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Ozone Layer, a region of the atmosphere from 19 to 48 km (12 to 30 mi) above Earth's surface. Ozone concentrations of up to 10 parts per million occur in the ozone layer. The ozone forms there by the action of sunlight on oxygen. This action has been taking place for many millions of years, but naturally occurring nitrogen compounds in the atmosphere apparently have kept the ozone concentration at a fairly stable level.

The ozone layer of the atmosphere protects life on Earth by absorbing harmful ultraviolet radiation from the Sun. If all the ultraviolet radiation given off by the Sun were allowed to reach the surface of Earth, most of the life on Earth’s surface would probably be destroyed. Short wavelengths of ultraviolet radiation, such as UV-A, B, and C, are damaging to the cell structure of living organisms. Fortunately, the ozone layer absorbs almost all of the short-wavelength ultraviolet radiation and much of the long-wavelength ultraviolet radiation given off by the Sun.

In the 1970s scientists became concerned when they discovered that chemicals called chlorofluorocarbons, or CFCs (see Fluorine)—long used as refrigerants and as aerosol spray propellants—posed a possible threat to the ozone layer. Released into the atmosphere, these chlorine-containing chemicals rise into the upper stratosphere and are broken down by sunlight, whereupon the chlorine reacts with and destroys ozone molecules—up to 100,000 per CFC molecule. The use of CFCs in aerosols has been banned in the United States and elsewhere. Other chemicals, such as bromine halocarbons, as well as nitrous oxides from fertilizers, may also attack the ozone layer. Thinning of the ozone layer is predicted to cause increases in skin cancer and cataracts, damage to certain crops and to plankton and the marine food web, and an increase in atmospheric carbon dioxide (see Global Warming) due to the decrease in plants and plankton.

Beginning in the early 1980s, research scientists working in Antarctica began to detect a periodic loss of ozone in the atmosphere high above that continent. The so-called ozone “hole,” a thinned region of the ozone layer, develops in the Antarctic spring and continues for several months before thickening again. Studies conducted with high-altitude balloons and weather satellites indicated that the overall percentage of ozone in the Antarctic ozone layer is actually declining. Measurements over the Arctic regions indicated that a similar problem was developing there.

In 1985 the Vienna Convention for the Protection of the Ozone Layer was adopted. In 1987 a protocol under the Vienna Convention, known as the Montréal Protocol, was signed and later ratified by 36 nations, including the United States. A total ban on the use of CFCs during the 1990s was proposed by the European Community (now called the European Union) in 1989, a move endorsed by U.S. President George H. W. Bush. In December 1995 over 100 nations agreed to phase out developed countries' production of the pesticide methyl bromide by the year 2000. The pesticide was estimated to cause about 15 percent of the ozone depletion. Production of CFCs in developed countries ceased at the end of 1995 and was to be phased out in developing countries by 2010.

Hydrochlorofluorocarbons, or HCFCs, which cause less damage to the ozone layer than CFCs do, began to be used as substitutes for CFCs following the adoption of the Montréal Protocol. HCFCs were to be used on an interim basis until 2030 in developed countries and until 2040 in developing countries. In addition, the United States passed legislation that would ban the production of the refrigerant HCFC-22, widely used in air conditioners, by 2010. Other industrialized nations also adopted measures to end HCFC-22 production prior to 2020. But production of HCFC-22 in developing nations was estimated in 2007 to be increasing at a rate of 20 to 35 percent each year.

Concerned about the increasing use of HCFCs, the United Nations Environment Program met again in September 2007 in Montréal, where more than 200 countries agreed to speed up the timetable for phasing out the use of HCFCs. Under the new agreement, developing countries would end all use of HCFCs by 2030, ten years earlier than previously agreed, and developed countries would end all use by 2020.

To monitor ozone depletion on a global level, in 1991 the National Aeronautics and Space Administration (NASA) launched the 7-ton Upper Atmosphere Research Satellite. Orbiting Earth at an altitude of 600 km (372 mi), the spacecraft measures ozone variations at different altitudes and provides thorough measurements of upper atmosphere chemistry.

The World Meteorological Organization (WMO), a specialized agency of the United Nations (UN), helps support the implementation of the Vienna Convention to protect the ozone layer. During the winter of 1995-1996 the WMO observed a 45 percent depletion of the ozone layer over one-third of the northern hemisphere, from Greenland to western Siberia, for several days. The deficiency was believed to have been caused by chlorine and bromine compounds combined with polar stratospheric clouds formed under unusually low temperatures.

The ozone hole over Antarctica reached a record size in 2001, the same year that the presence of CFCs in the atmosphere was thought to have peaked. Due to the international treaty to phase out production of CFCs, many scientists expected the ozone layer would begin to recover after the record thinning of 2001. To their surprise, however, measurements in 2006 indicated that the ozone hole had once again reached a record size. Most scientists attributed the increase in the ozone hole in 2006 to an unusually cold Antarctic winter. A study the same year by the WMO and the United Nations Environment Program, however, found that the ozone layer was recovering more slowly than predicted. This finding was expected to trigger an effort in 2007 to phase out the production of HCFC-22 more rapidly than previously planned.

Black holes.

It has yet to be proved that black holes—hypothetical bodies with gravitational fields so powerful that nothing, not even light, can escape from them—actually exist. But evidence continues to mount that these bizarre products of theoreticians' minds are real features of our universe. Since star-size black holes, if they exist, cannot be seen, they can only be detected by their gravitational effects on visible bodies. Perhaps the only way of hunting for a black hole is to look for a binary (double) star system in which a visible star has an unaccountably massive, unseen companion. (According to theory, any stellar object with a mass greater than about twice the sun's must either shed its excess mass in some way or eventually become a black hole.) In 1983 a scientific team found the best black-hole candidate yet, in the binary star LMC X-3 in the Large Magellanic Cloud. The scientists concluded that the unseen companion of LMC X-3's visible component has a mass of more than nine suns, and thus is very likely a black hole.

In 1994 astronomers used the Hubble Space Telescope (HST) to uncover the first convincing evidence that a black hole exists. They detected an accretion disk (disk of hot, gaseous material) circling the center of the galaxy M87 with an acceleration that indicated the presence of an object 2.5 to 3.5 billion times the mass of the Sun. By 2000, astronomers had detected supermassive black holes in the centers of dozens of galaxies and had found that the masses of the black holes were correlated with the masses of the parent galaxies. More massive galaxies tend to have more massive black holes at their centers. Learning more about galactic black holes will help astronomers learn about the evolution of galaxies and the relationship between galaxies, black holes, and quasars.

In other cases of massive stars collapsing, pressure or a nuclear explosion does not halt the final collapse. As the radius of such a star decreases, the gravitational force at its surface increases. Eventually the radius of the star is so small and its mass so dense that not even light can escape its gravitational pull. The star is then no longer visible from the outside and has become a black hole. The size of the black hole is proportional to the mass inside it. A black hole containing the mass of our sun would be about 1.5 km (0.93 mi) in radius. The matter inside the black hole continues to collapse. Scientists are not sure what happens to this matter, but it must remain inside the black hole. There may be many black holes in our galaxy, the Milky Way, but none have been discovered with certainty. Astronomers do believe they have found galactic black holes in other galaxies, including NGC 4258, NGC 4621, and M 87.

object in space: an area in space with such a strong gravitational pull that no matter or energy can escape from it.

Black holes are believed to form when stars collapse in on themselves.

place where things get lost: a place or thing into which objects disappear and are not expected to be seen again

Black Hole, an extremely dense celestial body that has been theorized to exist in the universe. The gravitational field of a black hole is so strong that, if the body is large enough, nothing, including electromagnetic radiation, can escape from its vicinity. The body is surrounded by a spherical boundary, called a horizon, through which light can enter but not escape; it therefore appears totally black.

Electromagnetic Radiation, energy waves produced by the oscillation or acceleration of an electric charge. Electromagnetic waves have both electric and magnetic components. Electromagnetic radiation can be arranged in a spectrum that extends from waves of extremely high frequency and short wavelength to extremely low frequency and long wavelength (see Wave Motion). Visible light is only a small part of the electromagnetic spectrum. In order of decreasing frequency, the electromagnetic spectrum consists of gamma rays, hard and soft X rays, ultraviolet radiation, visible light, infrared radiation, microwaves, and radio waves.

Tsunami, Japanese word used as the scientific term for a seismic sea wave, a large ocean wave generated by an undersea earthquake. The wave is thought to be triggered when the ocean floor is tilted or offset during the quake. Another possible cause is an undersea landslide or volcanic eruption. Most tsunamis originate along the so-called Ring of Fire, a zone of volcanoes and seismic activity, 32,500 km (24,000 mi) long, that encircles the Pacific Ocean. Since 1819, for example, about 40 tsunamis have struck the Hawaiian Islands.

A tsunami may travel hundreds of kilometres across the deep ocean, reaching speeds of about 725 to 800 km/h (450 to 500 mph). On entering shallow coastal waters, the wave, which may have been only about half a metre (a foot or two) high out at sea, suddenly begins growing rapidly. By the time it reaches the shore, it may become a towering wall of water 15 m (50 ft) high or more, capable of destroying entire coastal settlements.

Tsunamis have erroneously been called tidal waves, but they have nothing to do with the diurnal pattern of high and low tides. Such waves, however, in combination with meteorological phenomena, can also sometimes be destructive.

Earthquake, vibrations produced in the Earth's crust when rocks in which elastic strain has been building up suddenly rupture, and then rebound. The vibrations can range from barely noticeable to catastrophically destructive. Earthquakes can release energy thousands of times greater than the world's first atomic bomb.

Six kinds of shock waves are generated in the process. Two are classified as body waves—that is, they travel through the Earth's interior—and the other four are surface waves. The waves are further differentiated by the kinds of motions they impart to rock particles. Primary or compressional waves (P waves) send particles oscillating back and forth in the same direction as the waves are travelling, whereas secondary or transverse shear waves (S waves) impart vibrations perpendicular to their direction of travel. P waves always travel at higher velocities than S waves, so whenever an earthquake occurs, P waves are the first to arrive and be recorded at geophysical research stations throughout the world.

Volcano, fissure or vent through which molten rock material, or magma, and gases from the interior of the Earth erupt on to its surface, and the landform which is produced as a result of this eruption. The word “volcano” derives from Vulcano, one of the volcanic Lipari Islands in the Mediterranean Sea, and the place where, according to Roman mythology, Vulcan, the god of fire, kept his forge. The processes that create volcanoes and other volcanic structures are called volcanism or vulcanism.

As landforms, volcanoes are formed by the deposition of the magma that flows or is ejected, normally from one or several circular vents, as molten or solid material. Molten magma is known as lava when it reaches the Earth's surface; the solid material—classified as dust, ash, cinders, and bombs depending on size and shape—is called tephra. Volcanoes which form round circular vents are known as central volcanoes; the basin-like mouth of the vent is known as the crater. Most volcanoes tend to be conical in shape; some, however, are much larger structures with very gentle slopes. Often covering many square kilometres, they are known as shield volcanoes.

This Scientific American article discusses what happens in the time between the infection of a cell and the appearance of new viruses. The behaviour of bacteriophages suggests that this stage involves a new concept: the provirus.

Life Cycle of a Virus

Close your eyes and look. What you saw at first is there no more; and what you will see next has not yet come to life.—Leonardo da Vinci

We can apply these words very aptly to a virus—of the bacteria-infecting kind known as bacteriophage. When a phage particle enters a cell, it loses its infective power and its identity as a particle. Generally its entrance into the cell is followed within 15 minutes to an hour by the emergence of a new generation of infectious virus particles. Sometimes, however, there is no immediate pathological event. The genetic material of the virus that has passed into the cell combines with the genetic material of the cell itself. In doing so it is converted into something that has been named a “provirus,” meaning before virus. Days or years afterward the provirus may suddenly develop into virus and the bacterium give rise to a group of virus particles.

The term provirus needs some explanation. The expression “proman” would certainly not evoke the idea of a human egg, from which Homo sapiens always develops, but rather that of an evolutionary ancestor of man which would have to undergo a genetic transformation to become man. A provirus may perhaps correspond to an evolutionary ancestor of a virus. But it is also much more than that.

Before attacking the question of the nature of proviruses, we must know something about viruses themselves. What is a virus? We shall leave out of the discussion the much debated issue as to whether viruses are living organisms or not; our concern is to find out how they differ from “normal” organisms of the microbiologist’s world. The two attributes that are usually thought to define viruses are their very small size and the fact that they can multiply only inside living cells—usually requiring a specific kind of cell host. But to learn more about their peculiarities let us go beyond this definition and compare viruses with other small biological units.

First of all, how does a virus differ from a cell? Most cells are capable of reproducing themselves: they possess the genetic material which is the basis of heredity and the tools necessary to synthesize the essential building blocks and to organize these into a structure just like themselves. We can see three important differences between a cell and a virus, taking bacteriophage as a typical virus: (1) whereas cells contain both desoxyribonucleic acid (DNA) and ribonucleic acid (RNA), the phage contains only DNA; (2) whereas cells are reproduced from essentially all their constituents, bacteriophage is reproduced from its nucleic acid; (3) whereas cells are able to grow and to divide, the virus particle as such is unable to grow or to undergo fission. Bacterial viruses are never produced directly by division of an existing virus; invariably they are formed by organization of material produced in the host cell.

Next we must consider whether viruses bear any likeness to the particles within a cell, particularly the particles called plasmagenes. Here differences are less easy to find. The theory has been proposed that viruses may originate as mutated plasmagenes. But we know that some plasmagenes (e.g., the chloroplasts of green plants) can grow and divide. Furthermore, plasmagenes are not pathogenic or lethal to the cell, as virus particles are. Let us just note, for the time being, that nothing which resembles a bacteriophage in its properties, life cycle, shape or organization has been found in normal cells.

Let us now consider the peculiar behavior of the virus. The virus particle as such is only the beginning and the end of a life cycle. Its only physiological function is to obtain entry of the virus' genetic material into the host cell. After this occurs, what remains of the virus is devoid of infectious power. There follows a vegetative phase in which the specific constituents for new viruses are produced. Finally these constituents are organized into virus particles, which are liberated by lysis (dissolution) of the cell. The whole process usually takes from 15 to 60 minutes.

But a bacterial virus may multiply in another way, and this is where the provirus enters the picture. Ordinarily the virus nucleic acid passed into a cell proceeds promptly to multiply and to synthesize specific protein material for new phage particles. Sometimes, however, the nucleic acid may anchor onto a bacterial chromosome and act as if it were a normal constituent of the cell. It behaves as a bacterial gene, being replicated at each bacterial division and transmitted to each daughter bacterium. This is what we call a provirus. It is a potential virus; it may eventually give rise to virus particles. In the meantime the bacterial offspring go on growing and dividing as normal bacteria, and each daughter bacterium yields progeny capable of producing viruses. In other words, the ability to produce viruses is perpetuated inside the bacterium; no new infection from outside is needed.

Bacteria containing proviruses are called lysogenic. When a small number of such bacteria are broken down, no infectious particles can be found. This means that the provirus is not infectious. And yet in every large population of these bacteria some mature bacteriophage particles appear. From time to time a bacterium in such a culture suddenly disappears, and about 100 phage particles emerge. The probability of a lysogenic bacterium spontaneously giving rise to viruses varies from 1/100 to 1/100,000. In some systems the probability is apparently independent of external factors; it cannot be modified. In other lysogenic systems phage production may be initiated at will by inducing agents, such as X-rays, ultraviolet rays, nitrogen mustard and other substances—all of which are known to be capable of producing mutation. Within 30 to 60 minutes after exposure to one of these agents, practically all of the bacteria produce viruses and lyse.

How do lysogenic bacteria produce viruses? Before discussing this question we must know more about the proviruses. We are inclined to think that proviruses originally arose as mutants of normal bacterial genes. Whatever their origin, the reservoir of bacterial viruses seems to be the provirus-carrying bacteria. These bacteria may have perpetuated provirus, that is to say, the hereditary ability to produce virus, for many thousands of years.

The study of lysogenic bacteria has led to a clear picture of the provirus. Apparently it does not contain virus protein, for lysogenic bacteria do not cause the production of specific antibodies to phage protein in experimental animals. It is therefore tempting to visualize the provirus as a large molecule of nucleic acid. Secondly, the provirus is associated with a certain genetic character of bacteria and is located at a specific site on a bacterial chromosome. Thirdly, two genetically related proviruses in a bacterium may cross over and recombine. Fourth, a lysogenic bacterium is immune to infection by a phage particle related genetically to its provirus, though it can be killed by an unrelated phage. As long as the provirus remains in that state, a genetically related superinfecting phage is unable to develop into phage. Finally, the mere presence of the provirus may modify the properties of a bacterium: it may endow certain bacteria with the ability to produce a toxin they could not otherwise make, or it may change the typical appearance of bacterial colonies. Things happen as if the provirus either carries a specific gene or modifies the neighboring bacterial genes. From all these data it may be concluded that provirus is the bacterial virus’ genetic material, bound to a specific site in the bacterium and responsible for a specific bacterial immunity.

Now it is difficult to imagine that this immunity is due only to the presence of the provirus. A particle cannot exert a specific action by its mere presence. The only way the provirus can make the bacterium immune—that is, prevent multiplication of a virus invader—is by modifying or blocking a specific activity of the bacterium necessary for that reproduction. And the provirus can do this only if it is present at a specific site. As a matter of fact, we can account for all the properties of proviruses and of lysogenic bacteria by the hypothesis that the provirus is the genetic material of the virus anchored at a given site in the bacterium. The genetic material of an infecting virus becomes a provirus when and because it becomes bound at that site to a specific receptor, which modifies the material. It then gives the bacterium immunity against genetically related infecting particles. An inducing agent such as ultraviolet rays destroys the immunity because it displaces the genetic material of the virus from its specific site.

For a long time virologists have concentrated on the virus particle itself. Yet the particle is only a prelude to the infection. During the longest and most important part of the life cycle, the pathogenic phase in a cell, no virus particle is present. As a matter of fact, disappearance of the virus particle is the sine qua non for the development of the cellular lesion. Indeed, there are cases in which all the bacteria in a lysogenic population die although very few of them produce bacteriophage particles; the cells are killed by a defective development of proviruses initiated by an inducing agent. One could even conceive of a condition in which the probability of the virus ever appearing would be infinitely small, that is to say, practically absent. Some bacteria actually carry a gene which can initiate the synthesis of a protein lethal to themselves. But that is another story.

Biologists have long been accustomed to think of death in terms of the destruction or alteration of some vital structure. We have been less inclined to think of living cells as carrying the seeds of their own destruction, or of the possibility that lethal agents may kill in more than one way. For example, X-rays sometimes kill by destroying essential structures, but they may also destroy a cell by inducing a gene to express its lethal potentiality. This potentiality is sometimes the power to start a new synthesis which may or may not end in virus particles.

To what extent are the phenomena disclosed in bacteria valid for higher organisms? May animal or plant cells perpetuate proviruses? Are some viral diseases of man the result of the activation of a provirus? May immunity to virus diseases be explained in terms of proviruses? Do the findings concerning lysogeny have any bearing on cancer? Let us recall that the inducing agents which can trigger proviruses to give rise to viruses are all not only mutagenic but also carcinogenic—radiations, nitrogen mustard and so on. It is indeed tempting to theorize that carcinogens may induce malignancy by initiating the formation of a pathological structure from a proviruslike material. Many facts are in favor of the hypothesis that proviruses originate some animal diseases, but the problem cannot be discussed within the limits of this article. Suffice it to say that this is, at any rate, a working hypothesis.

I have tried to outline the concept of the provirus, to analyze its relations with the concept of the cell and of the virus and to show the impact of the newly acquired knowledge on our conceptions of cellular disease. The common denominator of the various phases of the life cycle of a virus is the genetic material—the nucleic acid—which may exist in three states: infectious, proviral and vegetative. Throughout these three states the genetic material apparently remains cssentially the same in structure, but it changes radically in dynamic potentialities and behavior. The virus particle, the end product of the vegetative phase, is a quiescent nucleoprotein particle, unable to grow or to divide. The provirus is an integrated nucleic acid, which behaves like a gene and is replicated like the host genes. Neither the virus particle nor the provirus is pathogenic per se; their pathogenic property is only potential. The only pathogenic phase of the virus is the vegetative phase, during which the specific viral nucleic acid multiplies and during which the specific viral protein is synthesized. Things happen as if the synthesis of the protein is responsible for pathogenicity.

The provirus produces provirus; it is order. The vegetative particle produces virus particles and a disease of the host; it is disorder. The virus particle does not produce anything; it is an extremely conservative particle—the absence of any activity, that is to say, a kind of order. Thus the virus is an alternation of order and disorder.

As a result, my presentation of the subject may seem somewhat disordered. For this I had decided to apologize, when I came across an unpublished letter which Martin de Barcos, Abbot of Saint-Cyran, wrote to Mother Angélique in 1652: “Allow me to tell you that you would be wrong to apologize for the disorder of your discourse and of your thoughts, because, if they were otherwise, things would not be in order, especially for a person belonging to your profession. As there is a wisdom which is folly before God, there is also an order which is disorder, and in consequence, there is a folly which is wisdom and a disorder which is the true rule.” This being exactly the case of the virus, I decided not to apologize.

Virus (biology) (Latin, “poison”), any of a number of organic entities consisting simply of genetic material surrounded by a protective coat. The term “virus” was first used in the 1890s to describe agents that caused diseases but were smaller than bacteria. By itself a virus is a lifeless form, but within living cells it can replicate many times and harm its host in the process. The hundreds of known viruses cause a wide range of diseases in humans, other animals, insects, bacteria, and plants (see Diseases of Animals).

The existence of viruses was established in 1892, when Russian scientist Dmitry I. Ivanovsky discovered microscopic particles later known as the tobacco mosaic virus. The name virus was applied to these infectious particles in 1898 by the Dutch botanist Martinus W. Beijerinck. A few years later, viruses were found growing in bacteria; these viruses were dubbed bacteriophages. Then, in 1935, the American biochemist Wendell Meredith Stanley crystallized tobacco mosaic virus and showed that it is composed only of the genetic material called ribonucleic acid (RNA) and a protein covering. In the 1940s development of the electron microscope made visualization of viruses possible for the first time. This was followed by development of high-speed centrifuges used to concentrate and purify viruses. The study of animal viruses reached a major turning point in the 1950s with the development of methods to culture cells that could support virus replication in test tubes. Numerous viruses were subsequently discovered, and in the 1960s and 1970s most were analysed to determine their physical and chemical characteristics.

Characteristics

Viruses are submicroscopic intracellular parasites that consist of either RNA or deoxyribonucleic acid (DNA)—never both—plus a protective coat of protein or of protein combined with lipid or carbohydrate components. The nucleic acid is usually a single molecule, either singly or doubly stranded. Some viruses, however, may have nucleic acid that is segmented into two or more pieces. The protein shell is termed the capsid, and the protein subunits of the capsid are called capsomeres. Together these form the nucleocapsid. Other viruses have an additional envelope that is usually acquired as the nucleocapsid buds from the host cell. The complete virus particle is called the virion. Viruses are obligate intracellular parasites; that is, their replication can take place only in actively metabolizing cells. Outside living cells, viruses exist as inert macromolecules (very large molecules).

Viruses vary considerably in size and shape. Three basic structural groups exist: isometric; rod shaped or elongated; and tadpole-like, with head and tail (as in some bacteriophages). The smallest viruses are icosahedrons (20-sided polygons) that measure about 18 to 20 nanometres wide (one-millionth of a millimetre = 1 nanometre). The largest viruses are rod shaped. Some rod-shaped viruses may measure several microns in length, but they are still usually less than 100 nanometres in width. Thus, the widths of even the largest viruses are below the limits of resolution of the light microscope, which is used to study bacteria and other large micro-organisms.

Many of the viruses with helical internal structure have outer coverings (also known as envelopes) composed of lipoprotein or glycoprotein, or both. These viruses appear roughly spherical or in various other shapes, and they range from about 60 to more than 300 nanometres in diameter. Complex viruses, such as some bacteriophages, have heads and a tubular tail, which attaches to host bacteria. The pox viruses are brick shaped and have a complex protein composition. Complex and pox viruses are exceptions, however; most viruses have a simple shape.

Replication

Viruses do not contain the enzymes and metabolic precursors necessary for self-replication. They have to get these from the host cells that they infect. Viral replication, therefore, is a process of separate synthesis of viral components and assembly of these into new virus particles. Replication begins when a virus enters the cell. The virus coat is removed by cellular enzymes, and the virus RNA or DNA comes into contact with ribosomes (cell organs that synthesize proteins) inside the cell. There the virus RNA or DNA directs the synthesis of proteins specified by the viral nucleic acid. The nucleic acid replicates itself, and the protein subunits constituting the viral coat are synthesized. Thereafter, the two components are assembled into a new virus. One infecting virus can give rise to thousands of progeny viruses. Some viruses are released by destruction of the infected cell. Others are released by budding through cell membranes and do not kill the cell. In some instances, infections are “silent”—that is, viruses may replicate within the cell but cause no obvious cell damage.

The RNA-containing viruses are unique among replicative systems in that the RNA can replicate itself independently of DNA. In some cases, the RNA can function as messenger RNA (see Genetics), indirectly replicating itself using the cell's ribosomal and metabolic precursor systems. In other cases, RNA viruses carry within the coat an RNA-dependent enzyme that directs the synthesis of virus RNA. Some RNA viruses, which have come to be known as retroviruses, may produce an enzyme that can synthesize DNA from the RNA molecule. The DNA thus formed then acts as the viral genetic material.

Bacterial viruses and animal viruses differ somewhat in their interaction with the cell surface during infection. The “T even” bacteriophage that infects the bacterium Escherichia coli, for instance, first attaches to the surface and injects its DNA directly into the bacterium. No absorption and uncoating take place. The basic events of virus replication, however, are the same after the nucleic acid enters the cell.

Viruses in Medicine

Viruses represent a major challenge to medical science in combating infectious diseases. Many cause diseases that are of major importance to humans and that are extraordinary in their diversity.

Included among viral diseases is the common cold, which affects millions of people every year. Other viral diseases are important because they are frequently fatal. These diseases include rabies, haemorrhagic fevers, encephalitis, poliomyelitis, and yellow fever. Most viruses, however, cause diseases that usually only create acute discomfort unless the patient develops serious complications from the virus or from a bacterial infection. Some of these diseases are influenza, measles, mumps, cold sores (also known as herpes simplex), chicken pox, shingles (also known as herpes zoster), respiratory diseases, acute diarrhoea, warts, and hepatitis. Still others, such as rubella (also known as German measles) virus and cytomegalovirus, may cause serious abnormalities or death in unborn infants. Acquired immune deficiency syndrome (AIDS) is caused by a retrovirus. Only two retroviruses are unequivocally linked with human cancers (see Leukaemia and HTLV), but some papilloma virus forms are suspected. Increasing evidence also indicates that other viruses may be involved in some types of cancer and in chronic diseases such as multiple sclerosis and other degenerative diseases. Some of the viruses take a long time to cause disease; kuru and Creutzfeldt-Jakob disease, both of which gradually destroy the brain, are slow virus diseases.

Viruses that cause important human disease are still being discovered. Most can be isolated and identified by laboratory methods, but these usually take several days to complete. One of the most recently discovered viruses is rotavirus, the causal agent of infant gastroenteritis.

Spread

To cause new cases of disease, viruses must be spread from person to person. Many viruses, such as those causing influenza and measles, are transmitted by the respiratory route when virus-containing droplets are put into the air by people coughing and sneezing. Other viruses, such as those that cause diarrhoea, are spread by the faecal-oral route. Still others, such as yellow fever and viruses called arboviruses, are spread by biting insects. Viral diseases are either endemic (present most of the time), causing disease in susceptible people, or epidemic—that is, they come in large waves and attack thousands of people. An example of an epidemic viral disease is the worldwide occurrence of influenza almost every year.

Treatment

Currently, no completely satisfactory treatments exist for viral infections, because most drugs that destroy viruses also damage the cell. The drug amantadine is used extensively in some countries for treatment of respiratory infections caused by influenza-A viruses, and the drug AZT is used in the treatment of HIV.

One promising antiviral agent, interferon, is produced by the cell itself. This non-toxic protein, which is produced by some animal cells infected with viruses, can protect other cells against such infection. The use of interferon for treating cancer is under intensive study. Until recently, study of the use of interferon has been restricted by its limited availability in pure form. However, new techniques of molecular cloning of genetic material (see Genetic Engineering) now make it possible for scientists to obtain the protein in larger quantities. Its relative value as an antiviral agent has already been established.

The only effective way to prevent viral infection is by the use of vaccines. For example, vaccination for smallpox on a worldwide scale in the 1970s eradicated this disease. Many antiviral vaccines have been developed for humans and other animals. Those for humans include vaccines for rubeola (also known as measles), rubella, poliomyelitis, and influenza. Immunization with a virus vaccine stimulates the body's immune mechanism to produce a protein—called an antibody—that will protect against infection with the immunizing virus. The viruses are always altered before they are used for immunization so that they cannot themselves produce disease.

Plant Infections

Viruses cause a wide variety of diseases in plants and frequently cause serious damage to crops. Common plant-disease viruses are turnip yellow mosaic virus, potato leaf roll virus, and tobacco mosaic virus. Plants have rigid cell walls that plant viruses cannot penetrate, so the most important means of plant-virus spread is provided by animals that feed on plants. Often, healthy plants are infected by insects that carry on their mouthparts viruses acquired while feeding on other infected plants. Nematodes (also known as roundworms) may also transmit viruses while feeding on the roots of healthy plants.

Plant viruses can accumulate in enormous quantities within infected cells. For instance, tobacco mosaic virus may represent as much as 10 per cent of the dry weight of infected plants. Studies on the interaction of plant viruses with plant cells are limited, because plants often cannot be infected directly, but only by means such as an insect vector. Cell cultures in test tubes, which can be infected with plant viruses, are not generally available.

Role in Research

The study of viruses and their interaction with host cells has been a major motivation for the host of fundamental biological studies at a molecular level. For example, the existence of messenger RNA, which carries the genetic code from DNA to define what proteins are made by a cell, was discovered during studies of bacteriophages replicating in bacteria. Studies of bacteriophages have also been instrumental in delineating the biochemical factors that start and stop the utilization of genetic information. Knowledge of how virus replication is controlled is fundamental to understanding biochemical events in higher organisms.

The reason that viruses are so useful as model systems for studying events that control genetic information is that viruses are, in essence, small pieces of genetic information that is different from the genetic information of the cell. This allows scientists to study a smaller and simpler replicating system, but one that works on the same principle as that of the host cell. Much of the research on viruses is aimed at understanding their replicative mechanism in order to find ways to control their growth, so that viral diseases can be eliminated. Studies on viral diseases have also contributed greatly to understanding the body's immune response to infectious agents. Antibodies in blood serum, as well as secretions of the mucous membranes, all of which help the body eliminate foreign elements such as viruses, have been more thoroughly characterized by studying their responses to viral infection. Intense scientific interest is now concentrated on studies designed to isolate certain viral genes. These genes can be used in molecular-cloning systems to produce large amounts of particular virus proteins, which can in turn be used as vaccines.

Severe Acute Respiratory (SARS Fear):

Syndrome (SARS), contagious respiratory illness that can cause a fatal form of pneumonia. The illness first appeared in November 2002 in people living in Guangdong province in southern China. Its cause was unknown and available treatments were ineffective. By February 2003 new cases of the illness were reported in Hong Kong, Vietnam, Singapore, and Canada. The fast spread of the disease, its deadly nature, and its unknown cause prompted the World Health Organization (WHO), an agency of the United Nations, to issue a global alert in March 2003 designating SARS as a worldwide health threat. The alert triggered governments around the world to establish infection-control procedures to prevent the illness from reaching epidemic proportions. Despite these public-health measures, more than 8,000 SARS cases were reported in 32 countries and the disease caused 800 deaths by the time the outbreak was declared contained in July 2003.

SYMPTOMS AND TREATMENT

SARS symptoms begin with a fever about 38°C (about 100.4°F) or higher, chills, headache, and malaise. Two to seven days later some people develop a dry cough and difficulty breathing. Symptoms may progress to a severe form of pneumonia, in which air sacs in the lungs fill with fluid, preventing oxygen from reaching blood cells and nourishing the other cells of the body. Aside from regular nursing care and the use of a respirator to help breathing in severe cases, there is no effective treatment for SARS. Recovery seems to depend on the health of the patient’s immune system. Epidemiologists (scientists that study the cause and spread of diseases) have found that those most susceptible to the fatal form of the illness are aged 40 or older and have a history of a chronic disease.

HOW THE ILLNESS SPREADS

nfection with SARS results from close contact with an infected person. SARS can spread if a person inhales droplets sprayed into the air when an infected person coughs or sneezes. SARS may also spread when a person touches an object that has been contaminated. Scientists are investigating if the infection can spread in other ways. Symptoms typically develop two to seven days after exposure, so someone may unknowingly become infected and spread the illness before developing symptoms. In Asia, before infection-control measures were established, many SARS cases occurred among hospital workers who cared for SARS patients. These infected hospital workers, in turn, spread the illness to people living in their households. Most SARS cases reported in Canada were in people who became infected with the illness while traveling abroad or people who were exposed to infected travelers from abroad.

CAUSE

Although studies are incomplete, scientists suspect that a newly discovered virus from the coronavirus family causes SARS. Until now coronaviruses have been known to cause only minor illnesses in humans, such as colds or diarrhea. Scientists theorize that the SARS virus may have passed to humans from an animal. The virus then underwent a series of genetic mutations (changes) to acquire properties that cause severe illness in humans.

Researchers have developed laboratory tests that identify the SARS virus in infected people. These tests can help epidemiologists determine how long someone infected with SARS remains contagious and if those infected develop long-term immunity to the disease.

PREVENTION

Researchers in Hong Kong have identified chemicals that may prevent the virus from replicating once it infects a human body. Other researchers are investigating if genetically engineered antibodies are effective in blocking the virus. In addition, efforts to develop a vaccine that would prevent SARS are underway.

Until effective treatments can be developed, public-health officials have established infection-control measures to contain the spread of SARS. Those people diagnosed with SARS or suspected of having the illness are treated in isolation in their homes, in hospitals, or in other designated health-care settings. Caregivers follow strict procedures to lessen their own risk of infection. The WHO also issues travel advisories recommending against nonessential travel to certain countries where the risk of infection is high.

September 11, 2001

Terrorists Strike United States

In a coordinated strike on the United States, terrorists crash hijacked commercial jetliners into the twin towers of the World Trade Center, in New York City, and the Pentagon, outside Washington, D.C. A fourth hijacked airliner crashes in Pennsylvania. The unprecedented terrorist attack destroys the World Trade Center, kills more than 3,000 people, and shakes the nation to its core. United States authorities soon identify the al-Qaeda terrorist network of Saudi Arabian exile Osama bin Laden as the group responsible for the attack. Within weeks, a U.S.-led coalition would launch a war on terrorism aimed at destroying al-Qaeda and preventing future terrorist attacks.

Terrorists Destroy World Trade Center

A fireball erupts from the south tower of the World Trade Center in New York City after a hijacked passenger jet crashed into it on September 11, 2001. Another hijacked jet had crashed into.

The first two planes, American Airlines Flight 11 and United Airlines Flight 175, left Boston within minutes of each other, around 8 am. Both were Boeing 767s bound for Los Angeles, and they carried between them 137 passengers and 20 crew members. The first indication of trouble came at about 8:25 am, when air traffic controllers in Boston heard a strange voice from the Flight 11 cockpit saying, “We have some planes. Just stay quiet, and you will be OK. We are returning to the airport.” A few minutes later the plane turned off course, heading south toward New York City. Flight 11 crashed into the World Trade Center north tower at 8:46 am, hitting the 110-story building between the 93rd and 99th floors. The hijackers of United Flight 175 followed a similar route. Flying much faster, they slammed their airplane into the World Trade Center south tower, also 110 stories tall, between the 77th and85th floors 16 minutes later, at 9:03 am.

New York firefighters rushed to the scene from stations across the metropolitan area and helped thousands of people evacuate the towers and buildings nearby. Nearly all of the World Trade Center workers caught in offices above the floors where the planes hit had no means of escape. Many, realizing they were doomed, jumped from their office windows rather than waiting to suffocate or burn to death.

The tower structures, built from 1966 to 1973, were designed to withstand the impact of a jetliner crash, and initially remained intact. However, Boeing 767s are much larger than 1960s-era jetliners, and carry much more fuel. In both towers the intense heat from the burning jet fuel eventually melted their interior steel supports. At 9:58:59 am the south tower collapsed: The steel supports gave way in the burning part of the tower, the floors above fell into the lower portion of the building, and the weight of the falling sections swiftly caused the lower floors to pancake. The north tower fell in a similar fashion 29 minutes later, at 10:28 am. More than 400 rescue workers, including more than 300 New York firefighters, were crushed in the ash and rubble. Including the World Trade Center workers who died and the aircraft crews and passengers, the total death toll in the New York attack was about 2,750.

American Airlines Flight 77, meanwhile, took off from Washington Dulles International Airport outside Washington, D.C., at about 8:20 am with 6 crew members and 58 passengers. Like the Boston flights, the airplane was bound for Los Angeles, and its fuel tanks were full. About 40 minutes later, the hijackers turned the Boeing 757 around and flew it back toward Washington, D.C. Flying low and fast, the airplane hit the Pentagon at 9:37 am. In a bit of good fortune, the plane crashed into the west side of the building, which had recently been reinforced with stronger construction and blast-resistant windows in order to withstand a terrorist attack. Even so, the plane penetrated three of the Pentagon’s five concentric rings, taking a chunk out of the building and incinerating dozens of offices and the people who worked in them. The plane’s burning fuel spilled through the ruins as military and civilian workers groped their way through smoky and burning offices to rescue colleagues. In all, 184 people died at the Pentagon, including everyone aboard the plane.

My Wife From Missouri!

Missouri Compromise:

Under the Constitution of the United States, the federal government had no authority to interfere with slavery within the states. Northern opponents of slavery could hope only to prevent it from spreading. They tried to do this in 1818, when Missouri sought admission to the Union with a constitution permitting slavery. After two years of bitter controversy a solution was found in the Missouri Compromise. This compromise admitted Missouri to the Union as a slave state and admitted Maine as a free state to keep the balance in the Senate. It also provided that slavery would be excluded from the still unorganized part of the Louisiana Territory. A line was drawn from Missouri’s southern boundary, at the latitude of 36°30’, and slavery would not be allowed in the territory north of that line,with the exception of Missouri.

Strategic Defense Initiative (SDI), United States military research program for developing an antiballistic missile (ABM) defense system, first proposed by President Ronald Reagan in March 1983. The Reagan administration vigorously sought acceptance of SDI by the United States and its North Atlantic Treaty Organization (NATO) allies. As initially described, the system would provide total U.S. protection against nuclear attack. The concept of SDI marked a sharp break with the nuclear strategy that had been followed since the development of the armaments race. This strategy was based on the concept of deterrence through the threat of retaliation (see Arms Control). More specifically, the SDI system would have contravened the ABM Treaty of 1972 (see Strategic Arms Limitation Talks). For this reason and others, the SDI proposal was attacked as a further escalation of the armaments race.

Many experts believed the system was impractical. With the dissolution of the Soviet Union, the signing of the START I and II treaties, and the election in 1992 of Bill Clinton as president, the SDI, like many other weapons programs, was given a lower budgetary priority. In 1993 U.S. secretary of defense Les Aspin announced the abandonment of SDI and the establishment of the Ballistic Missile Defense Organization (BMDO) to oversee a less costly program known as National Missile Defense that would make use of ground-based antimissile systems.

The SDI system was originally planned to provide a layered defense employing advanced weapons technologies, several of which were only in a preliminary research stage. The goal was to intercept incoming missiles in midcourse, high above the earth. The weapons required included space- and ground-based nuclear X-ray lasers, subatomic particle beams, and computer-guided projectiles fired by electromagnetic rail guns—all under the central control of a supercomputer system. (The space-based weapons and laser aspects of the system gained it the media name “Star Wars,” after the popular 1977 science-fiction film.) Supporting these weapons would have been a network of space-based sensors and specialized mirrors for directing the laser beams toward targets. Some of these weapons were in development, but others—particularly the laser systems and the supercomputer control—were not certain to be attainable.

The total cost of such a system was estimated at between $100 billion and $1 trillion. Actual expenditures for SDI amounted to about $30 billion. The initial annual budget for BMDO was $3.8 billion.

Cost was not the only controversial issue surrounding SDI. Critics of SDI, including several former government officials, leading scientists, and some NATO members, maintained that the system—even if it had proved workable—could have been outwitted by an enemy in many ways. Also, other nations feared that the SDI system could have been used offensively.

The administration of President George W. Bush gave missile defense a high priority when Bush took office in January 2001. The September 11 terrorist attacks that year gave further impetus to a missile defense system. Secretary of Defense Donald Rumsfeld said such a system was needed to protect the United States from possible attacks by terrorist groups or rogue states. In 2002 the Bush administration withdrew from the ABM Treaty so that it could pursue more vigorous testing of a missile defense program. Criticism of a missile defense system persisted. The Union of Concerned Scientists said the technology did not yet exist to deploy a reliable missile defense system. The group also argued that countermeasures could easily be taken against such a defense system. Other critics noted that terrorists would be unlikely to use missiles and could conceal nuclear weapons, if they obtained them, in a ship or van.

Missile Defense Test

A U.S. interceptor missile lifts off from Kwajalein Atoll in the Pacific Ocean in December 2001 in a test of a missile defense system. The interceptor successfully destroyed a Minuteman II missile in space, but officials with the U.S. Ballistic Missile Defense Organization said the test was not carried out under realistic conditions. Defense against intercontinental ballistic missiles has long been controversial because of its costs, doubts about its reliability, and its effect on arms control agreements.Encarta EncyclopediaReuters

Many experts believe that nations such as Iraq and North Korea may have acquired stocks of smallpox virus that they intend to use as biological weapons (see Chemical and Biological Warfare). Some experts fear that, in addition to the threat from belligerent nations, a terrorist or extremist group might illegally gain access to stocks of smallpox virus and release it into the air in aerosol form in a crowded public place, such as an airport. The effects of such smallpox exposure would be devastating—with the halt of regular smallpox vaccinations worldwide, many people have no immunity to smallpox.

With the intentional distribution of anthrax through the United States mail in 2001, government officials became even more concerned about the threat of smallpox as a bioterrorist weapon. In December 2002 U.S. president George W. Bush announced a plan to protect Americans from the threat of smallpox attack from terrorists or hostile governments. The plan called for state and local governments to form volunteer smallpox response teams made up of people who, in the event of an attack, will implement emergency mass vaccination programs, investigate and evaluate suspected cases of smallpox, and initiate measures to control an outbreak. Health-care workers and other members of the teams will be asked to volunteer to receive the smallpox vaccine. This will ensure that team members can vaccinate others without fear of becoming sick themselves and provide critical emergency services in the days following a smallpox attack.