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April 1, 2020
April 8, 5020 U
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World War III: War of the Clones
BACKGROUND FACTS
TIME TRAVEL
Part 4.
Excerpts from the book:
"VIRUSES"'
by Arnold J. Levine,
published by
Scientific American Library,
New York: 1992.
Year: 1900
US Army isolates a
Human Virus for study
Year: 1950
US Designs Lethal Virus
to Selectively Kill
a Race of Rabbits
* * * *
BACKGROUND
[p. 171-172]
A good case has been made that the earliest life forms on Earth used RNA polymers both to store information in the nucleotide sequence and to catalyze chemical reactions.
Studies over the past few years have shown that, under the right conditions, RNA polymers can replicate and even cut themselves into pieces of defined sizes.
RNA is a very reactive polymer, but this very property makes it poorly suited to store information.
If your goal were to store information stably, whether on a computer tape or in a polymer, we would not want all sorts of chemical reactions to occur over the length of our tape that might alter the information stored there.
For a variety of chemical reasons, DNA is much less reactive than RNA and therefore is better suited to serve as an inert storage molecule. Most living organisms, accordingly, use RNA to carry the messages for protein production, but not to store their genomic information.
Since RNA has greater reactivity than DNA, RNA viruses evolve more rapidly than do DNA viruses. The source of RNA's higher mutation rate can be seen by comparing the duplication of RNA with that of DNA. As the enzyme RNA replicase copies one strand of RNA into a complementary polymer, it averages one mistake per 10,000 nucleotides copied.
As DNA polymerase copies DNA into its complementary strand, it makes about one mistake in every million to ten million nucleotides. Part of this difference in accuracy is due to the reactivity of RNA and to the variable fidelity of the duplicating enzymes.
Another part reflects the fact that DNA polymerases have evolved the ability to correct mistakes in their synthesizing process.
. . . .
In effect DNA polymerases, but not RNA polymerases, have proofreading abilities. RNA genomes, therefore, retain more mistakes in their copies than do DNA genomes.
There is an additional reason that influenza A viruses evolve rapidly. All viruses, as we have seen, go through a very large number of duplication cycles in a short time. A single viral RNA genome may reproduce ten thousand copies of itself in six hours, while the generation time of the host for an influenza A virus is measures in years -- for humans, perhaps a quarter century.
Not only is the error frequency in the original RNA genome high, but the large number of generations yearly causes the progeny viruses to diverge rapidly. it has been estimated that 0.03 to 2 percent of the nucleotides in the genome of an RNA virus are altered every year.
EVOLVING FASTER THAN ANY OTHER LIVING ORGANISM
Some RNA viruses -- those whose polymerases have high error frequencies - are evolving much faster than any other living organism.
[p. 204]
HOW VIRUSES
CHANGE
Two major mechanisms act upon the genetic information of a virus (or any life form) to produce change: mutation and recombination. Mutation is a change in the sequence of the nucleotides in DNA (A, T, G, and C) or RNA (A, U, G, and C) polymers.
Recombination is the exchange and bringing together or new sequences of nucleotides, in new combinations, from two parental polynucleotide strands of DNA or RNA. Both processes generate diversity in all living organisms, which can then be tested for environmental advantages and replicative fitness in the real world.
Because viruses can encode the enzymes for their own replication and recombination, some viruses have a good deal of control over their mutation rates and frequencies of recombination.
[pp. 207-208]
YEAR 1900
FIRST HUMAN VIRUS
ISOLATED
BY
US ARMY
The yellow fever virus played a central role in the history of virology.
Walter Reed and the US Army Commission, in 1900, identified it as the first human virus to be isolated. Reed's team went on to prove that the virus was transmitted by mosquitoes and that eliminating the breeding grounds for these insects eliminated the disease.
Yellow fever is a zoonotic disease, which means that it has a major animal reservoir. In central Africa, where it is thought to have originated, wild nonhuman primates such as howler, owl, spider [monkeys], and squirrel monkeys are infected.
The virus replicates in many organs of their bodies and spends time in the bloodstream.
HOW MOSQUITOES TRANSMIT VIRUSES
The aedine mosquitoes, like Aedes africanus, breed and lay their eggs in tree holes; they feed in the forest canopy, taking blood meals from the monkeys to provide nutrients for their developing eggs. The virus is taken up with the monkey blood and replicates in the mosquito, principally in the cells of the gut.
When the mosquito bites again, the virus is in the saliva, which the insect regurgitates into the wound to prevent coagulation.
Thus the virus circulates from a primate host to an insect and replicates in both, even though they are very different types of animals.
[pp. 209-210]
US EXPERIMENT
IN THE YEAR 1950
LETHAL VIRUS
DESIGNED TO
SELECTIVELY KILL
The wild European rabbit was first introduced in Australia in 1859. It very rapidly spread over the southern half of the continent, where it became a major pest in agricultural and grazing areas.
The situation got so bad that, when other methods to keep the rabbit population under control failed, introduction of a lethal myxoma virus from the Americas was tried in 1950.
The virus was shown to be restricted to rabbit populations -- that was critical -- and was spread by a mosquito biting the host.
The original virus strain killed more than 99 percent of the infected animals, and the first few years after its introduction saw an enormous decline in the rabbit population.
The virus spread efficiently during the spring and summer, when mosquitoes were abundant, but the incidence and spread of disease were poor in each cold season because of the paucity of insects.
In some places the virus even died out over the winter because of the lack of infected rabbits and poor transmission; but on a continent-wide basis, the disease and the virus persisted.
During each winter, rabbits that were infected with the most virulent virus died, so this most lethal strain of myxoma virus was not efficiently delivered to mosquitoes the next spring.
By contrast, some mutations in the virus created less virulent strains, permitting its hosts longer life and a better chance to survive the winter: these rabbits were available in the spring for mosquitoes to bite, thereby transmitting the less lethal disease.
The requirement for survival over the winter months imposed a strong selection for a less lethal virus.
Attenuated strains appeared in the spring of the very first year after the introduction of the myxoma virus into Australia, and three of four years later they were dominant.
HERD IMMUNITY
Rabbit populations infected with this less virulent virus began to show herd immunity -- a phenomenon in which infection of a rabbit already immunized by previous exposure to a virus neutralizes that virus and lowers its probability of transmission to other animals, even if they are not immune. This accelerated the loss of the virulent strain, and the rabbit population resurged.
The rabbits that now bred were veterans of the initial exposure to the highly virulent myxoma virus. Among this group were rabbits that had survived because they were genetically resistant to the virus. The reasons for genetic resistance are complex (an unknown number of genes in specific combinations are thought to be involved), but such rabbits appeared quite rapidly.
Within seven years after the introduction of the most virulent myxoma strain, which killed 90 to 99 percent of rabbits in the field, the same virus reintroduced into a population of rabbits that was not immune -- a group with no previous exposure -- killed only 25 percent. The difference was due to genetic factors in the host rabbit that had been selected for and were present in most individuals seven years after selection began.
This experiment demonstrates that the most successful virus is one that can replicate many times in its host but is not recognized and causes little or no damage.
These requirements are difficult to achieve, however, and most viruses do not fall into this category.
[pp. 211-212]
VIRUSES GROWN
IN LABORATORIES
WORLDWIDE
Over the past thirty years [since 1992], vaccine production and testing have been carried out in cell culture, using tissue obtained from an organ -- say, a kidney -- placed in culture dishes to grow.
The African green monkey from Uganda is commonly used as a source of such cells, which are prepared at various laboratories around the world.
In 1967, twenty-five laboratory workers from three different locations . . . each processing monkey-kidney cell cultures, all contracted a similar disease: hemorrhagic fever.
The patient typically has a very high fever, rash, and swelling followed by an uncontrollable bleeding in the organs, skin, and mucous membranes. As these patients were admitted to hospitals, six attending medical personnel contracted the disease, indicating human-to-human spread of an infectious agent. Among these thirty-one cases, there were seven deaths.
A virus was isolated from the blood and tissues of these patients, and extensive tests showed that it was unrelated to any known virus.
The isolate caused a hemorrhagic-fever-like disease when inoculated into African green monkeys, and it was noted that several of the monkeys in a single shipment form Uganda had this hemorrhagic disease.
MARBURG VIRUS
CROSSED SPECIES
It seemed likely that a monkey virus had crossed species, becoming more virulent, and attacked these human hosts . . . now called Marburg virus.
The monkeys did not even have antibody against it, proving that these primates were not an animal reservoir for this virus.
. . . .
During this time, a closely related virus that also produced a hemorrhagic fever was detected. In 1976 in the Sudan and Zaire, an epidemic of about 550 cases occurred, with more than 430 deaths.
* *
MARBURG VIRUS
DEFEATED
HOST ANTIBODIES
BY
TRANSFORMING
INTO A NEW VIRUS
* *
MARBURG VIRUS
TRANSFORMED
INTO
EBOLA VIRUS
This new virus was isolated and named Ebola virus, after a small river in Zaire.
Electron micrographs showed it to be morphologically identical to Marburg virus, but antibodies made against it did not protect against Marburg virus: these isolates were related but distinct.
STEALTH VIRUSES
REPLICATE AND HIDE
BETWEEN
EPIDEMICS
Extensive tests of possible animal reservoirs have, to date, failed to find where the Ebola and Marburg viruses replicate and hide between epidemics.
[pp. 212-213]
CONCLUSIONS
What have we learned from these stories and observations? First, we have surely been taught that there are rules that govern life processes; try as we may, we cannot violate them.
All life forms are continually changing. Each generation brings new nucleotide sequences, information, and functions, and these are continuously tried out in various combinations in an ever-changing environment.
Some of these changes have been brought about by humanity within a remarkably short time frame, compared to the rates of biological change.
We have learned that all life processes follow the laws of chemistry and physics.
There is a difference, however, between events occurring in living organisms and those in the nonliving world. So long as an organism is capable of reproducing itself, rare events can be selected for and become the dominant form of life.
When a rare event that cannot be replicated happens in the nonliving universe, it often remains minor in the field of observation.
In contrast, a rare mutation that occurs in a virus only once in a million trials will, if it provides a replicative advantage, be selected for, and become, the virus of tomorrow.
If we change the environment, we change the field against which new viruses are selected -- in effect, we change the rules for selection, and new agents will certainly appear.
It has become clear that virus infections select the host that survives, just as we -- by altering the field -- select the virus that survives.
VIRUSES ARE PARASITES
We are what we are in part because we have survived the onslaught of our parasites. But the viruses we have studied have done more.
They have contributed some of their nucleotide sequences to our own genetic endowment. We carry and pass to each generation the vestiges of retroviruses, integrated in our chromosomes and possibly exercising a sustained impact upon our selection and survival.
Viruses
can be the conduit to move genetic information from one host to another.
Sometimes this results in diseases as dramatic as cancer, as with Rous
sarcoma virus and its oncogene; and sometimes this may contribute to an
organism's ability to survive, as seen in the T4 bacteriophage and its
eukaryotic-like genes.
That special relationship between host and parasite will continue to make human beings -- and all forms of life on Earth -- what we are and what we will be.
It is important for us to know the rules.