The study of viruses has historically provided and continues to provide the basis for much of our most fundamental understanding of modern biology, genetics, and medicine. Virology has had an impact on the study of biological macromolecules, processes of cellular gene expression, mechanisms for generating genetic diversity, processes involved in the control of cell growth and development, aspects of molecular evolution, the mechanism of disease and response of the host to it, and the spread of disease in populations. In essence, viruses are collections of genetic information directed toward one end: their own replication. They are the ultimate and prototypical example of “selfish genes.” The viral genome contains the “blueprints” for virus replication enciphered in the genetic code, and must be decoded by the molecular machinery of the cell that it infects to gain this end. Viruses are; thus, obligate intracellular parasites dependent on the metabolic and genetic functions of living cells.
Given the essential simplicity of virus organization – a genome containing genes dedicated to self replication surrounded by a protective protein shell – it has been argued that viruses are nonliving collections of biochemicals whose functions are derivative and separable from the cell. Yet this generalization does not stand up to the increasingly detailed information accumulating describing the nature of viral genes, the role of viral infections on evolutionary change, and the evolution of cellular function. A view of viruses as constituting a major subdivision of the biosphere as ancient as and fully interactive and integrated with the three great branches of cellular life becomes more strongly established with each investigational advance.
It is a major problem in the study of biology at a detailed molecular and functional level that almost no generalization is sacred, and the concept of viruses as simple parasitic collections of genes functioning to replicate themselves at the expense of the cell they attack does not hold up. Many generalizations will be made in the survey of the world of viruses introduced in this book, most if not all will be ultimately classified as being useful, but unreliable tools for the full understanding and organization of information. Even the size range of viral genomes, generalized to range from one or two genes to a few hundred at most (significantly less than those contained in the simplest free living cells), cannot be supported by a close analysis of data. While it is true that the vast majority of viruses studied range in size from smaller than the smallest organelle to just smaller than the simplest cells capable of energy metabolism and protein synthesis, the mycoplasma and simple unicellular algae, the recently discovered Mimivirus (distantly related to poxviruses such as smallpox or variola) contains nearly 1000 genes and is significantly larger than the smallest cells. With such caveats in mind it is still appropriate to note that despite their limited size, viruses have evolved and appropriated a means of propagation and replication that ensures their survival in freeliving organisms that are generally between 10 and 10,000,000 times their size and genetic complexity.
The effect of virus infections on the host organism and populations –viral pathogenesis, virulence, and epidemiology:-
Since a major motivating factor for the study of virology is that viruses cause disease of varying levels of severity in human populations and in the populations of plants and animals which support such populations, it is not particularly surprising that virus infections have historically been considered episodic interruptions of the well being of a normally healthy host. This view was supported in some of the earliest studies on bacterial viruses, which were seen to cause the destruction of the host cell and general disruption of healthy, growing populations of the host bacteria. Despite this, it was seen with another type of bacterial virus that a persistent, lysogenic, infection could ensue in the host population. In this case, stress to the lysogenic bacteria could release infectious virus long after the establishment of the initial infection. These two modes of infection of host populations by viruses, which can be accurately modeled by mathematical methods developed for studying predator–prey relationships in animal and plant populations, are now understood to be general for virus–host interactions. ndeed, persistent infections with low or no levels of viral disease are universal in virus–host ecosystems that have evolved together for extended periods – it is only upon the introduction of a virus into a novel population that widespread disease and host morbidity occurs. While we can, thus, consider severe virus-induced disease to be evidence of a recent introduction of the virus into the population in question, the accommodation of the one to the other is a very slow process requiring genetic changes in both virus and host, and it is by no means certain that the accommodation can occur without severe disruption of the host population – even its extinction. For this reason, the study of the replication and propagation of a given virus in a population is of critical importance to the body politic, especially in terms of formulating and implementing health policy. This is, of course, in addition to its importance to the scientific and medical communities. The study of effects of viral infection on the host is broadly defined as the study of viral pathogenesis. The sum total of the virus-encoded functions that contribute to virus propagation in the infected cell, in the host organism, and in the population is defined as pathogenicity of that virus. This term essentially describes the genetic ability of members of a given specific virus population (which can be considered to be genetically more or less equivalent) to cause a disease and spread through (propagate in) a population. Thus, a major factor in the pathogenicity of a given virus is its genetic makeup or genotype. The basis for severity of the symptoms of a viral disease in an organism or a population is complex. It results from an intricate combination of expression of the viral genes controlling pathogenicity, physiological response of the infected individual to these pathogenic determinants, and response of the population to the presence of the virus propagating in it. Taken together, these factors determine or define the virulence of the virus and the disease it causes.