Zella’s Fight: The Myxoma Virus
Andrea Rendel, Raven Hinton, Australia Gaither
Philander Smith College
Professor Bolden
Zella’s Fight: The Myxoma Virus
There are more than one million viruses found across the face of the Earth. Those same viruses could care less about who or what they infect, so long as they can continue to thrive within the host's body. Types of inhabitable hosts do not exclude the more adored organisms known to mankind, including ducklings, guppies, sugar gliders, pandas and the cutest of them all, bunny rabbits. While bunny rabbits are considered one of the cutest organisms ever, pesky viruses, like the Myxoma virus, still view them as acceptable hosts. Discovered first by Giuseppe Sanarelli in 1896 during a lab experiment, the Myxoma virus, also known as Myxomatosis, was initially introduced via field test in efforts to reduce the overpopulation of European rabbits ,however, at the time, the virus seemed ineffective. Several more tests were conducted in other parts of the world but with similar outcomes. Eventually, with the help of rainfall and perfect temperatures, the virus made its way into inland waters where it would then circulate to all parts of the world. With better living conditions, the Myxoma virus began to infect and soon posed a perpetual threat upon the existence of hares and rabbits in all nations and continues to do so even today. Before the first strain of myxoma began to take effect some time after, other strands of Myxoma were introduced such as Amoxomatous Myxomatosis which happens to spread through direct contact with an infected organism as opposed to actual inoculation. The Myxoma virus is associated with the Leporipoxvirus which happens to be a particular genus of a multitude of viruses. This particular virus could be compared to a seed from a Sweet Gumball tree but rather on a more microscopic level. Myxoma is mostly a non cancerous cyst-like tumor which happens to be filled with mucus and/or gelatinous content. By entering the organism through the bite of an infected arthropod such as a mosquito, tick, mite or some other insect and/or arachnid, the Myxoma virus leaves ulcers and tumors of many sizes on infected hosts body. The virus also affects the mucous membrane around the eyes of its victims. Death after infection is imminent as Myxomatosis does an exceptional job at deteriorating the internal organs of its host thus ceasing any chance of survival as there is no cure. Symptoms of this virus can be detected within the first 48 hours and once infected, all one can do is make the rabbit comfortable until it meets its fate with death three to four days later.
How does it infect?
While it is understood what the Myxoma virus is, understanding its means of infecting its host is just as important. When bitten by any infectious insect and/or arachnid, the virus first begins to attack the cells found within the epidermis. As the infection progresses, the virus begins to work its way deeper into the integument of the organism by further attacking the basal lamina, reticular lamina, and as expected, the dermis. At this point in the infection, inflammation of the skin should begin to take place within the affected host. Simultaneously, white blood cells, also referred to as neutrophils, are drawn to the infected site upon the detection of the invasive virus, however, the virus is too potent to be treated. With that in mind, the virus begins to attack other cells within the deeper layers of tissue including Langerhans cells which happen to be apart of the skin immune system and aid in antigen presentation. Those of the Langerhans cells that were to make contact with the myxoma virus would now be carriers of live traces of the virus. The infected Langerhans cells would then travel to and enter the lymph nodes thus making its way to the T-cell region. After making contact with the infected Langerhans cells, T-Lymphocytes would then be infected as well. The same infected T-Lymphocytes will then travel into the bloodstream where, unfortunately, the Myxoma virus will continue to spread and on a more aggressive note; a cell-to-cell basis. The virus will, then, travel to all other sensory organs found within the organism by means of the vascular blood system and disintegrate them. As the infection would have, now, rotted the interior organs found within the host, survival would be highly unlikely.
Living Conditions
Extracellular and Intracellular proteins
Extracellular proteins are molecules secreted by supporting cells that provide structural and biochemical support to the surrounding cell. Intracellular proteins are synthesized within the cytoplasm and cotranslationally inserted into the endoplasmic reticulum prior to being either sorted to their respective compartments or secreted. The myxoma virus living conditions and host tend to live in different places. The rabbit virus (pox-like virus) uses mosquitos and fleas as a vectors. The life cycle of the myxoma virus states that both extracellular, and intracellular proteins, produce virions to mature and bud to get through the surface membrane of the host to form and navigate to the immune system of the host body.
General Effects
Rabbits infected with the myxoma virus experience the myxomatosis disease. Infected rabbits often develop skin tumors, and sometimes blindness. Other symptoms of the disease, include fatigue, fever, foaming of the mouth, and swelling and discharge of the eyes. Unfortunately, infected rabbit die fourteen days after onset symptoms.
Co-Evolution Over Time
As stated earlier in this paper, the Myxoma virus was not only found in Europe. It’s coevolution has expanded over time throughout Australia as well. In the 1860s, European rabbits invaded Western Australia. During this time, Europe was attempting to westernize the lower continent by introducing non-native species that existed at manageable populations in Europe. However, the European rabbit had no natural predators in the continent and quickly proliferated as an invasive species to reach plague-like numbers. This caused a mass destruction of land, crops and an urge to find a solution to control the rabbit population. Researchers then introduced the pox virus Myxoma. The virus is easily carried as an intermediate host by biting insects, such as mosquitoes. Once it was introduced to the area, it’s continuation was able to spread from rabbit to rabbit as well. By the 1950s the virus became around 95% effective. As less virulent viruses were selected for, more room was created for a larger number of resistant individuals. The remaining rabbits that survived myxomatosis then gave rise to the resulting repopulation generations, and thus there was a strong selection for the resistant individuals to help rebound the population.
The disease was caused by small pathogens, such as viruses and certain bacteria that are able to change over time. A mosquito picked up the virus from the skin of an infected animal and then transmitted the disease to the skin of a new host. The virus traveled from skin into cells within the lymphatic system an organs throughout the rabbit. As it infected new areas, it replicated and caused cell death. Eventually the virus moved back into secondary sites in the skin, where there’s a high enough concentration of the virus in the skin for the mosquito to pick it up again. As a result, both the rabbits and myxomatosis continuously exerted selective pressures on another to collect sub populations within each species that possess the optimal traits for survival and reproduction. This was the basis for coevolution, which is where two species change to adapt to their constant interaction with each other in order to survive. The rabbits that died earlier kept the virus from moving to the skin. Since the virus was not present on the epidermis, mosquitoes could not pick it up. The decreased virulence of the myxoma virus was essential for the virus to survive, or else it would have completely eradicated the rabbit population and died along with its definitive/primary host. The cases where the rabbits lived longer allowed the virus to move and multiply in the skin of the rabbit, so the mosquitoes could receive the virus and transfer it to a new host. These attenuated strands of the virus let the rabbit live longer which allowed the cycle to continue. The selection of traits and rabbits came from those sub populations that were resistant, and thus their resistance was prevalent in the following generations. The attenuated viral strain was naturally selected for, as were the resistant rabbits. The resulting balance meant that the weaker virus had the ability to continue being spread and infecting while the stronger rabbits lived long enough to produce offspring. Overall, both participants co evolved to survive and continue their life cycles.
Below is a more detailed visual example taken from the text depicting the virulence analysis of the Myxoma virus in Australia and its evolution in Europe,
In Part A, viruses are color-coded according to their virulence grade. Grade 1 is red, grades 3–4 are green, and grade 5 is blue.
“The tree is rooted between the two oldest strains in the collection from 1949 and 1950, which were used to seed the European and Australian epidemics, respectively. The same root position is obtained under the mid-point method and from the Maximum Clade Credibility tree. “All horizontal branch lengths have been drawn to a scale of nucleotide substitutions per site, and bootstrap values greater than 70% are shown.” Part B represents the rate of the nucleotide substitution for the real MYXV genomic data set (which is In red on the right side) compared to 20 sequence data sets in which the year of sampling has been randomized among the taxa. Note that the lower 95% HPD value for the randomized data tends to a zero rate. Part C shows “regression of root-to-tip genetic distances against year of sampling for the 24 complete genomes of MYXV and inferred from the ML phylogenetic tree.” The correlation coefficient is 0.98 and the slope of the line, which is an estimator of the mean substitution rate, is 1.0×10−5 subs/site/year” (Kerr, P. J., Ghedin, E., DePasse, J. V., Fitch, A., Cattadori, I. M., Hudson, P. J., . . . Holmes, E. C.)
Treatments
At this time, the majority of wild bunnies are immune to this disease; but an infection in a domestic rabbit is nearly always fatal. There are no known proven treatments, and pet rabbits are highly recommended to be put under to end their suffering. Because of this, more research has been centered around prevention. The disease is recognized by swelling and discharge from the eyes, nose, and anogenital region. In some parts of the world (such as the UK) there has been progress made in vaccines for myxoma, but in Australia it is not available. It is recommended that owners invest in a mosquito proof rabbit hutch or have the rabbits avoid being outside at dawn and dusk where mosquitoes are most prevalent. Other methods such as flea control and two week isolation the first time an owner receives them is also encouraged.
Conclusion
The myxoma virus is a viral, fatal, and highly infectious disease designed to cull wild rabbits. It was introduced into Australia in 1950 in an attempt to control the rabbit population, but also ended up changing the entire evolutionary history of rabbits by coevolving over generations. According to the PLOS, is one of the best documented examples of host-virus coevolution (Kerr, P. J., Ghedin, E., DePasse, J. V., Fitch, A., Cattadori, I. M., Hudson, P. J., . . . Holmes, E. C.) . Development of resistance has been made by the coming of attenuated virus strains that allowed the survival of moderately resistant rabbits, which occurred far more rapidly in hot climates. Little research has been done to determine the evolutionary genetic basis to the major changes in virulence in both the Australian and European epidemics To this day, myxoma doesn’t have a cure and is still fatal to domestic rabbits.