Information

How did viruses come to be?


My question is out of curiosity and got me thinking. How did viruses with the head, tail and tail fibres actually evolve? These viruses look more like machines than biological entities. Are there any theories to how these viruses evolved?


I found a book chapter for you here

Quick summary: 3 hypotheses to Origin of viruses

  1. From pre-cellular world (virus first hypothesis)
  2. From reductive evolution of parasites (reduction hypothesis)
  3. From fragments of cellular genetic material (escape hypothesis)

Drawbacks:

  1. virus require cells (to infect) so how can they come first
  2. virus do not look like known reduced parasites from Bacteria/Eukarya/Archaea
  3. unlikely that genetic fragments form complex viral structures for viral function

Because of these drawbacks, the problem of virus origin was for a long time considered untractable and not worth serious consideration

The rest of the chapter looks more in-depth into the 3 hypotheses


The Discovery of Viruses

By the late nineteenth century, the work of Louis Pasteur (1822-1895) and other scientists had established the germ theory of disease and identified the bacteria that caused many ailments.

But they found that some diseases were caused by invisible agents that could not be filtered out, agents that came to be called viruses. The experiments by Martinus Beijerinck (1851-1931) and Dmitri Ivanovsky on the tobacco mosaic virus in the 1890s are generally thought of as the beginning of the science of virology, but it was not until 40 years later that viruses could be isolated with extra-fine filters and imaged using electron microscopes.


What are viruses

A virus essentially is genetic information in a capsule. That’s the blandest explanation I could come up with, but it works. Are viruses alive? The current consensus is that they are somewhere in between. They are not alive because they lack several properties of life, such as cellular organelles or metabolism, yet viruses are not non-living either, as they do share some life-like properties. For example, replication and evolution.

Evolution has lead to a large diversity of viruses around us. Don’t be alarmed, though. We tend to think about viruses as something bad, yet, the majority of them are harmless to us. For example, most viruses of other animals can’t hurt us. We can’t catch FIV (the cat equivalent of HIV) and we are completely out of reach of viruses that infect plants. But there is more. There are also viruses that infect bacteria, and, hell yeah, there are viruses that infect other viruses.

Evolution has lead to a large diversity in the viral world. Illustration by iimages.

In our immediate interest, of course, are viruses that infect humans. Equally interesting are also ones that infect other animals but potentially could evolve an ability to infect us.

You probably have heard that current coronavirus SARS-CoV-2 originally comes from bats after an evolutionary change that allowed it to infect us, as well. Evolution is also the reason why flu comes to us in a new shape each season or why HIV is now becoming resistant to previously established treatments. So, the question is how this happens.


Are viruses alive?

What does it mean to be &lsquoalive&rsquo? At a basic level, viruses are proteins and genetic material that survive and replicate within their environment, inside another life form. In the absence of their host, viruses are unable to replicate and many are unable to survive for long in the extracellular environment. Therefore, if they cannot survive independently, can they be defined as being &lsquoalive&rsquo?

Taking opposing views, two microbiologists discuss how viruses fit with the concept of being &lsquoalive&rsquo and how they should be defined.

No, viruses are not alive

NIGEL BROWN

In many ways whether viruses are living or non-living entities is a moot philosophical point. There can be few organisms other than humans that have caused such devastation of human, animal and plant life. Smallpox, polio, rinderpest and foot-and-mouth viruses are all well-known for their disastrous effect on humans and animals. Less well known is the huge number of plant viruses that can cause total failure of staple crops.

In teaching about simple viruses, I use the flippant definition of a virus as &lsquogift-wrapped nucleic acid&rsquo, whether that is DNA or RNA and whether it is double- or single-stranded. The gift-wrapping is virtually always a virus-encoded protein capsid and may or may not also include a lipid coat from the host. The viral nucleic acid is replicated and the viral proteins synthesised using the host cell&rsquos processes. In many cases the virus also encodes some of the enzymes required for its replication, a well-known example being reverse transcriptase in RNA viruses.

Over the last 15 years or so, giant viruses found in amoebae have complicated our picture of viruses as simple non-living structures. Mimiviruses and megaviruses can contain more genes than a simple bacterium and may encode genes for information storage and processing. Genes common to the domains Archaea, Bacteria and Eukarya can be found in different giant viruses, and some researchers argue on this basis that they constitute a fourth domain of life.

However, a crucial point is that viruses are not capable of independent replication. They have to replicate within a host cell and they use or usurp the host cell machinery for this. They do not contain the full range of required metabolic processes and are dependent on their host to provide many of the requirements for their replication. To my mind there is a crucial difference between viruses and other obligate intracellular parasites, such as bacteria namely, viruses have to utilise the host metabolic and replication machinery. Intracellular bacteria may merely use the host as the environment in which they can supplement their limited metabolic capacity and they usually have their own replication machinery. Organisms such as Chlamydia spp. have not yet been grown outside cell culture but they carry their own transcriptional and translational machinery and fall into the evolutionary kingdom of Bacteria. Like many other &lsquodifficult&rsquo pathogenic bacteria, we may eventually be able to grow them in cell-free systems.

Caetano-Anollés and colleagues examined the phylogenomic relationships of viruses to living organisms through analysis of viral proteomes and assigned protein fold superfamilies. The authors concluded that viruses originated in &lsquoproto-virocells&rsquo that were cellular in nature and they implied that viruses and modern bacteria evolved from common ancestors. They further claim that this means that viruses are indeed living organisms.

This is not an argument I am comfortable with. If a virus is alive, should we not also consider a DNA molecule to be alive? Plasmids can transfer as conjugative molecules, or be passively transferred, between cells, and they may carry genes obtained from the host. They are simply DNA molecules, although they may be essential for the host&rsquos survival in certain environments. What about prions? The argument reductio ad absurdum is that any biologically produced mineral that can act as a crystallisation seed for further mineralisation (hence meeting the criterion of reproducibility) might also be classified as living!

The explicit sexism apart contained in the wording, I can do no better than to quote Dr Kenneth Smith in the Preface to his classic book Viruses (Cambridge University Press, 1962): &ldquoAs to the question asked most frequently of all, &lsquoAre viruses living organisms?&rsquo, that must be left to the questioner himself to answer&rdquo. This questioner currently considers viruses to be non-living.

Yes, viruses are alive

DAVID BHELLA

The question of whether viruses can be considered to be alive, of course, hinges on one&rsquos definition of life. Where we draw the line between chemistry and life can seem a philosophical, or even theological argument. Most creation stories involve a deity that imbues inanimate matter with the &lsquospark of life&rsquo. From a scientific perspective, attempting to find a working definition for &lsquolife&rsquo seems to me to have little practical value, but it is fun to think about.

Arguments over the life/not life status of viruses are often rooted in evolutionary biology and theories of the origins of life. All cellular organisms can claim a direct lineage to a primordial cell or cells, a continuous chain of cell divisions along which the &lsquospark&rsquo has been passed. Are viruses able to claim a similar ancestry?

The contention that viruses have no place in the tree of life is often supported by the assertion that viruses do not have a comparable history &ndash viruses are polyphyletic. Viruses are at a terrible disadvantage in this comparison, however. We are aware of only a tiny fraction of the total genetic diversity of viruses. Moreover, their genomes evolve far more rapidly than cellular organisms. So, from the small islands of sequence data we have, it is hard to argue that a coherent phylogeny does or does not exist. Interestingly, conservation of folds in viral proteins has begun to highlight possible common ancestries that could never be inferred from genome sequence data. A striking example is domain duplication of the beta jelly roll motif which gives rise to the pseudo-sixfold symmetry of trimeric hexon capsomeres in adenovirus. This is also found in viruses that infect insects, Gram-positive and Gram-negative bacteria and extremophile archaea. Viruses assemble their capsids from surprisingly few distinct protein folds, such that convergent evolution seems highly implausible.

HUMAN ADENOVIRUS TYPE 5 (LEFT &ndash EM DATABANK 1579) AND SULFOLOBUS TURRETED ICOSAHEDRAL VIRUS 2 (RIGHT &ndash EM DATABANK 1679) ASSEMBLE THEIR CAPSIDS FROM TRIMERIC CAPSOMERES IN WHICH EACH PROTOMER COMPRISES A DOMAIN DUPLICATION OF THE BETA JELLY ROLL FOLD. THIS ALLOWS EACH TRIMER TO PACK WITH PSEUDO-SIXFOLD SYMMETRY &ndash THE GEOMETRIC CAGE INDICATES THE POSITIONS OF THE LOCAL SIX-FOLD SYMMETRY IN THE ICOSAHEDRAL CAPSID STRUCTURE. THIS HIGHLY CONSERVED FEATURE HAS LED TO THE PROPOSAL OF A COMMON VIRAL LINEAGE FOR THESE VIRUSES THAT INFECT EUKARYOTES AND ARCHAEA, RESPECTIVELY.

A recent study has investigated viral origins by analysis of the evolution and conservation of protein folds in the structural classification of proteins (SCOP) database. This work identified a subset of proteins that are unique to viruses. The authors conclude that viruses most likely originated from early RNA-containing cells. If viruses made an evolutionary leap away from the cellular form, casting off its weighty metabolic shackles to opt for a more streamlined existence, did they cease to be life? Have they reverted to mere chemistry?

Viruses are genetically simple organisms the smallest viral genomes are only 2&ndash3 kbp while the largest are

1.2 Mbp &ndash comparable in size to the genome of Rickettsia. They all have surprisingly complex replication (life) cycles, however they are exquisitely adapted to deliver their genomes to the site of replication and have precisely regulated cascades of gene expression. Viruses also engineer their environment, constructing organelles within which they may safely replicate, a feature they share with other intracellular parasites.

While a virion is biologically inert and may be considered &lsquodead&rsquo in the same way that a bacterial spore or a seed is, once delivered to the appropriate environment, I believe that viruses are very much alive.

Fundamental to the argument that viruses are not alive is the suggestion that metabolism and self-sustaining replication are key definitions of life. Viruses are not able to replicate without the metabolic machinery of the cell. No organism is entirely self-supporting, however &ndash life is absolutely interdependent. There are many examples of obligate intracellular organisms, prokaryote and eukaryote that are critically dependent on the metabolic activities of their host cells. Humans likewise depend on the metabolic activity of nitrogen-fixing bacteria and photosynthetic plants along with that of our microbiota. There are very few (if any) forms of life on Earth that could survive in a world in which all chemical requirements were present but no other life.

So, what does define life? Some have argued that the possession of ribosomes is a key ingredient. Perhaps the most satisfying definition, that explicitly excludes viruses, emerges from the &lsquometabolism first&rsquo model and concerns the presence of membrane-associated metabolic activity &ndash a tangible &lsquospark&rsquo of life. This draws a neat distinction between viruses and obligate intracellular parasites such as Chlamydia and Rickettsia. This definition also confers the status of life on mitochondria and plastids, however. The endosymbiosis that led to mitochondria is thought to have given rise to eukaryotic life. Mitochondria have metabolic activity on which we depend, they have machinery to manufacture proteins and they have genomes. Most would accept that mitochondria are part of a life form, but they are not independent life.

I would argue that the only satisfactory definition of life therefore lies in the most critical property of genetic heredity: independent evolution. Life is the manifestation of a coherent collection of genes that are competent to replicate within the niche in which they evolve(d). Viruses fulfil this definition.

It is estimated that there are 10 31 virus particles in the oceans &ndash they vastly outnumber all other organisms on the planet. Alive or not, viruses are doing rather well!

NIGEL BROWN
DAVID BHELLA

MRC-University of Glasgow Centre for Virus Research, Sir Michael Stoker Building, 464 Bearsden Road, Glasgow, UK
[email protected]

FURTHER READING

Bamford, D. H. & others (2002). Evolution of viral structure. Theor Popul Biol 61, 461&ndash470.

Boyer, M. & others (2010). Phylogenetic and phyletic studies of informational genes in genomes highlight existence of a 4 th domain of life including giant viruses. PLoS ONE 5, e15530. doi:10.1371/journal.pone.0015530.

Moreira, D. & López-García, P. (2009). Ten reasons to exclude viruses from the tree of life. Nat Rev Microbiol 7, 306&ndash311 and associated commentary.

Nasir, A. & Caetano-Anollés, G. (2015). A phylogenomic data-driven exploration of viral origins and evolution. Sci Adv, e1500527. doi:10.1126/sciadv.1500527.

Rybicki, E. P. (2014). A top ten list for economically-important plant viruses. Arch Virol. doi:10.1007/s00705-014-2295-9.

Scheid, P. (2015). Viruses in close associations with free-living amoebae. Parasitol Res 114, 3959&ndash3967. doi:10.1007/s00436-015-4731-5.

Image: Coloured transmission electron micrograph of a group of foot-and-mouth disease viruses. Power and Syred/Science Photo Library. Human adenovirus type 5 and sulfolobus turreted icosahedral virus 2. David Bhella..


We put this question to Cambridge University Researcher Ed Hutchinson.

In the case of flu, you've got the fact that flu will spread from organism to organism so although we're worried particularly about a human virus, or a virus of livestock as well, it actually starts off as a virus in waterfowl. Things like ducks, where it's not really a pathogen at all - it just lives in there and gets along with them. That doesn't really tell you where a virus has come from. We know that they can spread from organism to organism.

In the first place viruses probably evolve as just bits of the genetic sequence which just get out of hand and start copying themselves, moving to places they shouldn't and acquiring more and more abilities along the way. There are quite a few examples of this where thing start jumping around inside genomes eventually will get the ability to jump from cell to cell as well.

Chris - In the answer to what came first, chicken or the egg, the virus-cell situation has to be the cell came first, the virus came later?

Ed - Remember, the defining feature of the virus is that it's absolutely dependent on taking over a cell to work. Without a cell the virus isn't going to do anything at all.


Viruses revealed to be a major driver of human evolution

The constant battle between pathogens and their hosts has long been recognized as a key driver of evolution, but until now scientists have not had the tools to look at these patterns globally across species and genomes. In a new study, researchers apply big-data analysis to reveal the full extent of viruses' impact on the evolution of humans and other mammals.

Their findings suggest an astonishing 30 percent of all protein adaptations since humans' divergence with chimpanzees have been driven by viruses.

"When you have a pandemic or an epidemic at some point in evolution, the population that is targeted by the virus either adapts, or goes extinct. We knew that, but what really surprised us is the strength and clarity of the pattern we found," said David Enard, Ph.D., a postdoctoral fellow at Stanford University and the study's first author. "This is the first time that viruses have been shown to have such a strong impact on adaptation."

The study was recently published in the journal eLife and will be presented at The Allied Genetics Conference, a meeting hosted by the Genetics Society of America, on July 14.

Proteins perform a vast array of functions that keep our cells ticking. By revealing how small tweaks in protein shape and composition have helped humans and other mammals respond to viruses, the study could help researchers find new therapeutic leads against today's viral threats.

"We're learning which parts of the cell have been used to fight viruses in the past, presumably without detrimental effects on the organism," said the study's senior author, Dmitri Petrov, Ph.D., Michelle and Kevin Douglas Professor of Biology and Associate Chair of the Biology Department at Stanford. "That should give us an insight on the pressure points and help us find proteins to investigate for new therapies."

Previous research on the interactions between viruses and proteins has focused almost exclusively on individual proteins that are directly involved in the immune response -- the most logical place you would expect to find adaptations driven by viruses. This is the first study to take a global look at all types of proteins.

"The big advancement here is that it's not only very specialized immune proteins that adapt against viruses," said Enard. "Pretty much any type of protein that comes into contact with viruses can participate in the adaptation against viruses. It turns out that there is at least as much adaptation outside of the immune response as within it."

The team's first step was to identify all the proteins that are known to physically interact with viruses. After painstakingly reviewing tens of thousands of scientific abstracts, Enard culled the list to about 1,300 proteins of interest. His next step was to build big-data algorithms to scour genomic databases and compare the evolution of virus-interacting proteins to that of other proteins.

The results revealed that adaptations have occurred three times as frequently in virus-interacting proteins compared with other proteins.

"We're all interested in how it is that we and other organisms have evolved, and in the pressures that made us what we are," said Petrov. "The discovery that this constant battle with viruses has shaped us in every aspect -- not just the few proteins that fight infections, but everything -- is profound. All organisms have been living with viruses for billions of years this work shows that those interactions have affected every part of the cell."

Viruses hijack nearly every function of a host organism's cells in order to replicate and spread, so it makes sense that they would drive the evolution of the cellular machinery to a greater extent than other evolutionary pressures such as predation or environmental conditions. The study sheds light on some longstanding biological mysteries, such as why closely-related species have evolved different machinery to perform identical cellular functions, like DNA replication or the production of membranes. Researchers previously did not know what evolutionary force could have caused such changes. "This paper is the first with data that is large enough and clean enough to explain a lot of these puzzles in one fell swoop," said Petrov.

The team is now using the findings to dig deeper into past viral epidemics, hoping for insights to help fight disease today. For example, HIV-like viruses have swept through the populations of our ancestors as well as other animal species at multiple points throughout evolutionary history. Looking at the effects of such viruses on specific populations could yield a new understanding of our constant war with viruses -- and how we might win the next big battle.


Contents

Despite his other successes, Louis Pasteur (1822–1895) was unable to find a causative agent for rabies and speculated about a pathogen too small to be detected using a microscope. [1] In 1884, the French microbiologist Charles Chamberland (1851–1931) invented a filter – known today as the Chamberland filter – that had pores smaller than bacteria. Thus, he could pass a solution containing bacteria through the filter and completely remove them from the solution. [2]

In 1876, Adolf Mayer, who directed the Agricultural Experimental Station in Wageningen, was the first to show that what he called "Tobacco Mosaic Disease" was infectious. He thought that it was caused by either a toxin or a very small bacterium. Later, in 1892, the Russian biologist Dmitry Ivanovsky (1864–1920) used a Chamberland filter to study what is now known as the tobacco mosaic virus. His experiments showed that crushed leaf extracts from infected tobacco plants remain infectious after filtration. Ivanovsky suggested the infection might be caused by a toxin produced by bacteria, but did not pursue the idea. [3]

In 1898, the Dutch microbiologist Martinus Beijerinck (1851–1931), a microbiology teacher at the Agricultural School in Wageningen repeated experiments by Adolf Mayer and became convinced that filtrate contained a new form of infectious agent. [4] He observed that the agent multiplied only in cells that were dividing and he called it a contagium vivum fluidum (soluble living germ) and re-introduced the word virus. [3] Beijerinck maintained that viruses were liquid in nature, a theory later discredited by the American biochemist and virologist Wendell Meredith Stanley (1904–1971), who proved that they were in fact, particles. [3] In the same year, 1898, Friedrich Loeffler (1852–1915) and Paul Frosch (1860–1928) passed the first animal virus through a similar filter and discovered the cause of foot-and-mouth disease. [5]

The first human virus to be identified was the yellow fever virus. [6] In 1881, Carlos Finlay (1833–1915), a Cuban physician, first conducted and published research that indicated that mosquitoes were carrying the cause of yellow fever, [7] a theory proved in 1900 by commission headed by Walter Reed (1851–1902). During 1901 and 1902, William Crawford Gorgas (1854–1920) organised the destruction of the mosquitoes' breeding habitats in Cuba, which dramatically reduced the prevalence of the disease. [8] Gorgas later organised the elimination of the mosquitoes from Panama, which allowed the Panama Canal to be opened in 1914. [9] The virus was finally isolated by Max Theiler (1899–1972) in 1932 who went on to develop a successful vaccine. [10]

By 1928 enough was known about viruses to enable the publication of Filterable Viruses, a collection of essays covering all known viruses edited by Thomas Milton Rivers (1888–1962). Rivers, a survivor of typhoid fever contracted at the age of twelve, went on to have a distinguished career in virology. In 1926, he was invited to speak at a meeting organised by the Society of American Bacteriology where he said for the first time, "Viruses appear to be obligate parasites in the sense that their reproduction is dependent on living cells." [11]

The notion that viruses were particles was not considered unnatural and fitted in nicely with the germ theory. It is assumed that Dr. J. Buist of Edinburgh was the first person to see virus particles in 1886, when he reported seeing "micrococci" in vaccine lymph, though he had probably observed clumps of vaccinia. [12] In the years that followed, as optical microscopes were improved "inclusion bodies" were seen in many virus-infected cells, but these aggregates of virus particles were still too small to reveal any detailed structure. It was not until the invention of the electron microscope in 1931 by the German engineers Ernst Ruska (1906–1988) and Max Knoll (1887–1969), [13] that virus particles, especially bacteriophages, were shown to have complex structures. The sizes of viruses determined using this new microscope fitted in well with those estimated by filtration experiments. Viruses were expected to be small, but the range of sizes came as a surprise. Some were only a little smaller than the smallest known bacteria, and the smaller viruses were of similar sizes to complex organic molecules. [14]

In 1935, Wendell Stanley examined the tobacco mosaic virus and found it was mostly made of protein. [15] In 1939, Stanley and Max Lauffer (1914) separated the virus into protein and nucleic acid, [16] which was shown by Stanley's postdoctoral fellow Hubert S. Loring to be specifically RNA. [17] The discovery of RNA in the particles was important because in 1928, Fred Griffith (c.1879–1941) provided the first evidence that its "cousin", DNA, formed genes. [18]

In Pasteur's day, and for many years after his death, the word "virus" was used to describe any cause of infectious disease. Many bacteriologists soon discovered the cause of numerous infections. However, some infections remained, many of them horrendous, for which no bacterial cause could be found. These agents were invisible and could only be grown in living animals. The discovery of viruses paved the way to understanding these mysterious infections. And, although Koch's postulates could not be fulfilled for many of these infections, this did not stop the pioneer virologists from looking for viruses in infections for which no other cause could be found. [19]

Discovery Edit

Bacteriophages are the viruses that infect and replicate in bacteria. They were discovered in the early 20th century, by the English bacteriologist Frederick Twort (1877–1950). [20] But before this time, in 1896, the bacteriologist Ernest Hanbury Hankin (1865–1939) reported that something in the waters of the River Ganges could kill Vibrio cholerae – the cause of cholera. The agent in the water could be passed through filters that remove bacteria but was destroyed by boiling. [21] Twort discovered the action of bacteriophages on staphylococci bacteria. He noticed that when grown on nutrient agar some colonies of the bacteria became watery or "glassy". He collected some of these watery colonies and passed them through a Chamberland filter to remove the bacteria and discovered that when the filtrate was added to fresh cultures of bacteria, they in turn became watery. [20] He proposed that the agent might be "an amoeba, an ultramicroscopic virus, a living protoplasm, or an enzyme with the power of growth". [21]

Félix d'Herelle (1873–1949) was a mainly self-taught French-Canadian microbiologist. In 1917 he discovered that "an invisible antagonist", when added to bacteria on agar, would produce areas of dead bacteria. [20] The antagonist, now known to be a bacteriophage, could pass through a Chamberland filter. He accurately diluted a suspension of these viruses and discovered that the highest dilutions (lowest virus concentrations), rather than killing all the bacteria, formed discrete areas of dead organisms. Counting these areas and multiplying by the dilution factor allowed him to calculate the number of viruses in the original suspension. [22] He realised that he had discovered a new form of virus and later coined the term "bacteriophage". [23] [24] Between 1918 and 1921 d'Herelle discovered different types of bacteriophages that could infect several other species of bacteria including Vibrio cholerae. [25] Bacteriophages were heralded as a potential treatment for diseases such as typhoid and cholera, but their promise was forgotten with the development of penicillin. [23] Since the early 1970s, bacteria have continued to develop resistance to antibiotics such as penicillin, and this has led to a renewed interest in the use of bacteriophages to treat serious infections. [26]

Early research 1920–1940 Edit

D'Herelle travelled widely to promote the use of bacteriophages in the treatment of bacterial infections. In 1928, he became professor of biology at Yale and founded several research institutes. [27] He was convinced that bacteriophages were viruses despite opposition from established bacteriologists such as the Nobel Prize winner Jules Bordet (1870–1961). Bordet argued that bacteriophages were not viruses but just enzymes released from "lysogenic" bacteria. He said "the invisible world of d'Herelle does not exist". [28] But in the 1930s, the proof that bacteriophages were viruses was provided by Christopher Andrewes (1896–1988) and others. They showed that these viruses differed in size and in their chemical and serological properties. In 1940, the first electron micrograph of a bacteriophage was published and this silenced sceptics who had argued that bacteriophages were relatively simple enzymes and not viruses. [29] Numerous other types of bacteriophages were quickly discovered and were shown to infect bacteria wherever they are found. Early research was interrupted by World War II. d'Herelle, despite his Canadian citizenship, was interned by the Vichy Government until the end of the war. [30]

Modern era Edit

Knowledge of bacteriophages increased in the 1940s following the formation of the Phage Group by scientists throughout the US. Among the members were Max Delbrück (1906–1981) who founded a course on bacteriophages at Cold Spring Harbor Laboratory. [26] Other key members of the Phage Group included Salvador Luria (1912–1991) and Alfred Hershey (1908–1997). During the 1950s, Hershey and Chase made important discoveries on the replication of DNA during their studies on a bacteriophage called T2. Together with Delbruck they were jointly awarded the 1969 Nobel Prize in Physiology or Medicine "for their discoveries concerning the replication mechanism and the genetic structure of viruses". [31] Since then, the study of bacteriophages has provided insights into the switching on and off of genes, and a useful mechanism for introducing foreign genes into bacteria and many other fundamental mechanisms of molecular biology. [32]

In 1882, Adolf Mayer (1843–1942) described a condition of tobacco plants, which he called "mosaic disease" ("mozaïkziekte"). The diseased plants had variegated leaves that were mottled. [33] He excluded the possibility of a fungal infection and could not detect any bacterium and speculated that a "soluble, enzyme-like infectious principle was involved". [34] He did not pursue his idea any further, and it was the filtration experiments of Ivanovsky and Beijerinck that suggested the cause was a previously unrecognised infectious agent. After tobacco mosaic was recognized as a virus disease, virus infections of many other plants were discovered. [34]

The importance of tobacco mosaic virus in the history of viruses cannot be overstated. It was the first virus to be discovered, and the first to be crystallised and its structure shown in detail. The first X-ray diffraction pictures of the crystallised virus were obtained by Bernal and Fankuchen in 1941. On the basis of her pictures, Rosalind Franklin discovered the full structure of the virus in 1955. [35] In the same year, Heinz Fraenkel-Conrat and Robley Williams showed that purified tobacco mosaic virus RNA and its coat protein can assemble by themselves to form functional viruses, suggesting that this simple mechanism was probably the means through which viruses were created within their host cells. [36]

By 1935, many plant diseases were thought to be caused by viruses. In 1922, John Kunkel Small (1869–1938) discovered that insects could act as vectors and transmit virus to plants. In the following decade many diseases of plants were shown to be caused by viruses that were carried by insects and in 1939, Francis Holmes, a pioneer in plant virology, [37] described 129 viruses that caused disease of plants. [38] Modern, intensive agriculture provides a rich environment for many plant viruses. In 1948, in Kansas, US, 7% of the wheat crop was destroyed by wheat streak mosaic virus. The virus was spread by mites called Aceria tulipae. [39]

In 1970, the Russian plant virologist Joseph Atabekov discovered that many plant viruses only infect a single species of host plant. [37] The International Committee on Taxonomy of Viruses now recognises over 900 plant viruses. [40]

By the end of the 19th century, viruses were defined in terms of their infectivity, their ability to be filtered, and their requirement for living hosts. Up until this time, viruses had only been grown in plants and animals, but in 1906, Ross Granville Harrison (1870–1959) invented a method for growing tissue in lymph, [41] and, in 1913, E Steinhardt, C Israeli, and RA Lambert used this method to grow vaccinia virus in fragments of guinea pig corneal tissue. [42] In 1928, HB and MC Maitland grew vaccinia virus in suspensions of minced hens' kidneys. [43] Their method was not widely adopted until the 1950s, when poliovirus was grown on a large scale for vaccine production. [44] In 1941–42, George Hirst (1909–94) developed assays based on haemagglutination to quantify a wide range of viruses as well as virus-specific antibodies in serum. [45] [46]

Influenza Edit

Although the influenza virus that caused the 1918–1919 influenza pandemic was not discovered until the 1930s, the descriptions of the disease and subsequent research has proved it was to blame. [47] The pandemic killed 40–50 million people in less than a year, [48] but the proof that it was caused by a virus was not obtained until 1933. [49] Haemophilus influenzae is an opportunistic bacterium which commonly follows influenza infections this led the eminent German bacteriologist Richard Pfeiffer (1858–1945) to incorrectly conclude that this bacterium was the cause of influenza. [50] A major breakthrough came in 1931, when the American pathologist Ernest William Goodpasture grew influenza and several other viruses in fertilised chickens' eggs. [51] Hirst identified an enzymic activity associated with the virus particle, later characterised as the neuraminidase, the first demonstration that viruses could contain enzymes. Frank Macfarlane Burnet showed in the early 1950s that the virus recombines at high frequencies, and Hirst later deduced that it has a segmented genome. [52]

Poliomyelitis Edit

In 1949, John F. Enders (1897–1985) Thomas Weller (1915–2008), and Frederick Robbins (1916–2003) grew polio virus for the first time in cultured human embryo cells, the first virus to be grown without using solid animal tissue or eggs. Infections by poliovirus most often cause the mildest of symptoms. This was not known until the virus was isolated in cultured cells and many people were shown to have had mild infections that did not lead to poliomyelitis. But, unlike other viral infections, the incidence of polio – the rarer severe form of the infection – increased in the 20th century and reached a peak around 1952. The invention of a cell culture system for growing the virus enabled Jonas Salk (1914–1995) to make an effective polio vaccine. [53]

Epstein–Barr virus Edit

Denis Parsons Burkitt (1911–1993) was born in Enniskillen, County Fermanagh, Ireland. He was the first to describe a type of cancer that now bears his name Burkitt's lymphoma. This type of cancer was endemic in equatorial Africa and was the commonest malignancy of children in the early 1960s. [54] In an attempt to find a cause for the cancer, Burkitt sent cells from the tumour to Anthony Epstein (b. 1921) a British virologist, who along with Yvonne Barr and Bert Achong (1928–1996), and after many failures, discovered viruses that resembled herpes virus in the fluid that surrounded the cells. The virus was later shown to be a previously unrecognised herpes virus, which is now called Epstein–Barr virus. [55] Surprisingly, Epstein–Barr virus is a very common but relatively mild infection of Europeans. Why it can cause such a devastating illness in Africans is not fully understood, but reduced immunity to virus caused by malaria might be to blame. [56] Epstein–Barr virus is important in the history of viruses for being the first virus shown to cause cancer in humans. [57]

Late 20th and early 21st century Edit

The second half of the 20th century was the golden age of virus discovery and most of the 2,000 recognised species of animal, plant, and bacterial viruses were discovered during these years. [58] [59] In 1946, bovine virus diarrhea was discovered, [60] which is still possibly the most common pathogen of cattle throughout the world [61] and in 1957, equine arterivirus was discovered. [62] In the 1950s, improvements in virus isolation and detection methods resulted in the discovery of several important human viruses including varicella zoster virus, [63] the paramyxoviruses, [64] – which include measles virus, [65] and respiratory syncytial virus [64] – and the rhinoviruses that cause the common cold. [66] In the 1960s more viruses were discovered. In 1963, the hepatitis B virus was discovered by Baruch Blumberg (b. 1925). [67] Reverse transcriptase, the key enzyme that retroviruses use to translate their RNA into DNA, was first described in 1970, independently by Howard Temin and David Baltimore (b. 1938). [68] This was important to the development of antiviral drugs – a key turning-point in the history of viral infections. [69] In 1983, Luc Montagnier (b. 1932) and his team at the Pasteur Institute in France first isolated the retrovirus now called HIV. [70] In 1989 Michael Houghton's team at Chiron Corporation discovered hepatitis C. [71] New viruses and strains of viruses were discovered in every decade of the second half of the 20th century. These discoveries have continued in the 21st century as new viral diseases such as SARS [72] and nipah virus [73] have emerged. Despite scientists' achievements over the past one hundred years, viruses continue to pose new threats and challenges. [74]


The Institute for Creation Research

Viruses have a bad reputation. They are ultra-tiny, well-designed machines that copy themselves in a process that sometimes causes disease in the organisms in which they reside. One class called retroviruses is equipped with machinery that splices its own viral code into the DNA of a host cell.

Retroviruses have been portrayed as genetic "leftovers" from an evolutionary past, but how did they really originate?

A report published in Science showed how one retrovirus was "born." Researchers discovered that a retrovirus named XMRV was formed when two DNA sequences called "proviruses" were brought together through "recombination." 1 This occurs during gamete development when genetic material from the parent cells is rearranged into new combinations of genes in the offspring, resulting in more genetic variations.

The study authors wrote, "We conclude that XMRV was generated as a result of a unique recombination event." 1

Could other—or perhaps all—viruses have entered the world by recombining unique DNA sequences that were already present in animal genomes? Perhaps God made viruses during the creation week as integral parts of plants and animals.

If so, He certainly did not form them to cause disease. At the end of that week, He declared His works "very good." 2 But like many other created features, their original purpose was warped because of "the bondage of corruption" brought about by mankind’s sin. 3 For example, God made sharp teeth to equip animals to eat vegetation, but many have long since abandoned herbivory and become carnivores. 4

It is possible that God made viruses as tiny robots to carry life-enhancing genetic information from one cell to another. 5 At some point after the Fall, the once-balanced cell-virus interactions would have begun to falter and fail.

Another implication of this research concerns evolutionary claims regarding human-chimpanzee ancestry. Both species appear to share certain retrovirus-like DNA sequences. These have been assumed by evolutionists to have originated from a retroviral infection of the ancestral population that supposedly gave rise to both chimpanzees and humans. 6

This assumption, however, ignores the fact that in the supposed six million years since the species diverged, the useless retroviral DNA would have mutated beyond recognition. It also presumes that the virus came first. The Science study demonstrated that the animal DNA came first and brought forth a retrovirus.

The finding also implies that the "provirus" DNA sequences that combined to become a retrovirus were situated on the chromosome right where they could be joined by the precise cellular machinations that perform recombination. Thus, what appears to be shared retrovirus infections in chimps and humans could have come from "proviruses" in their genomes—created for originally good and similar purposes—that were later activated by recombination.

This study is consistent with the idea that retroviruses, and even the retroviral-like DNA sequences found in genomes, began as created genetic features and were not the products of evolution.

  1. Paprotka, T. et al. 2011. Recombinant Origin of the Retrovirus XMRV. Science. 333 (6038): 97-101. . .
  2. Criswell, D. 2009. Predation Did Not Come from Evolution. Acts & Facts. 38 (3): 9.
  3. Indeed, viral machinery is exploited by man for gene therapy. If man can use viruses to accomplish a good purpose, then so can God.
  4. Thomas, B. 2010. Evolution's Best Argument Has Become Its Worst Nightmare. Acts & Facts. 39 (3): 16-17.

* Mr. Thomas is Science Writer at the Institute for Creation Research.


How do viruses multiply?

Due to their simple structure, viruses cannot move or even reproduce without the help of an unwitting host cell. But when it finds a host, a virus can multiply and spread rapidly.

To identify the correct host, viruses have evolved receptors on their surfaces that match up with those of their ideal target cell, letting the virus get its genetic material inside and hijack its host's cellular machinery to help it reproduce by multiplying the virus' genetic material and proteins.

Using that strategy, the minute marauders have flourished and evolved in step with their hosts. By one estimate, at least 320,000 different viruses can infect mammals alone, and even this massive number may be on the low side. This viral army can cause symptoms as mild as a cough or as deadly as internal bleeding. Some viruses may even cause the runaway cellular growth that is the root of cancer, as is thought to be the case with human papillomavirus and cervical cancer.


Isn’t That Evolution?

It is important to recognize that biologists use several distinct definitions for evolution that are often blurred together as if they are synonymous.13 Evolution is sometimes defined as “change in the genetic makeup (or gene frequency) of a population over time.” This has been observed both creationists and evolutionists recognize this as important in building models to help us understand what likely happened in the past. A second definition of evolution involves the idea that all life descended from a common ancestor over millions of years through naturalistic processes. This has not been observed. In fact, it is in direct opposition to the testimony God (the eyewitness to creation) gives us in the Bible. The idea that all life has a common ancestor requires the assumption that the Bible’s history is false, and the assumption that changes which do occur could produce the variety of life we see today from a single-celled ancestor.14

With regard to the first definition of evolution, creationists and evolutionists differ in the pattern of genetic changes they should expect to see. The creation model predicts that degenerative changes can occur because mankind sinned and brought death into the world ( Genesis 3 ). It also predicts that adaptive changes could occur because God cares for His creation and intends for the earth to be inhabited ( Psalm 147:8–9 Isaiah 45:18 Matthew 6:25–34 ). Both types of changes have been observed. The fact that some foxes are adapted to live in the arctic while others are adapted to live in the desert fits perfectly with this biblical teaching. While evolutionists accept that these types of changes occur, their model requires that most genetic changes add information to the genome. This pattern has not been observed. Without this pattern, they cannot account for the many organs and complex biochemical pathways that exist in animals today.15 Scientific observations show that there is an overall pattern of decay seen in the genome, which is the opposite of what the evolutionary model would predict.16

Another difference is the source of the genetic change. Evolutionists assume that random mutations and natural selection can account for the genetic changes that are seen. Since the underlying mechanism is naturalistic, changes were expected to be very slow. Contrary to their expectations, rapid adaptation has been observed,17 and evolutionists have had to adjust their thinking to accept this. Furthermore, detailed studies of the pattern in genetic differences within related animals don’t make sense if mutations are assumed to always be essentially random events.18 Something else is clearly going on here. It appears that God has placed some incredible programming into the genomes of the animals He created, and viruses may play some role in this.


Scouring the skies

To track the invisible microbial highways in the sky &mdash and find out how many viral passengers they carried &mdash the authors of the new study ascended platforms in Spain's Sierra Nevada Mountains, and collected samples from the atmosphere at altitudes of about 9,840 feet (3,000 m) above sea level, scooping up free-floating microbes and those attached to airborne dust and water vapor.

When the scientists separated and analyzed the microbial hitchhikers, they found that not only were billions of microbes showering Earth's surface on a daily basis, but that viruses could be up to 461 times more abundant than bacteria. In the samples, viruses were attached to more of the organic, lighter particles than bacteria were, hinting that viruses could stay airborne longer and thereby travel greater distances, the study authors reported.

Their findings also answer a long-standing mystery as to why genetically similar virus populations could be found in areas that are separated by great distances, a discovery that dates to decades ago, Suttle said in the statement.

"Roughly 20 years ago we began finding genetically similar viruses occurring in very different environments around the globe. This preponderance of long-residence viruses travelling the atmosphere likely explains why," he said.

"It's quite conceivable to have a virus swept up into the atmosphere on one continent and deposited on another," he said.

The findings were published online Jan. 29 in the Multidisciplinary Journal of Microbial Ecology.