Viruses: A Summary of Lecture
by Dr. Arnold Levine
Aleta Sullivan and Karen Wickersham
There are three reasons to talk about viruses. First of all, they are very easy to study for evolution because they evolve so fast. Secondly, viruses are obligate parasites which shape their hosts dramatically. Finally, viruses should be studied because they are very interesting.
Taking a closer look at the speed of virus evolution, viruses have a very short generation time with in a cell, producing even 20-30 generations in a single day. As to viruses shaping their hosts, we simply have to look at how humans are shaped by parasitic load. Ninety percent of the Aztecs were killed by smallpox, and yellow fever ran rampant in the Americas after the slave trade began in Africa.
Viruses are defined as sub-microscopic, obligate intracellular parasites. They are called sub-microscopic because they cannot be seen with a light microscope. The largest virus is 0.2 mm in length, the size of a single ribosome. They are called obligate intracellular (degenerate) organisms because they must live within a cell to duplicate. Viruses are classified by size, shape and structure. For example, the pox virus is made of a brick shaped unit of double stranded DNA surrounded by a protein and carbohydrate capsid. DNA viruses are much more stable than RNA viruses. Vaccinations are possible for smallpox and polio because they are DNA viruses which evolve more slowly.
RNA viruses are less stable than those made with DNA. They change more rapidly and make more mistakes while replicating. It is thought that life arose as RNA, because it is more reactive. RNA's instability is due to its hydroxide group on the ribose. Lack of fidelity drives the mutation rate. During DNA replication, the normal rate of error is 1 per 100,000 in copying the genome. This gives each of us humans approximately 30 errors to pass on. However, correcting enzymes reduced this number. In DNA replication, correcting enzymes act like a "spell-check" on a computer, catching many of these mistakes before they can be passed on. There is no "spell check" in the RNA world; retroviruses make mistakes about 1 in 10,000 base pairs replicated.
Ivanovsky showed that viruses were smaller than bacteria. He used porcelain filters whose pores inhibited bacterial passage, but allowed passage of plaques. He thought something was wrong with his filter, but he published anyway, and others repeated his experiment hoping to disprove his findings. He and others proved that smaller units, viruses, passed through the filters.
Wendell Stanley (1935) crystallized the tobacco mosaic virus. Because he was able to force a virus into a crystalline structure, he thought it could not be alive. When he rehydrated the crystals, they functioned normally. Virus have symmetrical shapes. A good example of this is the adenovirus, an icosohedron made of equilateral triangle subunits. This provides two-fold rotational symmetry. This symmetry provides the strongest structure with the fewest subunits (also seen in geodesic dome buildings).
The introduction of European rabbits into Australia generated an interesting study in virus evolution. Rabbits were introduced to Australia to give hunters something to shoot. But, they multiplied so fast that they competed with the sheep for the available grass. There were too many rabbits to shoot. So scientists developed a pox virus called myxooma to kill the rabbits. They introduced the virus, which is carried by mosquitoes. In the first year after introduction, 90% of the rabbits were killed. In the second year, the virus killed another 90% of the remaining rabbits. But by the third year only 50% of the rabbits died. Each year those rabbits with the weak form of the virus survived the winter and reproduced the next spring. Seven years after the introduction of the virus, the rabbit population was back to its original size. When scientists reintroduced the virus by reinoculating rabbits, only 25% died because 75% had immunity to the virus. Resistance to the virus was selected in the rabbits.
Both viruses and hosts evolve over time. Human viruses can evolve from animal viruses, the more interesting coming from highly diverse and isolated rainforest animals. An example of a transmission sequence would be from a monkey, to a mosquito, to a human, to a different mosquito, and finally, to a new human. Some people believe that viruses may have evolved through degenerative evolution from human genetic information. DNA could have degraded into a small unit and replicated over and over. Therefore, following this hypothesis, new viruses could appear at any time.
The Influenza (flu) virus (an RNA virus) can cause two types of epidemics. The first type is a local epidemic. These occur every two to three years. They are driven by the high mutation rates of the viruses. Epidemics recur because the virus undergoes mutational changes in its protein coat where antibodies attach. The second type of epidemic is called a pandemic because it is world-wide. The flu virus is made of eight RNA chromosomes and surrounded by a protein coat of hemagglutinin which attaches the virus to a cell. To fight a virus, antibodies will change the hemoglutinin and prevent it from being able to attach to and invade cells. Flu replicates in ducks, pigs and several other animals, so sometimes the human and animal forms of the virus recombine to become a slightly different virus. Since no one has immunity to the new viral form, new virulent viruses may lead to world wide pandemics. Cohabitation with animals is a chief cause of these viral changes and subsequent epidemics. There were pandemics in 1908, 1900, 1918 (Spanish Flu), 1957 (Asian Flu), 1968 (Hong Kong Flu), and 1977 (Swine Flu).
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