It is with those thoughts etched into our memories that we dedicate this edition of Basic Virology to Edward K. Wagner. Basic Virology Third Edition Edward K. Basic Virology, 3rd Edition Downloadable artwork, original animations and online resources are available at wm-greece.info Edward K. Wagner - Goodreads Basic Virology Wagner 3rd Edition PDF Download virology, 3rd edition pdf free download, basic virology in.
|Language:||English, Spanish, Indonesian|
|Distribution:||Free* [*Sign up for free]|
Edition/Format: Print book: English: 3rd edView all editions and formats Notes: Revised edition of: Basic virology / Edward K. Wagner, Martinez J. Hewlett. You should truly to review the book Basic Virology 3rd Edition Pdf because you will basic virology, third edition by wagner, hewlett, bloom. basic virology, third edition by wagner, hewlett, bloom and camerini answers to edition third ed 3e by edward wagner pdf or read basic.
Barnaviruses Barnaviridae. BF23 phage See T5-like phage and related phages. Birnaviruses - animal Birnaviridae. Border disease virus See Bovine diarrhea virus and Border disease virus. Borna disease virus Bornaviridae. Bovine diarrhea virus and border disease virus flaviviridae.
Bovine herpesvirus Herpesviridae. Bovine immunodeficiency virus Retroviridae. Bovine lukemia virus Retroviridae. Bovine parvovirus See Parvoviruses - rodents, pigs, cattle and waterfowl. Bovine spongiform encephalopathy See Prions.
Bromoviruses Bromaviridae. Bunyaviruses Bunyaviridae. Caliciviruses Caliciviridae. Canine distemper virus See Rinderpest and canine distemper viruses. Canine parvoviruses See Parvoviruses. Caprine arthritis encephalitis virus. Csardioviruses Picornaviridae. Carmoviruses Tombusviridae. Cell structure and function in virus infections. Central European encephalitis virus See Encephalitis viruses. Chandipura, Piry and Isfahan viruses Rhabdoviridae. Channel catfish virus See Fish herpesviruses.
Chicken herpesvirus See Marek's disease virus. Chickenpox virus See Varicella-zoster virus. Chikungunya, O'nyong nyong and Mayaro viruses Togaviridae. Chilo iridescent virus See Tipula iridescent virus. Chimpanzee herpesvirus See Herpesvirus - baboon and chimanzee. Chlorella virus See Algal viruses. Closteroviruses Closteroviridae. Coltiviruses See Orbiviruses and coltiviruses.
Coliphage lambda Siphoviridae. Comoviruses Comoviridae. Coronaviruses Coronaviridae. Cowpox virus Poxviridae. Coxsackieviruses Picornaviridae. Creutzfeld-Jakob disease See Prions. Cricket paralysis virus See Picornaviruses - insect. Cryptoviruses Partitiviridae. Cucumoviruses Bromoviridae. Cypoviruses Reoviridae.
Cytokines and chemokines. Cytomegaloviruses Herpesviridae. Defective interfering viruses. Dengue viruses Flaviviridae. Densonucleosis viruses Parvoviridae. Diagnostic techniques. Dianthoviruses Tombusviridae. Drosophila C virus See Picornaviruses - insect. Eastern equine encephalitis virus See Equine encephalitis viruses.
Ebola virus See Marburg and Ebola viruses. Many people contributed to the physical process of putting this book together. Spaete of the Aviron Corp carefully read every page of the manuscript and suggested many important minor and a couple of major changes. This was done purely in the spirit of friendship and collegiality.
Christensen used her considerable expertise and incredible skill in working with us to generate the art. Not only did she do the drawings, but also she researched many of them to help provide missing details. Two undergraduates were invaluable to us. Finally, J.
Wagner carried out the very difficult task of copyediting the manuscript. A number of people at Blackwell Publishing represented by Publisher N. Hill-Whilton demonstrated a commitment to a quality product. We especially thank Elizabeth Frank, Caroline Milton, and Rosie Hayden who made great efforts to maintain effective communications and to expedite many of the very tedious aspects of this project. All of these colleagues and friends represent the background of assistance we have received, leading to the preparation of this third edition.
We would especially like to acknowledge Dr.
Luis Villareal and the Center for Virus Research at the University of California, Irvine, for supporting our efforts in bringing this book to a timely completion. 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. 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.
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 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,, 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.
Indeed, 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. 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. A basic factor contributing to virulence is the interaction among specific viral genes and the genetically encoded defenses of the infected individual. It is important to understand, however, that virulence is also affected by the general health and genetic makeup of the infected population, and in humans, by the societal and economic factors that affect the nature and extent of the response to the infection.
The distinction and gradation of meanings between the terms pathogenesis and virulence can be understood by considering the manifold factors involved in disease severity and spread exhibited in a human population subjected to infection with a disease-causing virus.
Consider a virus whose genotype makes it highly efficient in causing a disease, the symptoms of which are important in the spread between individuals — perhaps a respiratory infection with accompanying sneezing, coughing, and so on. This ideal or optimal virus will incorporate numerous, random genetic changes during its replication cycles as it spreads in an individual and in the population. Some viruses generated during the course of a disease may, then, contain genes that are not optimally efficient in causing symptoms.
Such a virus is of reduced virulence, and in the extreme case, it might be a virus that has accumulated so many mutations in pathogenic genes that it can cause no disease at all i. While an avirulent virus may not cause a disease, its infection may well lead to complete or partial immunity against the most virulent genotypes in an infected individual. This is the basis of vaccination, which is described in Chapter 8, Part II.
But the capacity to generate an immune response and the resulting generation of herd immunity also means that as a virus infection proceeds in a population, its virulence either must change or the virus must genetically adapt to the changing host.
Other factors not fully correlated with the genetic makeup of a virus also contribute to variations in virulence of a pathogenic genotype. The same virus genotype infecting two immunologically naive individuals i.
One individual might only have the mildest symptoms because of exposure to a small amount of virus, or infection via a suboptimal route, or a robust set of immune and other defense factors inherent in his or her genetic makeup. Another individual might have a very severe set of symptoms or even death if he or she receives a large inoculum, or has impaired immune defenses, or happens to be physically stressed due to malnutrition or other diseases.
Also, the same virus genotype might cause significantly different levels of disease within two more or less genetically equivalent populations that differ in economic and technological resources. Taken in whole, the study of human infectious disease caused by viruses and other pathogens defines the field of epidemiology in animals it is termed epizoology.
The interaction between viruses and their hosts The interaction between viruses and other infectious agents and their hosts is a dynamic one. As effective physiological responses to infectious disease have evolved in the organism and more recently have developed in society through application of biomedical research, viruses themselves respond by exploiting their naturally occurring genetic variation to accumulate and select mutations to become wholly or partially resistant to these responses.
In extreme cases, such resistance will lead to periodic or episodic reemergence of a previously controlled disease — the most obvious example of this process is the periodic appearance of human influenza viruses caused disease.
Evidence of this is the ongoing acquired immune deficiency syndrome AIDS epidemic, as well as sporadic occurrences of viral diseases, such as hemorrhagic fevers in Asia, Africa, and southwestern United States. Investigation of the course of a viral disease, as well as societal responses to it, provides a ready means to study the role of social policies and social behavior of disease in general.
The recent worldwide spread of AIDS is an excellent example of the role played by economic factors and other aspects of human behavior in the origin of a disease. There is strong evidence to support the view that the causative agent, human immunodeficiency virus HIV , was introduced into the human population by an event fostered by agricultural encroachment of animal habitats in equatorial Africa.
This is an example of how economic need has accentuated risk. HIV is not an efficient pathogen; it requires direct inoculation of infected blood or body fluids for spread. In the Euro-American world, the urban concentration of homosexual males with sexual habits favoring a high risk for venereal disease had a major role in spreading HIV and resulting in AIDS throughout the male homosexual community. A partial overlap of this population with intravenous drug users and participants in the commercial sex industry resulted in spread of the virus and disease to other portions of urban populations.
The result is that in Western Europe and North America, AIDS has been a double-edged sword threatening two disparate urban populations: the relatively affluent homosexual community and the impoverished heterosexual world of drug abusers — both highly concentrated urban populations. In the latter population, the use of commercial sex as a way of obtaining money resulted in further spread to other heterosexual communities, especially those of young, single men and women.
This led to the sudden appearance of AIDS in hemophiliacs and sporadically in recipients of massive transfusions due to intensive surgery. Luckily, the incidence of disease in these last risk populations has been reduced owing to effective measures for screening blood products.
In these areas of the world, the disease is almost exclusively found in heterosexual populations.
The periodic travel by men to their isolated village homes resulted in the virus being found with increasing frequency in isolated family units.
Further spread resulted from infected women leaving brothels and prostitution to return to their villages to take up family life. Another overweening factor in the spread of AIDS is technology. HIV could not have spread and posed the threat it now does in the world of a century ago.
Generally lower population densities and lower concentrations of individuals at risk at that time would have precluded HIV from gaining a foothold in the population. Slower rates of communication and much more restricted travel and migration would have precluded rapid spread; also the transmission of blood and blood products as therapeutic tools was unknown a century ago.
Of course, this dynamic interaction between pathogen and host is not confined to viruses; any pathogen exhibits it. The study and characterization of the genetic accommodations viruses make, both to natural resistance generated in a population of susceptible hosts and to humandirected efforts at controlling the spread of viral disease, provide much insight into evolutionary processes and population dynamics. Indeed, many of the methodologies developed for the study of interactions between organisms and their environment can be applied to the interaction between pathogen and host.
The history of virology The historic reason for the discovery and characterization of viruses, and a continuing major reason for their detailed study, involves the desire to understand and control the diseases and attending degrees of economic and individual distress caused by them.
As studies progressed, it became clear that there were many other important reasons for the study of viruses and their replication. Since viruses are parasitic on the molecular processes of gene expression and its regulation in the host cell, an understanding of viral genomes and virus replication provides basic information concerning cellular processes in general.
The bacterial viruses bacteriophage were discovered through their ability to destroy human enteric bacteria such as Escherichia coli, but they had no clear relevance to human disease. It is only in retrospect that the grand unity of biological processes from the most simple to the most complex can be seen as mirrored in replication of viruses and the cells they infect.
The biological insights offered by the study of viruses have led to important developments in biomedical technology and promise to lead to even more dramatic developments and tools. For example, when infecting an individual, viruses target specific tissues. The resulting specific symptoms, as already noted, define their pathogenicity.
The normal human, like all vertebrates, can mount a defined and profound response to virus infections. This response often leads to partial or complete immunity to reinfection. The study of these processes was instrumental to gaining an increasingly clear understanding of the immune response and the precise molecular nature of cell—cell signaling pathways.
It also provided therapeutic and preventive strategies against specific virus-caused disease. The study of virology has and will continue to provide strategies for the palliative treatment of metabolic and genetic diseases not only in humans, but also in other economically and aesthetically important animal and plant populations.
There are also somewhat imperfect historical records of viral disease affecting human populations in classical and medieval times. While the recent campaign to eradicate smallpox has been successful and it no longer exists in the human population owing to the effectiveness of vaccines against it, the genetic stability of the virus, and a well-orchestrated political and social effort to carry out the eradication , the disease periodically wreaked havoc and had profound effects on human history over thousands of years.
Smallpox epidemics during the Middle Ages and later in Europe resulted in significant population losses as well as major changes in the economic, religious, political, and social life of individuals.
Although the effectiveness of vaccination strategies gradually led to decline of the disease in Europe and North America, smallpox continued to cause massive mortality and disruption in other parts of the world until after World War II. Despite its being eradicated from the environment, the attack of September 11, on the World Trade Center in New York has lead some government officials to be concerned that the high virulence of the virus and its mode of spread might make it an attractive agent for bioterrorism.
Other virus-mediated epidemics had equally major roles in human history. Much of the social, economic, and political chaos in native populations resulting from European conquests and expansion from the fifteenth through nineteenth centuries was mediated by introduction of infectious viral diseases such as measles. Significant fractions of the indigenous population of the western hemisphere died as a result of these diseases. Potential for major social and political disruption of everyday life continues to this day.
Remarkable medical detective work using virus isolated from cadavers of victims of this disease frozen in Alaskan permafrost has lead to recovery of the complete genomic sequence of the virus and reconstruction of the virus itself some of the methods used will be outlined in Part V.
While we may never know all the factors that caused it to be so deadly, it is clear that the virus was derived from birds passing it directly to humans.
Further, a number of viral proteins have a role in its virulence. At the present time, human transmission of H5N1 influenza has not been confirmed, but further adaptation of this new virus to humans could lead to its establishing itself as a major killer in the near future.
A number of infectious diseases could become established in the general population as a consequence of their becoming drug resistant, human disruption of natural ecosystems, or introduced as weapons of bioterrorism.
As will be discussed in later chapters, a number of different viruses exhibiting different details of replication and spread could, potentially, be causative agents of such diseases.
Animal and plant pathogens are other potential sources of disruptive viral infections. Sporadic outbreaks of viral disease in domestic animals, for example, vesicular stomatitis virus in cattle and avian influenza in chickens, result in significant economic and personal losses.
Rabies in wild animal populations in the eastern United States has spread continually during the past half-century. The presence of this disease poses real threats to domestic animals and through them occasionally, to humans. The loss of coconut palms led to serious financial hardship in local populations. Examples of the evolutionary impact of the virus—host interaction There is ample genetic evidence that the interaction between viruses and their hosts had a measurable impact on evolution of the host.
Viruses provide environmental stresses to which organisms evolve responses. The genomes of viruses encode proteins which are essential for their structural components and replication of their genomes. Viruses do not produce energy through metabolism of small oxidizable molecules. In addition, genes for enzymes involved in energy metabolism are completely absent from viral genomes.
Viroids and prions 4. Like other parasites, viruses need their hosts for replication. A deadly virus may destroy its host before it can be spread, thus losing the opportunity to survive. Viruses can be a selective pressure for adaptation in cells and organisms that make them resistant to infection by viruses.
Moreover, viruses can be vectors of gene transfer from cell to cell or organism to organism.