Effect of viruses

Incubate at least four series, cells with three or more different concentrations of the preparation to be examined and the reference preparation in a microtitre plate and include in each series appropriate controls of untreated cells. Choose the concentrations of the preparations such that the lowest concentration produces some protection and the largest concentration produces less than maximal protection against the viral cytopathic effect. At a suitable time add the cytopathic virus to the wells with the exception of a sulScient number of wells in ah series, which are left with uninfected control cells. Determine the cytopathic effect of virus quantitatively with a suitable method. Calculate the potency of the preparation to be examined by the usual statistical methods for a parallel line assay. 

Middelboe, M., N. O. G. Jorgensen, and N. Kroer. 1996. Effects of viruses on nutrient turnover and growth efficiency of noninfected marine bacterioplankton. Applied and Environmental Microbiology 62 1991-1997. 

Weinbauer, M. G., and Peduzzi, P. (1995). Effect of virus-rich high molecular weight concentrates of seawater on the dynamics of dissolved amino acids and carbohydrates. Mar. Ecol. Prog. Ser. 127, 245-253. 

Hewson, 1., Vargo, G. A., and Fuhrman, J. A. (2003). Bacterial diversity in shallow ohgotrophic marine benthos and overlying waters Effects of virus infection, containment and nutrient enrichment. Microb. Ecol. 46, 322—336. 

Effects of Virus Characteristics on Adsorption. We noted previously that enteroviruses are quite consistent in regard to general shape and size, about 27 nm in diameter (6), and that they (i) are thought to represent the most significant category of viruses in regard to waterborne virus transmission. However, in some cases viruses that could be possible environmental hazards, for example, adenoviruses—70 to 80 nm in diameter (6) and rotaviruses—60 to 70 nm in diameter (59,60), are obviously larger in size. 

The effects of virus infection with the TrD strain of VEE on the CNS also demonstrated considerable species variability. Mice exhibited a severe paralytic episode prior to death from diffuse encephalomyelitis.89,90 Monkeys, however, showed few if any clinical signs of CNS involvement following peripheral inoculation, and only modest pathological changes in the CNS (found mainly in the thalamus, hypothalamus, and olfactory areas of the brain).90 However, the extent of neuroinvasion in animals is also a function of both the strain of VEE and the route of infection. Cynomolgus monkeys infected by the intranasal route developed immunoglobulin (Ig) M and IgG antibodies in the cerebrospinal... 

Cohen, M. M., and Shaw, M. W. (1965), The specific effects of viruses and antimetabolites on mammalian chromosomes, in "In Vitro The Chromosome Structural and Functional Aspects" (C. Dawe, ed.), Waverly Press, Maryland. 

Modern drugs which counteract the effects of viruses are usually called anti-virals but these have not yet proved to be as successful as have antibiotics when used against bacterial infections. 

Although the effect of virus infection on cellular RNA and DNA synthesis will be considered, this review will be concerned primarily with the inhibition of cellular protein synthesis. Several reviews on virus-induced changes in the synthesis of macromolecules have been written in the past few years (1,2,5,4)5 and thus the reference list is selective rather than exhaustive. This review will consist of three parts the first will be concerned with the properties of the shut-off phenomenon. The second part will deal with theories that have been proposed to explain shut-off. 

In 1961, Hampar and Ellison reported chromosomal alterations in Chinese hamster culture cells [181] infected with herpesvirus, and Nichols [182, 183] demonstrated an abnormal incidence of chromosome breaks in cultured leukocytes obtained from children with measles. Since then the list of publications on the effect of viruses on chromosomes has grown into an innumerable bibliography, and chromosomal anomalies have been described after infection with rubella, mumps, chicken pox, and even after vaccination for smallpox or yellow fever. 

Studies of the role of viruses in chromosomal anomalies are of two types the studies in which the infection takes place in vivo and the infected cells, usually leukocytes, are cultured in vitro to study chromosomal anomalies [184-187] and studies in which the effect of viruses on the mammalian karyotype has been investigated in vitro using either primary cell cultures or cell lines (cells capable of indefinite division—in humans, at least 70 consecutive divisions with 3-day intervals between cell subculture). When primary cell cultures are used (cells freshly derived from a living organism), usually lymphocytes stimulated with phytohemagglutinin are infected with the virus. Since only one cell division can be observed in primary cell cultures, established cell lines, such as HeLa cells, would seem to be preferable for studying the effect of viruses on the karyotype. But these cultures are heteropioid, and therefore most cell lines are inadequate for chromosomal studies. Fortunately, diploid cell lines are now available. 

Conclusive studies on the effect of viruses on the karyotype must of course be conducted in a system in which spontaneous alterations of the karyotype do not occur and no other agents capable of inducing chromosomal alterations are present. 

Shapiro, M. Farrar, Jr, R. R. Domek, J. Javaid, I. Effects of virus concentration and ultraviolet irradiation on the activity of com earworm and beet armyworm (Lepidoptera Noctuidae) nucleopolyhedrovirases. J. Econ. Enrowo/. 2002.95.243-249. 

In quite a different approach to the effect of viruses on cell membrane, Levanon et al. (1977) reported that adsorption of encephal-omyocarditis, Semliki Forest, and polyoma viruses to BHK-21 and mouse 3T3 cells resulted in a rapid increase in membrane fluidity as measured by depolarization of the fluorescent dye, diphenylhexa-triene. The degree of fluidity increase was virus dose dependent and could be reversed by low temperature or by blocking virus receptors on the host cell surface. These investigators suggest that an increase in membrane fluidity is an early event in viral cytopathogen-icity. 

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