baglioni (1979). They showed that, in extracts of interferon-treated cells, VSV mRNA hybridized with poly (U) at its poly (A) tail or EMC RNA hybridized with poly (I) at its poly (C) tract are more rapidly degraded than the corresponding control mRNAs. They proposed that, in infected, interferon-treated cells, activation of the endoribonuclease takes place near the replicative intermediate of RNA viruses, because the dsRNA moiety therein promotes the formation of (2 -5 )oligo (A) in its vicinity. As a result, the viral mRNA portion in the replicative intermediate may be more sensitive to degradation than host mRNA. 

Herpesvirus-induced inhibition of host protein synthesis has been primarily associated to a viral component which is either synthesized during the replication of herpesvirus type 1 (Stenberg and Pizer, 1982 Hill et al., 1983) or is a component of the parental herpesvirus type 2 (Fenwick and Walker, 1978). In addition, herpesvirus type 1 causes the degradation of host cell mRNA (Nishioka and Sil-verstein, 1978 Inglis, 1982 Stenberg and Pizer, 1982). All the three virus-cell systems mentioned above also cause inhibition of host RNA and DNA synthesis during virus replication which may contribute to shut-off. 

The viral products most commonly implicated in shut-off in many virus-cell systems have been structural components of the virus particles. Structural components of adenovirus (Pereira, 1960), frog virus-3 (Maes and Granoff, 1967), vesicular stomatitis virus (Baxt and Bablanian, 1976), herpesvirus type 1 (Fenwick and Walker, 1978), and vaccinia virus (Moss, 1968) have been implicated as the agents responsible for inhibition of host protein synthesis. 

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