Viruses are submicroscopic, obligate intracellular parasites. This definition differentiates viruses from all other groups of living organisms. There exists more biological diversity within viruses than in all other known life-forms combined. This is the result of viruses successfully parasitizing all known groups of living organisms. Viruses have evolved in parallel with other species by capturing and using genes from infected host cells for functions that they require to produce their progeny, to enhance their escape from their host’s cells and immune system, and to survive the intracellular and extracellular environment. At the molecular level, the composition and structures of virus genomes are more varied than any others identified in the entire bacterial, botanical, or animal kingdoms. Unlike the genomes of all other cells composed of DNA, virus genomes may contain their genetic information encoded in either DNA or RNA. The nucleic acid comprising a virus genome may be single-stranded or double-stranded and may occur in a linear, circular, or segmented configuration.
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It must be understood that virus particles themselves do not grow or undergo division. Virus particles are produced from the assembling of pre-formed components, whereas other agents actually grow from an increase in the integrated sum of their components and reproduce by division. The reason is that viruses lack the genetic information that encodes the apparatus necessary for the generation of metabolic energy or for protein synthesis (ribosomes). The most critical interaction between a virus and a host cell is the need of the virus for the host’s cellular apparatus for nucleic acid and for the synthesis of proteins. No known virus has the biochemical or genetic potential to generate the energy necessary for producing all biological processes. Viruses depend totally on a host cell for this function.
Viruses are therefore not living in the traditional sense, but they nevertheless function as living things; they do replicate their own genes. Inside a host cell, viruses are “alive,” whereas outside the host they are merely a complex assemblage of metabolically inert chemicals—basically a protein shell. Therefore, while viruses have no inner metabolism and cannot reproduce on their own, they carry with them the means necessary to get into other cells and then use those cells’ own reproductive machinery to make copies of themselves. Viruses thrive at the host cells’ expense.
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The sole goal of a virus is to replicate its genetic information. The type of host cell infected by a virus has a direct effect on the process of replication. For viruses of prokaryotes (bacteria, primarily), reproduction reflects the physical simplicity of the host cell. For viruses with eukaryotic host cells (plants and animals), reproduction is more complex. The coding capacity of the genome forces the virus to choose a reproductive strategy. The strategy might involve near-total reliance on the host cell, resulting in a compact genome encoded for only a few essential proteins (+), or could involve a large, complex virus genome encoded with nearly all the information necessary for replication, relying on the host cell only for energy and ribosomes. Those viruses with an RNA genome plus messenger RNAs (mRNAs) have no need to enter the nucleus of their host cell, although during replication many often do. DNA genome viruses mostly replicate in the host cell’s nucleus, where host DNA is replicated and the biochemical apparatus required for this process is located. Some DNA viruses (poxviruses) have evolved to contain the biochemical capacity to replicate in their host’s cytoplasm, with a minimal need for the host cell’s other functions.
Virus replication involves several stages carried out by all types of viruses, including the onset of infection, replication, and release of mature virions from an infected host cell. The...
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Becker, Yechiel, and Gholamreza Darai, eds. Molecular Evolution of Viruses: Past and Present. Boston: Kluwer Academic, 2000. Detailed research of the evolution of viruses by acquisition of cellular RNA and DNA, and how virus genes evade the host immune responses.
Dimmock, N. J., A. J. Easton, and K. N. Leppard. Introduction to Modern Virology. 6th ed. Malden, Mass.: Blackwell, 2007. Part 2 of this textbook focuses on virus growth in cells, with information about the replication of viral DNA, genome replication in RNA viruses, and the replication of RNA viruses with a DNA intermediate and vice versa.
Domingo, Esteban, Colin R. Parrish, and John J. Holland, eds. Origin and Evolution of Viruses. 2d ed. Boston: Elsevier/Academic Press, 2008. An interdisciplinary reference book consisting of chapters authored by leading researchers in the fields of RNA and DNA viruses. Deals with the simplest, as well as the most complex, viral genomes known.
Holland, J. J., ed. Current Topics in Microbiology and Immunology: Genetic Diversity of RNA Viruses. New York: Springer-Verlag, 1992. Detailed collection of papers concerning the genetic and biological variabilities of RNA viruses, replicase error frequencies, the role of environmental selection pressures in the evolution of RNA populations, and the emergence of drug-resistant virus genomes.
Shors, Teri. Understanding Viruses....
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Microbial Genetics, Genetics of Viruses. http://student.ccbcmd.edu/courses/bio141/lecguide/unit6/Genetics/virus/virus.html. Gary Kaiser, a teacher at Community College of Baltimore County, includes a page on viral genetics in the site he created for his microbiology course.
Microbiology and Immunology On-Line, Virology. http://pathmicro.med.sc.edu/book/virol-sta.htm. The virology section of this site, which was created by the University of South Carolina School of Medicine, contains a page on viral genetics, pages on DNA and RNA virus replication strategies, and other information about viruses.
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Viral genetics, the study of the genetic mechanisms that operate during the life cycle of viruses, utilizes biophysical, biological, and genetic analyses to study the viral genome and its variation. The virus genome consists of only one type of nucleic acid, which could be a single or double stranded DNA or RNA. Single stranded RNA viruses could contain positive-sense (+RNA), which serves directly as mRNA or negative-sense RNA (NA) that must use an RNA polymerase to synthesize a complementary positive strand to serve as mRNA. Viruses are obligate parasites that are completely dependant on the host cell for the replication and transcription of their genomes as well as the translation of the mRNA transcripts into proteins. Viral proteins usually have a structural function, making up a shell around the genome, but may contain some enzymes that are necessary for the virus replication and life cycle in the host cell. Both bacterial virus (bacteriophages) and animal viruses play an important role as tools in molecular and cellular biology research.
Viruses are classified in two families depending on whether they have RNA or DNA genomes and whether these genomes are double or single stranded. Further subdivision into types takes into account whether the genome consists of a single RNA molecule or many molecules as in the case of segmented viruses. Four types of bacteriophages are widely used in biochemical and genetic research. These are the T phages, the temperate phages typified by bacteriophage lambda, the small DNA phages like M13, and the RNA phages. Animal viruses are subdivided in many classes and types. Class I viruses contain a single molecule of double stranded DNA and are exemplified by adenovirus, simian virus 40 (SV40), herpes viruses and human papilloma viruses. Class II viruses are also called parvoviruses and are made of single stranded DNA that is copied in to double stranded DNA before transcription in the host cell. Class III viruses are double stranded RNA viruses that have segmented genomes which means that they contain 102 separate double stranded RNA molecules. The negative strands serve as template for mRNA synthesis. Class IV viruses, typified by poliovirus, have single plus strand genomic RNA that serves as the mRNA. Class V viruses contain a single negative strand RNA which serves as the template for the production of mRNA by specific virus enzymes. Class VI viruses are also known as retroviruses and contain double stranded RNA genome. These viruses have an enzyme called reverse transcriptase that can both copy minus strand DNA from genomic RNA catalyze the synthesis of a complementary plus DNA strand. The resulting double stranded DNA is integrated in the host chromosome and is transcribed by the host own machinery. The resulting transcripts are either used to synthesize proteins or produce new viral particles. These new viruses are released by budding, usually without killing the host cell. Both HIV and HTLV viruses belong to this class of viruses.
Virus genetics are studied by either investigating genome mutations or exchange of genetic material during the life cycle of the virus. The frequency and types of genetic variations in the virus are influenced by the nature of the viral genome and its structure. Especially important are the type of the nucleic acid that influence the potential for the viral genome to integrate in the host, and the segmentation that influence exchange of genetic information through assortment and recombination.
Mutations in the virus genome could either occur spontaneously or be induced by physical and chemical means. Spontaneous mutations that arise naturally as a result of viral replication are either due to a defect in the genome replication machinery or to the incorporation of an analogous base instead of the normal one. Induced virus mutants are obtained by either using chemical mutants like nitrous oxide that acts directly on bases and modify them or by incorporating already modified bases in the virus genome by adding these bases as substrates during virus replication. Physical agents such as ultra-violet light and x rays can also be used in inducing mutations. Genotypically, the induced mutations are usually point mutations, deletions, and rarely insertions. The phenotype of the induced mutants is usually varied. Some mutants are conditional lethal mutants. These could differ from the wild type virus by being sensitive to high or low temperature. A low temperature mutant would for example grow at 88°F (31°C) but not at 100°F (38°C), while the wild type will grow at both temperatures. A mutant could also be obtained that grows better at elevated temperatures than the wild type virus. These mutants are called hot mutants and may be more dangerous for the host because fever, which usually slows the growth of wild type virus, is ineffective in controlling them. Other mutants that are usually generated are those that show drug resistance, enzyme deficiency, or an altered pathogenicity or host range. Some of these mutants cause milder symptoms compared to the parental virulent virus and usually have potential in vaccine development as exemplified by some types of influenza vaccines.
Besides mutation, new genetic variants of viruses also arise through exchange of genetic material by recombination and reassortment. Classical recombination involves the breaking of covalent bonds within the virus nucleic acid and exchange of some DNA segments followed by rejoining of the DNA break. This type of recombination is almost exclusively reserved to DNA viruses and retroviruses. RNA viruses that do not have a DNA phase rarely use this mechanism. Recombination usually enables a virus to pick up genetic material from similar viruses and even from unrelated viruses and the eukaryotic host cells. Exchange of genetic material with the host is especially common with retroviruses. Reassortment is a non-classical kind of recombination that occurs if two variants of a segmented virus infect the same cell. The resulting progeny virions may get some segments from one parent and some from the other. All known segmented virus that infect humans are RNA viruses. The process of reassortment is very efficient in the exchange of genetic material and is used in the generation of viral vaccines especially in the case of influenza live vaccines. The ability of viruses to exchange genetic information through recombination is the basis for virus-based vectors in recombinant DNA technology and hold great promises in the development of gene therapy. Viruses are attractive as vectors in gene therapy because they can be targeted to specific tissues in the organs that the virus usually infect and because viruses do not need special chemical reagents called transfectants that are used to target a plasmid vector to the genome of the host.
Genetic variants generated through mutations, recombination or reassortment could interact with each other if they infected the same host cell and prevent the appearance of any phenotype. This phenomenon, where each mutant provide the missing function of the other while both are still genotypically mutant, is known as complementation. It is used as an efficient tool to determine if mutations are in unique or in different genes and to reveal the minimum number of genes affecting a function. Temperature sensitive mutants that have the same mutation in the same gene will for example not be able to complement each other. It is important to distinguish complementation from multiplicity reactivation where a higher dose of inactivated mutants will be reactivated and infect a cell because these inactivated viruses cooperate in a poorly understood process. This reactivation probably involves both a complementation step that allows defective viruses to replicate and a recombination step resulting in new genotypes and sometimes regeneration of the wild type. The viruses that need complementation to achieve an infectious cycle are usually referred to as defective mutants and the complementing virus is the helper virus. In some cases, the defective virus may interfere with and reduce the infectivity of the helper virus by competing with it for some factors that are involved in the viral life cycle. These defective viruses called "defective interfering" are sometimes involved in modulating natural infections. Different wild type viruses that infect the same cell may exchange coat components without any exchange of genetic material. This phenomenon, known as phenotypic mixing is usually restricted to related viruses and may change both the morphology of the packaged virus and the tropism or tissue specificity of these infectious agents.
See also Viral vectors in gene therapy; Virology; Virus replication; Viruses and responses to viral infection