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World eradication of polio has reached major heights, but is still far from being a complete success. India is one of the four countries where polio is still, to this day, endemic. The polio virus is the causative agent for poliomyelitis, more commonly known as polio (Younger, 1999). Polio is infamous for causing muscle paralysis. With the number of poliovirus infected individuals on the rise around many countries in the world during the late 19th and early 20th century, scientists and researchers were determined more than ever to find a way to stop the rapid spread of this crippling disease. The first step to stopping this virus was learning about its every detail. The poliovirus consists of a positive-sense single-stranded RNA genome inside its icosahedral capsid (Glenn et al., 1982). The poliovirus follows a lytic life cycle ("The Poliovirus Life Cycle," 2002). Attachment of the virus onto host cells occurs through binding of the poliovirus receptor (PVR) CD155. The virus then enters the host cell via endocytosis and uncoats its capsid, releasing its genome. Since the poliovirus is positive-sense single-stranded RNA, its skips transcription and proceeds directly to translating its genome into protein. New viral progeny are assembled and they egress by lysing the cell. The poliovirus targets cells of the intestine, throat, and central nervous system. A minor illness due to infection can result in having symptoms similar to the flu or paralytic polio may develop causing immobilization of muscles (Younger, 1999). Post-polio syndrome (PPS) can also occur as a result of acute paralytic polio. Physical therapy is available for the management of this disease. Preventative measures for this disease include vaccination, either orally or by injection. The poliovirus is transmitted via a fecal-oral route and is a waterborne disease. Areas with poor sanitation and hygiene having water contaminated with poliovirus-laden feces have populations that are at a high risk of getting polio (Younger, 1999).
Under the Baltimore classification system, the polio virus is placed in group IV (Peters, 2005). Viruses in this group exhibit similar genomic properties of having positive-sense single-stranded RNA (ssRNA). Another type of classification used by the International Committee on Taxonomy of Viruses classifies the poliovirus as belonging to the family Picornaviridael, subgroup enterovirus ("Poliomyelitis," 2009). While the Baltimore classification is primarily based on genomic similarities, the International Committee on Taxonomy of Viruses classification is based on a variety of common characteristics. The structure of the poliovirus was determined using x-ray diffraction (Glenn et al., 1982). The poliovirus spans 20 nanometers in diameter. Compared to the host cells this virus attacks, the polio virus is 1000 times smaller. The capsid of the polio virus is geometrically icosahedral in structure. The major function of the capsid is to protect and enclose the genome of the virus. The poliovirus' genome is made of single-stranded, positive RNA with 7,450 nucleotides. Sixty protomers of each of four different kinds of capsid proteins (VP1, VP2, VP3, and VP4) make up the poliovirus capsid. Although the VP1, VP2, VP3, and VP4 proteins mainly function to collectively hold and protect the genome, they serve other major functions in the virion's life cycle. These four proteins enable the virus to recognize and bind to target host cells (e.g. motor neurons). They are also capable of inducing an antigenic host immune response. In addition to the capsid, some viruses have an additional layer surrounding their genome-an envelope. The major function of an envelope is to assist the entry of the viral genome into the host cell. The polio virus, however, does not contain an envelope (Glenn et al., 1982).
The transmission of the poliovirus is via a fecal-oral route (Peters, 2005). This implies that humans who ingest water or food contaminated with poliovirus laden feces can develop the polio themselves. Once the poliovirus is in the gut, it can take its next step towards invasion-attachment and entry ("The Poliovirus Life Cycle," 2002). The VP1, VP2, VP3, and VP4 proteins on the capsid of the poliovirus bind only to the poliovirus receptor (PVR) CD155 present on the host cell membrane (Glenn et al., 1982). The only cells that display the poliovirus receptor are cells lining the intestine, the nerve cells, and the throat cells (Peter, 2005). Therefore, the poliovirus can only attach and invade specific target host cells containing the PVR on their surface. The ability of this virion to target specific cells in the human body is termed cell tropism. Once the viral capsid proteins attach to PVR, the virus can take one of two paths for entry ("The Poliovirus Life Cycle," 2002). The poliovirus can either directly inject its genomic material into the host cell via a tiny pore formed during the conformational changes of the capsid or it can become entirely endocytosed into the host cell's cytoplasm. Since the poliovirus does not contain an envelope, it can pass through the plasma membrane of the host cell or be endocytosed into endosomes. After endocytosis, the virion uncoats its capsid to release its genomic information into the host cell's cytoplasm. Since the genomic material of the poliovirus is positive, ssRNA, the virus need not enter the nucleus for replication (Peters, 2005). Its RNA is directly translated into protein in the cytoplasm. The product of translation is one polyprotein containing many different varying proteins attached to each other ("The Poliovirus Life Cycle," 2002). The attached proteins are cleaved into individual, fully functional proteins via proteases. In order to make additional viruses which can then go on to infect healthy host cells, the virion must be able to replicate its own genetic information. The poliovirus contains its own RNA polymerase in its genome to transcribe its positive, ssRNA into negative, ssRNA and back into positive, ssRNA to be used as the genetic information in the progeny cells. The last thing left for the virus to do after accumulating all the necessary materials for new progeny production is to assemble the new viral particles. Once the progeny particles have been assembled in the host cell's cytoplasm, the progeny exit the host cell by lysing the cell and, thereby, killing the host cell ("The Poliovirus Life Cycle," 2002).
The poliovirus invades the cells of the throat, first, and then the intestine after entry into the gut (Younger, 1999). The incubation period of the virus is between 3 to 35 days. Any signs of infection can take anywhere from between 4 to 14 days to appear; however, sometimes, cases may go asymptomatic. The virus may even appear in the stool prior to the onset of illness ("Poliomyelitis," 2009). At this level of infection, mild symptoms may appear similar to those of having a cold e.g. sore throat, fever, and headache (Younger, 1999). This type of polio is the minor form of the illness called inapparent polio. Some patients may have additional symptoms to these such as vomiting, diarrhea, and abdominal pain. This type of polio is called abortive polio. And, 90% of the patients are asymptomatic. However, as the virus continues to infect more tissues the symptoms worsen and become more apparent. From the intestinal mucosae, the poliovirus travel via the bloodstream to infect the lymphatic tissue. Furthermore, infection can travel to the anterior horn of the spinal cord affecting neural tissue. The gray matter of the anterior horn of the spinal cord consists of the motor neurons that control the movement of various muscles such as the respiratory muscles and leg muscles. Damage to motor neurons can be catastrophic leading to paralysis or sometimes even death. Non-paralytic polio may occur when damage does not induce paralysis, but exhibits symptoms of muscle stiffness and sore limbs. Non-paralytic symptoms last for about 2 to 10 days. Paralytic polio results when the ability to move muscles is lost. Paralytic poliomyelitis occurs in 1 out of every 100 people diagnosed. Spinal polio is paralysis of limbs; while, bulbar polio is paralysis of breathing and swallowing and, bulbar-spinal polio is the combination of the two. No matter the severity of the infection, the cytopathic effect (CPE) of the virus is the same on all host cells ("Poliomyelitis," 2009). Patients who have acute paralytic polio may, as a long-term consequence of this disease, develop the post-polio syndrome (PPS) (Halstead and Grimby, 1995). PPS usually occurs 30 to 50 after the onset of paralytic polio. Although the exact cause of PPS has not been determined, it has been suggested that PPS is primarily caused by premature exhaustion of new nerve terminal that connect to muscle fibers located in a paralytic muscle. The symptoms of PPS are new muscle weakening, chronic fatigue, and even atrophy of muscles (Halstead and Grimby, 1995).
There are different types of the poliovirus: type 1, type 2, type 3 (Younger, 1999). They all produce the same symptoms; however, separate antibodies are produced by the host cell for each type of poliovirus. Being immune to one type of poliovirus will not afford immunity to all three types of viruses since different antibodies are required. After entry into the host cell, some of the proteins synthesized from the poliovirus' genome function to inhibit the production of the host cell's proteins ("The Poliovirus Life Cycle," 2002). This alteration in the host cell function enables the virus to use all of the host cell's energy and ribosomes to produce its own proteins. Other cytopathic effects of this virus are that it increases the host cell's membrane permeability and also the condensation of the chromatin structure in the nucleus (Peters, 2005). The polioviruses lyse the host cell for the release of new progeny poliovirus ready to infect healthy cells (Peters, 2005).
Up until 1929, the only treatment for polio was physical therapy (Peters, 2005). In order to keep newly sprouted nerve terminal around paralytic muscles from degenerating, exercise is recommended (Younger, 1999). Also, to help alleviate the pain, hot packs are placed on sore muscles. The expected prognosis of polio with the use of physical therapy treatment is increased muscle movement involving new nerve terminals connecting muscle fibers than without the use of physical therapy treatment. In 1929, the iron lung was invented to aid those whose upper torso muscles were paralyzed to breathe (Peters, 2005). Prior to this invention, those who suffered from this crippling disease would die gasping for breath. While the iron lung saved lives for thousands of individuals, the quality of life suffered. Many patients, especially young children, spend years lying flat on their back inside a metal tube, unable to move anything. The expected prognosis of polio with the use of the iron lung machine treatment is enabling the survival of patients with paralyzed respiratory muscles. Without the use of the iron lung machine, patients would not be able to breath and would die (Peters, 2005).
Although no antiviral drugs for polio are available, vaccines are present. Dr. Jonas Salk was the first person to discover a successful vaccine for polio (Peters, 2005). Dr. Salk created an injectable vaccine using inactivated, killed poliovirus particles. This vaccine effectively prevents against paralytic polio. Seven years later, Dr. Albert Sabin created an oral vaccine from attenuated (live, but weakened) poliovirus particles (Collier, 2004). The Salk vaccine is administered in three doses, while the Sabin vaccine is administered in only one dose. The benefit of using the Sabin oral vaccine over the Salk vaccine is that it provides immunity to all three poliovirus strains; however, the down side of using this vaccine is that since live, weakened polioviruses are used, they can replicate and shed in the feces. The benefit of using the Salk vaccine is that all the viral particles are killed so there is no chance of replication inside the human body; however, the down side of using this vaccine is that it does not provide life-long immunity to the poliovirus and also one dose does not include immunity to all three strains (Collier, 2004).
There is, however, no vaccine for post-polio syndrome (PPS) (Halstead and Grimby, 1995). There are a few management treatments for PPS. Patients with respiratory muscle paralysis are put on a non-invasive nasal mask with positive pressure ventilation. Physical therapy including muscle exercise is also recommended for PPS. The expected prognosis for using physical therapy for PPS is not much different than without using physical therapy for PPS. After acute paralysis and post-polio syndrome, there is little to no hope that the patient will be able to recovery any movement in muscles that are paralyzed. The physical therapy most commonly helps alleviate any pain that the patient may have. However, the expected prognosis for the use of positive pressure ventilation treatment in PPS is much different than without the use of this treatment. Patients can die without the use of this treatment due to paralyzed respiratory muscles (Halstead and Grimby, 1995).
Preventative measures for the polio is the administration of the polio vaccine. When traveling to places where polio is still endemic, the Sabin oral vaccine is preferred as a preventative measure (Collier, 2004). This is because since it takes an oral route, the human body can create antibodies in the blood for the poliovirus and also block the virus from replicating in the intestines. Also, since the poliovirus is transmitted via oral-fecal route, as a preventative measure, it is cautioned feces contaminated water be not used in any way (e.g. drinking, cooking, swimming) (Collier, 2004).
Efforts to eradicate polio in the world have been fruitful due to the use Dr. Salk's and Dr. Sabin's vaccines; however, eradication of polio in the world is not yet completely successful. Some countries, such as India, still have few cases of polio every year (Younger, 1999). Despite the presence of the National Polio Eradication Program in India which works to vaccinate children the age of 5, the poliovirus still thrives. The geographic location of this country makes this country prone to poliovirus infections. The polio virus is endemic in regions of the world where hot, humid temperatures are present all year round. While in places located in the temperate zones, the polio virus is usually epidemic around the summer (Younger, 1999).
Certain populations are more susceptible to the poliovirus than others ("Poliomyelitis," 2009). Poor sanitation and hygiene is one of the biggest factors that make populations extremely susceptible to the poliovirus. Since polio is transmitted via fecal-oral route, infections rates spike in populations living in crowded areas where the water is contaminated with poliovirus feces. Thus, disadvantaged socioeconomic classes are most susceptible to the poliovirus since they are most likely to live in such crowded areas (Younger, 1999). Age is another factor that plays a role in susceptibility. Adults, adolescents, and older children are more susceptible to contracting polio with more server symptoms and extensive muscle paralysis than infants and younger children. While infants and younger children are more susceptible to the polio disease in general, whether it be non-paralytic or abortive polio. Gender is another factor that plays a role in susceptibility. Males are more likely to get polio than women. There are also certain risk factors which predispose individuals to getting polio. Pregnant women have an increased risk of getting paralytic polio by about three times. Physical exertion is another risk factor which causes individual to get paralytic polio (Younger, 1999).
Transmission of the 20 nanometer poliovirus occurs via a fecal to oral route (Peters, 2005). Selectivity of the poliovirus to the host intestine, throat, and motor neurons is due to the presence of the poliovirus receptor CD155 only on these host cells (Glenn et al., 1982). After attaching to the host cell, the poliovirus is endocytosed and releases its positive-sense single-stranded 7,450 nucleotide based RNA genome into the cytoplasm of the host cell ("The Poliovirus Life Cycle," 2002). Production of one long polypeptide takes place, then cleavage into individual proteins. New viral progeny are assembled and released after lysing the cell open. Paralytic or non-paralytic polio can develop as a result of infection (Younger, 1999). In most cases flu-like symptoms develop, while in some cases muscle paralysis, most commonly of the limbs, occurs. Three different types of poliovirus are present, each eliciting the production of a different antibody by the host cell, but causing the same symptoms. In some cases, post-paralytic syndrome develops after acute paralysis causing new muscle weakness. Although no antiviral is available for polio, both an oral and injectable vaccine is available (Collier, 2004). Sanitation is a key factor in the spread of this disease (Younger, 1999). Countries having a high population density, such as India, lead to living areas containing unsanitary water. The poliovirus is waterborne disease. Individuals who ingest water contaminated with poliovirus laden fecal matter develop polio. India is one of the few countries left in which polio is still endemic. With India's booming population, the eradication of polio will be a long and hard road. However, the number of cases reported each progressive year is continuing to drop (Younger, 1999).