The Virus

The virus has derived its name from the Latin term ‘virus’ denoting toxin or poison and is an ultramicroscopic infectious agent that reproduces itself only inside the cells of living hosts. Many viruses are pathogenic or disease bearing microorganisms that can contaminate all types of organisms, including animals, plants, bacteria as well as archaea. While these microscopic organisms possibly existed since life began on earth, they were discovered only a few centuries back. In fact, in 1892, while Dmitry Ivanovsky, a Russian botanist, was engaged in examining tobacco mosaic disease that resulted in blemishes and swelling up of the tobacco leaves. During the course of his investigation, Ivanovsky allowed the juice obtained from contaminated tobacco plants to go through a porcelain filter that was supposed to enmesh all kinds of microorganisms, inclusive of bacteria and other most diminutive pathogens known to mankind. In fact, the porcelain filter had been developed by a trustworthy junior of Louis Pasteur named Charles Chamberlain and was extensively made use of domestically to filter as well as disinfect drinking water.

Ivanovsky was surprised to note that despite filtering the sap from the infected tobacco plants, they lead to contamination. This made him come to the conclusion that the filter was unable to trap the agent responsible for the contagion, which was eventually passing through strain. This made the Russian botanist wonder if any toxin or poison produced by bacteria was responsible for tobacco mosaic disease - the malady affecting the tobacco plants. His suspicion was on the basis of the fact that it had been found that certain human ailments like diphtheria were actually had their origin in certain powerful poisons produced by bacteria and these were able to go through the filters invented by Charles Chamberlain with no difficulty. Like Ivanovsky, several other scientists of the time held a similar opinion on this issue.

Unfortunately, Ivanovsky as well as the other scientists of the day were proved to be wrong. Around some six years after Ivanovsky carried out his investigation on tobacco mosaic disease, a Dutch botanist called Martinus Beijerinck picked up the research from where the Russian botanist finished. The Dutch botanist adopted a different approach - something very dissimilar to Ivanovsky’s experimentations. Beijerinck used the sap collected from a diseased plant and sprinkled it on a healthy plant. Next, he collected the juice from the plant after it too became contaminated and continued the process passing the sap from the diseased plants to numerous tobacco plant generations. As a result of such consecutive jabs, the plants kept on developing the blemishes that are typical of the tobacco mosaic disease. In fact, even after innumerable plant passages, the sap of the contaminated tobacco plants preserve its belligerence in full strength. Such non-dilutable characteristic of the sap hinted that the agent responsible for the disease was replicating itself inside the plant. Thus, the concept that a toxin was responsible for the disease was eliminated. This was enough to give an idea that the agent causing the contagion was neither bacteria nor any toxin or poison. Hence, Beijerinck initially named the disease causing pathogen as a contagium vivium fluidum denoting a ‘contagious living fluid’. However, afterwards he named the agent virus borrowing the term from Latin. As mentioned earlier, virus in Latin denotes a ‘poison’ or a ‘poisonous substance’. Despite all this, at that time, nobody was actually aware of the precise substance they were coping with.

Although the scientists of that time were still not aware regarding the temperament or natural history of viruses, in a little while they discovered that this ‘soluble living germ’ was also responsible for a number of other maladies. In fact, scientists first discovered that the ‘foot-and-mouth’ disease prevalent in cattle was also caused by this contagious agent. They found that this ailment was caused by the infectious agent that was capable of passing through the finest filters available in those days and were much smaller compared to bacteria. In 1900, it was established that a human ailment known as the yellow fever was also caused by a germ that had its roots in virus. And, as of date, we are familiar with over 5,000 dissimilar types of viruses that are capable of contaminating any living organism.

The manner wherein viruses function

Many people confuse bacteria with viruses. They believe that viruses are extremely diminutive forms of bacteria. However, this is not true. In effect, bacteria and viruses are basically so dissimilar that in several aspects a bacterium is more intimately associated with humans compared to a virus. In any case, both humans and bacteria are both composed of living cells. On the contrary, apart from viruses, each and every living thing is composed of cells. Actually, the elements comprising a cell have a variety of functions, such as generating energy, development eating, as well as responding to ecological alterations. However, these aspects are missing in a virus. So long as the viruses remain outside a cell, they are actually nothing, but diminutive elements that are completely inert or lifeless. Unfortunately, viruses are developed with the intension to enter the living cells and when they succeed in penetrating the cells they commence the lethal work of viral contagion.

Each and every virus comprises of two elements - a nucleic acid at the centre and a protein coating that encircles the core. In a number of instances, the viruses have an extra fatty or lipid covering. The role of the protein coating or the lipid covering, if present, is crucial. They are not only responsible for binding the virus to the cell membrane of a living thing, but also to work and enable the virus to penetrate the cell in any way. However, doing so is not an uncomplicated or easy task. In fact, the exterior of the virus coating needs to precisely match with the ‘receptor’ sites on the membrane or covering of the living cell. The virus is neither able to attach itself to the cell or penetrate it when exterior viral coating does not exactly match with the membrane of the cell. Believe it or not, even when perfect matching occurs, perhaps only one in a number of thousands of viruses is able to bind to as well as penetrate the cell membranes. In other words, the bond and penetration of a virus into a living cell is really a very complicated task. Such accuracy in matching for viruses to bind with living cell membranes and penetrate them perhaps elucidates why they are generally species-specific and will never contaminate any cell from an entirely dissimilar species. However, there are some exceptions to this theory. For instance, the influenza and rabies viruses actually infect an assortment of hosts.

While the viruses will rarely contaminate entirely dissimilar species, but very often they are very particular regarding invading specific types of cells in a living being. For instance, while the hepatitis B virus aims at invading the liver cells, the HIV is on the look for specific sites to bind or marker on particular white blood cells. On the other hand, viruses responsible for common cold attach themselves to the coating of the respiratory tract. It is important to note that when a virus succeeds in binding to a cell membrane, it is able to break through the covering and go into the cell in many different ways. One of the ways is to compel the cell membrane to double up and envelope a small vesicle along with the virus inside the cell. Viruses having a fatty covering are able to mingle their coatings with the cell membrane, thereby breaking through it and allowing the remaining part of the virus to enter the cell.

When a virus enters a cell by any possible means, it is able to do a number of things. And, whatever action the virus takes actually establishes the course of the ailment caused by it. There are several instances when the virus begins to reproduce itself instantly after penetrating the cell membrane of a living organism. On fact, it may be said that rapid replication as well as extensive distribution are the two main causes for its very existence. In order to achieve these two tasks, the virus activates the mechanism of a cell soon after entering it and forces the cell to turn out an increasing number of viral units. Many scientists describe this activity of the virus as an implausible act of piracy that is basically coordinated and regulated by the nucleic acid core of the virus.

Although the nucleic acid present in the core of a virus is an extraordinary substance, the scientists had failed to comprehend its significance till as late as 1953. Actually, it was in that very year that two scientists James Watson and Francis Crick settled on the molecular construction of DNA or deoxyribonucleic acid, which is a long linear polymer found in the nucleus of a cell. In fact, there is another type of nucleic acid known as RNA or ribonucleic acid that is a close cousin of DNA.

In fact, the DNA is a genetic material that is present in all types of living cells, barring the mature red blood cells. In other words, this genetic substance is hereditary and responsible for giving any living thing its form as well as characteristics. DNA is the substance that actually makes a human a human, a tree a tree and a bacterium a bacterium. Again this is the genetic substance that is responsible for making one human different from another and one species of trees dissimilar to other species. The structure of the DNA is seen as an extremely long microscopic charm bracelet. For instance, the human DNA comprises three billion charms. Speaking precisely, the DNA is actually two charm bracelets that are arranged in such a manner that their charms are able to attach with each other. Looking at it closely, you will find that there are four different types of charms that are known as nitrogen bases and named by the English language alphabets A, T, C and G. The dual chain also possesses a noticeable coil making it generally appear like a twisted rope ladder or the spiral arrangement of the two complementary strands of DNA having rungs or girdles that are a manifestation of the paired nitrogen bases.

Similar to an alphabet comprising four letters, the arrangement or series of the rungs or base nitrogen pairs makes obvious the functions a particular cell will carry out and what they will eventually turn out to be. In fact, the DNA can be described as a master plan for every life, as it regulates the performance of a cell by deciding on the proteins made by particular cells. However, it is important to note that the DNA does not function individually. In other words, the DNA never directly regulates the synthesis of protein that takes place on the diminutive elements, often called protein factories, which remain buoyant in the region of the cells. In fact, the DNA is found concealed deeply inside the nucleus and is intertwined into the structure of the chromosomes. Actually, the DNA is a very precious element of the cell and, hence, it does not move around all over the cell. As an alternate, the DNA prepares a messenger filament with nucleic acid making use of its base pair series as a guide. This messenger molecule is known as the RNA and its function is to communicate the signals from the DNA to the protein factories located outside the nucleus.

Although viruses do not have much resemblance to the living cells, like the living cells, they also possess nucleic acid as their genetic substance. Any specific virus may enclose DNA or RNA, but no types of viruses contain both. The difference between the DNA contained in a living cell and that in any virus is that while the DNA in living cells transmit codes for manufacture of cellular proteins by the protein factories located outside the nucleus of the cell, in the instance of viruses, the viral nucleic acid signal is sent not for manufacture of cellular proteins, but to produce proteins essential for reproducing more viruses. In fact, the viral nucleic acid actually compels the host cells to produce proteins in large amounts that are required by the virus to replicate it rapidly. This process is somewhat similar to a clever invasion in a phased manner and may be explained as below:

• Proteins produced inside the cells are primarily enzymatic biologically. These cellular proteins stimulate reactions that generate several thousand duplicates of viral nucleic acid.
• The structural covering proteins are manufactured following the amalgamation of the viral nucleic acid.
• The virus is assembled once the coat protein forms a covering structure around the core of the nucleic acid.
• When the new viral elements are set free, they sometimes, and not always, kill the host cell in the procedure. In some cases, the virus gets hold of a fragment of cell membrane that is ultimately converted into the virus’ lipid wrapping.

The exact method by which the viruses begin their reproduction largely depends on the genetic substance enclosed by the virus. The manner of functioning of a DNA virus is very much comparable to the DNA of the host cell. Initially, the virus produces a viral RNA making use of the virus’ DNA as a model. Next, the RNA carries instructions from the viral nucleic acid to the protein factories of the host cell to manufacture viral proteins - proteins necessary for the replication of the virus. In brief, the virus replication process begins with the viral DNA, passes on to the viral RNA and concludes with the production of viral protein. However, in the instance of majority of the RNA viruses, the first step has to be done away with as they do not contain DNA (viruses may contain DNA or RNA, but not both). In this case, the viral nucleic acid just goes on to produce the requisite viral proteins. In brief, in the case of RNA viruses, the replication process begins with the viral RNA instructing the host cell’s protein factory to produce proteins necessary for reproduction of more viruses and it concludes with the production of such viral proteins by the host cells.

The perception that the DNA produces the RNA, which, in turn, produces protein is so fundamental to biology that it today it is widely accepted by scientists as the most vital doctrine or ‘central dogma’. It needs to be mentioned here that the RNA never produces DNA, and the process is actually the other way around. However, there is a rare exception to this doctrine and that is in the instance of a retrovirus. This type of RNA virus, includes HIV - the AIDS virus, and has actually amazed the molecular biologists by doing something incredible - by functioning in a retreating manner. It is interesting to note that rather than producing proteins, the RNA of the retrovirus initially goes into a reverse mode and functions as a prototype for the synthesis of DNA. Following the DNA synthesis, the newly formed DNA produces a new RNA that eventually starts mass producing protein molecules needed for virus replication. Precisely speaking, the reproduction process of retrovirus begins with viral RNA that undertakes DNA synthesis and, in turn, the new DNA model produces another RNA, which manufactures viral protein necessary for replication of this microscopic organism.

Genesis of viruses

Viruses are actually very obstinate microscopic organisms and what may come they will find some way or the other to enter the living cells to gain genetic advantage at our cost. According to past records, the viruses have been engaged in this task for several thousand years. The presence of small pox in ancient Egypt is evident from the blemished mummified face of Ramses V. Bas-relief (a type of structural relief) engravings done in that era also portray a priest having shrunk legs that indicates that polio also existed in ancient Egypt. And there is little doubt among scientists as well as historians that viral infections were very common in ancient Egypt. It is also believed that even the earliest man living in the caves too had to confront viruses. In fact, the manners wherein the viruses get inside the cells and take hold of control can only happen by means of a prolonged involvement that have helped the viruses to become accustomed to the host cells. In fact, even to this day, viruses are continually working to adapt themselves to their hosts.

However, it is only possible to guess the time from when such association actually started. One of the several theories on the subject says that viruses appeared earlier than the cells as they are much smaller and simpler compared to the cells. According to this assumption, the nucleic acids present in the viruses became more and more complicated before they turned out to be the material that comprise the cells. While this theory was widely accepted at one time, presently scientists think that this is a very implausible situation. In fact, there is another theory on this subject that appears to be more plausible. According to the second hypothesis, the viruses developed from fragments of the genetic substances present in the cells. These bits of genetic substances are believed to have run off from their cells. Advocators of the second hypothesis say that on due course, these ‘run off’ genetic materials or the fragments developed from the host nucleic acid acquired the aptitude to exist as independent parasites that reproduced by themselves within the cells. These ‘escaped’ genetic fragments eventually developed into viruses.

A renowned British scientist and astronomer, Fred Hoyle provided a third theory regarding the origin of viruses. According to Hoyle, the viruses actually fell on the earth from outer space and they continue to fall even to this day. However, most contemporary virologists do not concur to this view regarding the genesis of viruses. All said and done, no matter what may have been responsible for the origin of viruses, the fact remains that once the viruses have set themselves up on the earth, they became a force to be prepared for.

When viruses work as genetic change agents

In the 1970s, during researched conducted on Rous sarcoma virus, scientists first became aware of the fact that, in addition to making us ill, the viruses were capable of doing more things. In fact, this virus is responsible for a fatal cancer in chickens. The virus causes cancer in the chickens by introducing a gene that causes cancer, known as oncogene, straight away into the DNA of the host cell by means of a procedure known as integration.

Gradually, scientists became inquisitive regarding this oncogene and started examining the microscopic organism more minutely. During the course of their researches, scientists were amazed to note that oncogene was a very familiar gene normally present in hale and hearty chicken. It appeared that the sarcoma virus was seizing this gene from the host cell and taking it to different cells in other chickens. While seizing the gene it came into close connection with viral genes and this transformed the typical chicken gene, converting it into a cancer provoking agent.

Despite having detected so much about oncogene, the gene continued to remain an alien to the scientists. It was unbelievable that the ‘abducted’ gene was found to be virtually omnipresent as it began to be found in an assortment of vertebrates, such as fish, cow, rats and even humans. And, possibly this omnipresent nature of the gene was not a happenstance. This was possibly owing to the fact that viruses were responsible for spreading this gene in chickens as well as other animals. Going by this theory, it may be rationally concluded that viruses would later emerge as agents for dispersing a complete host of genes. And if this happens, viruses would be graded on the upper side with sexual reproduction being a key power to result in genetic inconsistency and eventually the progression of different species.

A scientific discovery achieved in 1977 really astounded the entire genetics community. In that year, scientists researching oncogene happened to come upon introns in the genes of rabbits and chickens. It may be mentioned that an intron is an expanse of worthless DNA - DNA that does not code or send any signal for producing proteins and, till so far, has no perceptible role. Hence, it is not surprising that scientists talk about introns as junk DNA. Additional research on the topic led the scientists to discover the presence of introns in several other animals and most surprisingly, even humans. Scientists were also surprised to learn one truth - the better evolved an organism is the more number of meaningless DNA or introns it had. Although it may seem to be incredible, the fact is that over 95 per cent of the DNA in humans comprises useless expanses of introns or junk DNA.

Well, this made scientists wonder if the introns were actually the residual fragments of very old viral contagions, a remnant inheritance of the bygone days of our evolutions. Well, this is very much possible because ever since scientists discovered junk DNA, various researches undertaken by molecular biologists have shown that particular expanses of the human DNA has very close resemblance to the genomes of specific viruses. On the other hand, a number of viral DNA found in the humans are very much similar to the fragments found in the chimpanzees, the non-humans who are most intimately related to the humans. According to hypothesis put forward by the researchers, around 10 million or a hundred million years ago this virus entered the DNA of an ape that would later evolve into chimpanzees and humans. They also assume the existence of a virus during that period that might have resulted in a fatal epidemic - possibly an ancient form of AIDS. Now, the virus is something akin to an excess baggage present in the inheritor cells of living organisms those continued to live even after enduring its horror. In fact, the introns are now considered to be silent reminders of various prehistoric contagions.

Marburg (a deadly hemorrhagic virus)

Sometime in August 1967, three factory employees engaged with the vaccine-manufacturing firm Behring Works suddenly developed muscle pain and mild fevers. Initially, the physicians who attended on these ailing workers were of the opinion that they might have developed some kind of influenza. However, as the days passed and these workers were still not cured of their illness, it became obvious that they were not suffering from any type of flu. Gradually, the affected workers were experiencing nausea and vomiting. Soon, they also developed diarrhea. Simultaneously, they developed symptoms, such as bloodshot eyes and painful red rashes. This was a fall-out of the blood clots formed in several thousand capillaries just beneath the skin. Their throats became so sore that they were unable to swallow and needed to be fed by means of intravenous injections. However, this was only the beginning of a deadly infective ailment, as the virus responsible for the contagion was simply limbering up. In ten days from the time the symptoms first appeared, these workers started vomiting and discharging blood.

In fact, numerous shattering viral contagions, including Marburg and Ebola, are called hemorrhagic fevers as the patients begin to bleed profusely during the last phase of the ailments. When the clotting aspects of the body becomes weak, blood discharge begins from every opening of the body carrying along layers of dead tissues. In such cases, blood and Marburg viruses spurt in every direction. This is a contagious disease and in case any other person comes in contact with the infected blood, it will result in a fresh cycle of infection by the virus all over again.

Altogether, the Marburg virus affected as many as 31 Europeans and after this the virus disappeared all of a sudden, almost as unexpectedly as it had emerged. After the virus had left its scar, or, more precisely, following the consequences of the viral attack, scientists worked frenetically to find answers to some of the most fundamental queries in their mind. They wondered about the type of virus that created such devastation and the place of its origin. Well, the scientists found the answer to the second question first. They soon learnt that all the people who were infected by the deadly virus in the initial stages of the spread of the disease were either dealing with monkeys or monkey tissues. In addition, the scientists discovered that all the monkeys belonged to the species of the African green monkeys and were imported from Uganda by ships in three different batches. It may be mentioned here that pharmaceutical firms manufacturing polio inoculation ought to make use of monkeys to make their products, as poliovirus are able to develop only within the monkey kidney cells. Every year around 16,000 monkeys are imported to the United States only for this purpose, but nothing such was ever reported. Hence, it may be concluded that there was something wrong with the batches of monkeys that were sent to Germany in 1967.

Needless to say that several people who had been infected by this virus succumbed to massive hemorrhages or profuse loss of blood from their body. In fact, the cause of deaths of hundreds of monkeys in their native places in the jungles of Africa, have accidentally been imported to Europe and the virus was being transmitted to a new species - the humans. The new virus was now developing in a new place and, in general, when any virus transmits to a new animal species it usually proves to be exceptionally deadly. This is primarily owing to the fact that the new host of the virus had never been exposed to the pathogen earlier and it is usually already too late when the immune system of the host becomes active to combat the microorganism. It was on the basis of this that the scientists did not consider the African green monkeys to be the natural host of the Marburg virus. In fact, they found out that compared to the human victims, this virus had proved to be much more overwhelming for these monkeys when it first infected them. Actually, the virus had killed them with full fierceness when it first invades the apes. Scientists were of the view that most probably there still was a pool of the Marburg viruses concealed in some yet to be known animal native to the rain forest.

During the subsequent years, the World Health Organization and the United States along with a number of nations in Europe dispatched teams of scientists to Uganda and Kenya to hunt the rural areas to find the animal that could be the natural host of the Marburg virus. During the course of their investigations, the scientists nabbed and examined several thousand organisms, including apes, monkeys, mice, bats, cats, ticks and even mosquitoes. However, it is regrettable that the scientists were unable to find the animal that was the natural host of the Marburg virus, as it remained obscure. Neither could they discover the existence of any pool for the virus.

Although the scientists failed to identify, let alone catch the living organism that is supposed to be the original host of the Marburg virus, the electron micrographs of tissue and blood samples collected from those infected by the virus revealed that notwithstanding its hiding place, this virus was different from the others. One major difference is the shape of the virus. While majority of the viruses have a spherical or an ovular form, Marburg appeared to resemble a small piece of thread. And when the virus multiplies itself inside a cell by replicating several thousand viral copies, it looked like a bowl of enmeshed spaghetti. Owing to its appearance, scientists named the virus as filovirus, getting the name from the Latin term ‘filo’ denoting a ‘thread’. In fact, there is no other virus that has an appearance like the Marburg.

The Marburg virus first struck in Germany in 1967 and since then it has only infected humans on two occasions, second time in 1976 and the last time in 1990. During the subsequent attacks by the virus, altogether four people, all Europeans, were infected. And, interestingly enough, all the four victims came in contact with the virus while they were traveling in Africa. Among these four patients, one person succumbed to the disease. Presently, the virus has been frozen and preserved in a number of laboratories across the world.

Unfortunately, scientists are no longer enthusiastically engaged in undertaking further researches involving the Marburg virus simple owing to the fact that it is too ‘hot’. It may be mentioned here that a virus is known as ‘hot’ when it has the aptitude to transmit by far, claims its victim’s life with a high humanity rate and does not have any remedy or preventive vaccine. Among the ‘hot’ viruses, Marburg is ranked on the upper side and it needs extremely specialized handling. While treating patients infected by the virus, physicians need to wear heavy dresses something resembling spacesuits that have independent air supplies to avoid any direct contact with the disease-bearing virus with any part of their body. The doctors also need to wear extra rubber gloves below their suit and often also over the suit as additional fortification against any accidental slashes or perforations when they are working with surgical instruments, such as scalpels and hypodermic needles. On the other hand, animals and tissue samples infected by the virus are usually dealt with in hermetically sealed glass or steel boxes with lastingly fixed gloves.

According to statistics available, the deadly virus has claimed about 25 per cent lives of patients it has infected and this makes Marburg one of the deadliest viruses known. In fact, humanity has witnessed several devastating plagues and very few among them had such a high mortality rate. For instance, yellow fever is a lethal viral ailment caused by a single bite of a female mosquito (incidentally, male mosquitoes never sting) and transmitted easily, normally claimed one out of every ten persons it infected. In spite of this, the Marburg still cannot be called the most horrible hemorrhagic fevers that have emerged from the rain forests of Africa. In fact, around nine years after the Marburg virus first invaded the humans in 1967, another virus, more lethal compared to this virus, struck the people in the central African countries of Sudan and Zaire. This fatal virus was later named Ebola.

Ebola

People first became aware of the existence of Ebola in July 1976 when it emerged in the southern regions of Sudan. This happened when a gentleman developed some illness and succumbed to it. However, his death was not only excruciating, but also bloody. Following the death of this man, the virus transmitted externally contaminating his mistress, friends and members of his family. And before the outbreak of the virus was over, it had infected a total of 284 persons among whom 150 patients succumbed to the viral infection. This took the mortality rate owing to the virus infection to a little over 50 per cent!

The menace caused by the virus was yet to be over, as Ebola launched another attack in September the same year and this time in neighboring Zaire. In fact, the strains of Ebola that struck people in Zaire appeared to be somewhat different from the strains of the virus that attacked people in Sudan earlier. In Zaire, the virus appeared in a more ferocious form claiming the lives of 90 per cent of the people it infected. During a number of months of rage during the latter part of 1976, the virus invaded people in as many as 50 villages claiming 325 lives of the 358 persons infected by Ebola.

It has been found that the Ebola virus is able to infect as well as multiply itself in practically every type of body tissue, possibly barring bone and the skeletal muscles. When this deadly virus infects an individual, he or she initially experiences an intense headache accompanies by fever and muscle aches. Soon after this, bleeding takes place. Initially, the hemorrhage occurs internally and the factors responsible for blood clotting become active. As a result of blood clotting in the internal organs, the liver and spleen are hardened eventually transforming into dehydrated masses of condensed blood and tissues. The kidneys, which are considered to be the filter plants inside the body, become so congested with thickets of blood that they ultimately stop functioning. All these put together creates an enormous workload on the heart as it tries to pump the condensed mass through the blood vessels to the different parts of the body. And when all the aspects that help in the clotting of blood tire out, it results in unrestrained bleeding. At this stage, the Ebola is said to be going berserk multiplying itself billions of time to devastate the body. As the capillaries worsen, the supply of blood to vital organs, such as the lungs, kidneys, stomach and the intestines, come to a halt. People infected by the virus may also experience inflation of the skin as the blood seeps out of the tissues just beneath it. In fact, the condition of the patients deteriorate to such an extent that blood even oozes out of their eyes. In fact, at this stage the virus Ebola is changing the host or patient’s internal organs into a viral broth. The only relief for the patients at this stage of the disease is that they succumb to the infection soon. Either they die due to shock witnessing such heavy loss of blood from the body and extremely low blood pressure or owing to heart failure or blocking of the lungs.

Researches have shown that the Ebola viruses are closely related to Marburg. When examined under an electronic microscope, they appeared almost alike - both seemed to appear filoviruses, denoting they have the shape of threads. Both Marburg and the Ebola viruses possessed analogous genetic substances - a solitary filament of RNA (ribonucleic acid). In addition, like in the case of Marburg, scientists are yet to find the natural host of any of the various Ebola strains.

What is more remarkable regarding the strains of Ebola virus is that these filoviruses are actually not as infective as they were initially seemed to be. While both viruses - Ebola and Marburg, have the aptitude to communicate a disease as well as kill monkeys that breathe in the virus, they cannot be easily transmitted taking help of the air or atmosphere. In fact, these viruses are also highly unlikely to be transmitted by means of casual human to human contact. It has been found that during its outbreak in Sudan and Zaire in 1976, the strains of Ebola did not spread owing to people meeting casually on the streets or visiting the same eateries. In fact, it is paradoxical that the hospitals treating patients infected by Ebola were responsible to a great extent for the small endemics caused by the virus. First, practically there were inadequate supplies of medical requirements. Second, professionals at the hospitals were negligent and irresponsible. For instance, when people came to the hospitals for treatment of malaria or various other diseases, they were injected with the same needles time and again. In fact, either the needles were not sanitized between two injections, as the time between two shots was too small to even wash them.

Lassa

Like Marburg and Ebola, Lassa fever is also a hemorrhagic fever caused by a deadly viral infection. Thus disease is widespread in the western regions of Africa and is responsible for approximately 5000 deaths in the region every year. Like the Marburg and Ebola viruses, Lassa is also a vicious killer and functions almost in the same manner as the other two viruses. While the virus has been rampaging in the African regions for time unknown, scientists only became aware of Lassa in 1969 when it infected a number of American nurses working in a hospital run by the church in Nigeria. The symptoms of Lassa fever extremely reminds one of the Marburg that was discovered by scientists about two years back in 1967 in the central African nation Sudan. When examined under the electronic microscope, the Lassa virus was found to appear sphere-shaped, very much different from the filoviruses like Marburg and Ebola. In fact, when the Lassa virus, a deadly pathogen, was combined with antibodies for Marburg, there was no reaction whatsoever. In fact, during the investigations, it was found that the Lassa virus was encouraging the body to produce antibodies that were unlike Marburg. Speaking precisely, the Lassa viruses were a completely different type of viruses.

In fact, during the research the scientists observed that the Lassa virus not only had any reaction with the antibodies of Marburg, but they also did not have any interaction with any other known antibody. In other words, all these denoted that the scientists and medical community were now aware of an entirely new ‘hot’ virus. This led the medical authorities to launch another hunt to find the natural host of this new and deadly ‘hot’ virus. According to an intuition, the researchers came to a conclusion that Lassa was by no means an arbovirus (arthropod-borne viruses), which are a large group of viruses that are spread mainly by blood-sucking insects. During their investigations, researchers found out that all the infections by this new ‘hot’ virus took place in the house. They also discovered another fact regarding the spread of the Lassa fever - the virus mainly infected the adults. Generally, insect-borne diseases demonstrate an inclination to infect the children first, as they play in the damp breeding grounds of insects, such as mites, mosquitoes, ticks and others.

The gut feeling of the researchers actually proved to be right. Thus, during their search for the natural host of the Lassa virus, scientists captured over 640 animals, primarily small mammals like rats, mice and bats from the rural areas were people had already been infected by the virus. The scientists collected blood samples of these captured animals and later also removed their hearts, lungs, kidneys and spleens by means of surgery. Finally, all the samples collected were preserved in liquid nitrogen and later shipped abroad for examinations at the Special Pathogens Branch in the United States. When the tests were complete, the results showed that one of the specimens tested proved to be positive. From the tests scientists came to learn that the species Mastomys matalensis or the common brown rat was the natural host of this deadly ‘hot’ virus.

In fact, viral infectious diseases, such as the Black Death and typhus, were both atrocious exterminators. These diseases were silently initiated among the humans by the brown rats. However, further studies revealed that these maladies were in reality fleas or lice living on and biting the diseased rats, and passed onto the humans. Next, the scientists wanted to find out if this was the actual approach for transmitting the Lassa virus onto the humans or if the rats themselves were responsible for passing on the virus to humans by biting the victims. When those infected by the virus were queried in this regard, they were unable to recall if they were bitten by rodents.

Incidentally, on one occasion when one researcher held an infected rat, the infuriated mammal urinated on him and, regrettably enough, the scientist succumbed to Lassa fever two weeks from this incident. Later, it was discovered that the urine of the infected rat was swarming with Lassa viruses. What was worse is the fact that these infected brown rats were almost present everywhere all over the eight countries in the western parts of Africa and they looked for human dwellings of their choice to reside in. This made life precarious for the people residing in these regions. The infected rats not only urinated on the food, floors and beds, but also on the people while they were asleep. The virus had the capability to enter the human body even through the most minuscule break or pore in the skin. This was really dangerous, as the disease spread rapidly, with no remedy or vaccination in sight.

Dengue

Before we discuss the topic, it needs to be mentioned here that compared to the common dengue fever, its close relative, the dengue hemorrhagic fever is much harsher in form. Both the diseases are infectious and result in agonizing bone and joint pain and the diseases have acquired their name ‘break bone fever’ from such symptoms. While the common dengue fever does not lead to hemorrhage, but internal bleeding and ensuing shock caused by dengue hemorrhagic fever results in death in approximately 15 per cent cases.

Dengue is closely related to yellow fever and is an arbovirus like its cousin. This means that the viral disease is transmitted by insect bites or sting of any arthropod. In fact, both forms of dengue are spread by the same agent - a mosquito called A. aegypti. Several researches have shown that mosquitoes are basically most effectual in transmitting diseases. As discussed earlier, the ‘hot’ virus Ebola spread rapidly in Zaire in 1976 owing to the reuse of hypodermic needles by callous hospital authorities. In this case, a female mosquito (male mosquitoes never bite) is like an airborne hypodermic needle. The long proboscis (nose of an animal) of the mosquito is akin to a needle and is used by the female insect to draw her blood meal from other animals. However, before the female mosquito sticks her long proboscis into the victim’s body, she usually performs a peculiar practice. In fact, the female mosquito first prepares the area on the skin to be attacked by spitting on it. The saliva of the mosquito contains an anti-coagulant substance that helps the blood to continue flowing and this saliva may often be full of viral elements. Next, A. aegypti penetrates her long proboscis and ravines herself on a large volume of blood, swelling to the extent of increasing her actual weight four-fold. At this stage the A. aegypti virtually turns out to be something in excess of a hypodermic syringe. In case the blood sucked by the mosquito is infected by dengue virus, the pathogen will start reproducing itself right inside her salivary glands. When this female mosquito spits and bites another target for her blood meal, the dengue virus will be transmitted to the new body causing innumerable miseries to this new victim.

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