The Nature of Viruses

Viruses are sub-cellular agents of infection that must utilize the cellular machinery of bacteria, plants or animals in order to reproduce. Composed of a single strand of genetic material (DNA or RNA) encased in a protein capsid, a virus is too small to be seen by standard light microscopy; indeed, most are less than one hundredth the size of a bacterium. Specific proteins on the viral capsid attach to receptors on the host cell; this attachment process is essential to viral infectivity and explains why viruses may only infect the cells of certain species or may only infect certain cells or tissues within a given host species.

While the infecting virus triggers an immune response in the host, some are capable of suppressing that response by infecting and killing cells that control immunity (e. g. HIV attacks lymphocytes). In addition, while most infected cells are destroyed by viral replication, some viruses enter a latent phase within cells, reactivating in the future to produce chronic or relapsing infections.

Many viruses use specific carriers (known as vectors) such as mosquitoes, ticks, bats and rodents that transmit the virus to a susceptible host while others are spread between individuals via blood contact or through respiratory, intestinal or sexual secretions. Of special concern is the fact that mutations within the viral genome may allow viruses to skip from one host (e. g. birds, swine, monkeys) to another (e. g. humans), unleashing pandemics.

Many common human infections are produced by viruses; these include the common cold, influenza, mononucleosis, herpes infections (including shingles), viral hepatitis (A, B, C and others), HIV, viral gastroenteritis, conjunctivitis, viral pneumonia, encephalitis, viral meningitis and viral infections of the heart, including pericarditis and myocarditis. While viruses do not respond to antibiotics, specific antiviral agents may control (though not cure) chronic disease (such as HIV, Hepatitis B and Hepatitis C) or may modify the severity of acute infection (as in influenza and herpes infections).

However, in most viral infections, treatment is, for now, purely symptomatic and supportive. On the other hand, vaccines are capable of preventing some viral infections (e. g. herpes simplex, measles, mumps, rubella, varicella, Hepatitis B) or reducing the severity of an acute infection (e. g. influenza). Beyond the acute or chronic illness that they produce, some viral infections (such and Hepatitis C and certain strains of herpes simplex) are known to be precursors of malignancy. Finally, many researchers suspect that viruses play a role in the pathogenesis of chronic illnesses such as multiple sclerosis and autoimmune disorders. ttp://naturesblog. blogspot. com/2013/01/the-nature-of-viruses. html The Nature of Viruses Viruses exist in two different states, the extracellular infectious particle or virion and the intracellular state consisting of viral nucleic acid. The capsid may be a polyhedron or a helix, or a combination of both (in some phages). Viruses are infective micro¬organisms that show several differences from typical microbial cells. 1. Size. The size range of viruses is from about 20 to 300 nm. On the whole, viruses are much smaller than bacteria.

Most animal viruses and all plant viruses and phages are invisible under the light microscope. 2. Simple structure. Viruses have very simple structures. The simplest viruses are nucleoprotein particles consisting of genetic material (DNA or RNA) surrounded by a protein capsid. In this respect they differ from typical cells which arc made up) of proteins, carbohydrates, lipids and nuc1eicacids. The more complex viruses contain lipids and carbohydrates in addition to proteins and nucleic acids, e. g. the enveloped viruses 3. Absence of cellular structure.

Viruses do not have any cytoplasm, and thus cytoplasmic organelles like mitochondria, Golgi complexes, lysosomes, ribosomes, etc. , are absent. They do not have any limiting cell membrane. They utilize the ribosomes of the host cell for protein synthesis during reproduction. 4. No independent metabolism. Viruses cannot multiply outside a living cell. No virus has been cultivated in a cell-free medium. Viruses do not have an independent metabolism. They are metabo¬lically inactive outside the host cell because they do not posses enzyme systems and protein synthesis machinery.

Viral nucleic acid replicates by utilizing the protein synthesis machinery of the host. It codes for the synthesis of a limited number of viral proteins, including the subunits or capsomeres of the capsid, the tail protein and some enzymes concerned Viruses have only one nucleic acid, either DNA or RNA. Typical cells have both DNA and RNA. Genomes of certain with the synthesis or the release of virions. 5. Nucleic acids. RNA viruses can be transcribed into complementary DNA strands in the infected host cells, e. g. Rous Sarcoma Virus (RSV).

Such RNA viruses are therefore also called RNA-DNA viruses. 6. Crystallization. Many of the smaller viruses can be crystallized, and thus behave like chemicals. 7. No growth and division. Viruses do not have the power of growth and division. A fully formed virus does not increase in, size by addition of new molecules. The virus itself cannot divide. Only its genetic material (RNA or DNA) is capable of reproduction and that too only in a host cell. It will thus be seen that viruses do not show all the characteris¬tics of typical living organisms.

They, however, possess two funda¬mental characteristics of living systems. Firstly, they contain nucleic acid as their genetic material. The nucleic acid contains instructions for the structure and function of the virus. Secondly, they can reproduce themselves, even if only by using the host cells synthesis machinery. Viral genomes The nucleic acid comprising the genome may be single-stranded or double-stranded, & in a linear, circular or segmented configuration. Single-stranded virus genomes may be: • positive (+)sense, i. e. of the same polarity (nucleotide sequence) as mRNA • negative (-)sense Ambisense – a mixture of the two. N/B. Virus genomes range in size from approximately 3,200 nucleotides (nt) to approximately 1. 2 million base pairs Unlike the genomes of all cells, which are composed of DNA, virus genomes may contain their genetic information encoded in either DNA or RNA. Since viruses are obligate intracellular parasites only able to replicate inside the appropriate host cells, the genome must contain information encoded in a form which can be recognized & decoded by the particular type of cell parasitized.

Thus, the genetic code employed by the virus must match or at least be recognized by the host organism. Similarly, the control signals which direct the expression of virus genes must be appropriate to the host. Many of the DNA viruses of eukaryotes closely resemble their host cells in terms of the biology of their genomes: Some DNA virus genomes are complexed with cellular histones to form a chromatin-like structure inside the virus particle. http://expertscolumn. com/content/nature-viruses http://www. mcb. uct. ac. za/tutorial/virorig. html Viral evolution

Viral evolution is a subfield of evolutionary biology and virology that is specifically concerned with the evolution of viruses. Many viruses, in particular RNA viruses, have short generation times and relatively high mutation rates (on the order of one point mutation or more per genome per round of replication for RNA viruses). This elevated mutation rate, when combined with natural selection, allows viruses to quickly adapt to changes in their host environment. Viral evolution is an important aspect of the epidemiology of viral diseases such as influenza (influenza virus), AIDS (HIV), and hepatitis (e. . HCV). It also causes problems in the development of successful vaccines and antiviral drugs, as resistant mutations often appear within weeks or months after the beginning of the treatment.

One of the main theoretical models to study viral evolution is the quasispecies model, as the viral quasispecies. | Origins Viruses are ancient. Studies at the molecular level have revealed relationships between viruses infecting organisms from each of the three domains of life, and viral proteins that pre-date the divergence of life and thus the last universal common ancestor. 1] This indicates that viruses emerged early in the evolution of life and existed before modern cells. [2] There are three classical hypotheses on the origins of viruses: Viruses may have once been small cells that parasitised larger cells (the degeneracy hypothesis[3][4] or reduction hypothesis[5]); some viruses may have evolved from bits of DNA or RNA that “escaped” from the genes of a larger organism (the vagrancy hypothesis[6] or escape hypothesis); or viruses could have evolved from complex molecules of protein and nucleic acid at the same time as cells first appeared on earth (the virus-first hypothesis). 5]

None of these hypotheses was fully accepted: the regressive hypothesis did not explain why even the smallest of cellular parasites do not resemble viruses in any way. The escape hypothesis did not explain the complex capsids and other structures on virus particles. The virus-first hypothesis was quickly dismissed because it contravened the definition of viruses, in that they require host cells. [5] Virologists are, however, beginning to reconsider and re-evaluate all three hypotheses. [7][8] http://en. wikipedia. org/wiki/Viral_evolution Evolution Time-line of paleoviruses in the human lineage[9]

Viruses do not form fossils in the traditional sense, because they are much smaller than the grains of sedimentary rocks that fossilize plants and animals. However, the genomes of many organism contain endogenous viral elements (EVEs). These DNA sequences are the remnants of ancient virus genes and genomes that ancestrally ‘invaded’ the host germline. For example, the genomes of most vertebrate species contain hundreds to thousands of sequences derived from ancient retroviruses. These sequences are a valuable source of retrospective evidence about the evolutionary history of viruses, and have given birth to the science of paleovirology. 9] The evolutionary history of viruses can to some extent be inferred from analysis of contemporary viral genomes.

The mutation rates for many viruses have been measured, and application of a molecular clock allows dates of divergence to be inferred. [10] Viruses evolve through changes in their DNA (or RNA), some quite rapidly, and the best adapted mutants quickly outnumber their less fit counterparts. In this sense their evolution is Darwinian, just like that of their host organisms. [11] The way viruses reproduce in their host cells makes them particularly susceptible to the genetic changes that help to drive their evolution. 12] The RNA viruses are especially prone to mutations. [13] In host cells there are mechanisms for correcting mistakes when DNA replicates and these kick in whenever cells divide. [13] These important mechanisms prevent potentially lethal mutations from being passed on to offspring. But these mechanisms do not work for RNA and when an RNA virus replicates in its host cell, changes in their genes are occasionally introduced in error, some of which are lethal. One virus particle can produce millions of progeny viruses in just one cycle of replication, therefore the production of a few “dud” viruses is not a problem.

Most mutations are “silent” and do not result in any obvious changes to the progeny viruses, but others confer advantages that increase the fitness of the viruses in the environment. These could be changes to the virus particles that disguise them so they are not identified by the cells of the immune system or changes that make antiviral drugs less effective. Both of these changes occur frequently with HIV. [14] Phylogenetic tree showing the relationships of morbilliviruses of different species[15] Many viruses (for example, influenza A virus) can “shuffle” their genes with other viruses when two similar strains infect the same cell.

This phenomenon is called genetic shift, and is often the cause of new and more virulent strains appearing. Other viruses change more slowly as mutations in their genes gradually accumulate over time, a process known as genetic drift. [16] Through these mechanisms new viruses are constantly emerging and present a continuing challenge to attempts to control the diseases they cause. [17][18] Most species of viruses are now known to have common ancestors, and although the “virus first” hypothesis has yet to gain full acceptance, there is little doubt that the thousands of species of modern viruses have evolved from less numerous ancient ones. 19] The morbilliviruses, for example, are a group of closely related, but distinct viruses that infect a broad range of animals.

The group includes measles virus, which infects humans and primates; canine distemper virus, which infects many animals including dogs, cats, bears, weasels and hyaenas; rinderpest, which infects cattle and buffalo; and other viruses of seals, porpoises and dolphins. 20] Although it not possible to prove which of these rapidly evolving viruses is the earliest, for such a closely related group of viruses to be found in such diverse hosts suggests a possible ancient common ancestor. [21] The Nature of Viruses Viruses are sub-cellular agents of infection that must utilize the cellular machinery of bacteria, plants or animals in order to reproduce. Composed of a single strand of genetic material (DNA or RNA) encased in a protein capsid, a virus is too small to be seen by standard light microscopy; indeed, most are less than one hundredth the size of a bacterium.

Specific proteins on the viral capsid attach to receptors on the host cell; this attachment process is essential to viral infectivity and explains why viruses may only infect the cells of certain species or may only infect certain cells or tissues within a given host species. While the infecting virus triggers an immune response in the host, some are capable of suppressing that response by infecting and killing cells that control immunity (e. g. HIV attacks lymphocytes).

In addition, while most infected cells are destroyed by viral replication, some viruses enter a latent phase within cells, reactivating in the future to produce chronic or relapsing infections. Many viruses use specific carriers (known as vectors) such as mosquitoes, ticks, bats and rodents that transmit the virus to a susceptible host while others are spread between individuals via blood contact or through respiratory, intestinal or sexual secretions.

Of special concern is the fact that mutations within the viral genome may allow viruses to skip from one host (e. g. birds, swine, monkeys) to another (e. g. humans), unleashing pandemics. Many common human infections are produced by viruses; these include the common cold, influenza, mononucleosis, herpes infections (including shingles), viral hepatitis (A, B, C and others), HIV, viral gastroenteritis, conjunctivitis, viral pneumonia, encephalitis, viral meningitis and viral infections of the heart, including pericarditis and myocarditis.

While viruses do not respond to antibiotics, specific antiviral agents may control (though not cure) chronic disease (such as HIV, Hepatitis B and Hepatitis C) or may modify the severity of acute infection (as in influenza and herpes infections). However, in most viral infections, treatment is, for now, purely symptomatic and supportive. On the other hand, vaccines are capable of preventing some viral infections (e. g. erpes simplex, measles, mumps, rubella, varicella, Hepatitis B) or reducing the severity of an acute infection (e. g. influenza). Beyond the acute or chronic illness that they produce, some viral infections (such and Hepatitis C and certain strains of herpes simplex) are known to be precursors of malignancy. Finally, many researchers suspect that viruses play a role in the pathogenesis of chronic illnesses such as multiple sclerosis and autoimmune disorders. development of viruses (images)