The Ebola virus and its genus are named after the country Zaire, now known as the Democratic Republic of Congo, where it was first discovered.

Ebola virus disease (EVD), also known as Ebola haemorrhagic fever, is a severe illness in humans.Ebola virus is a member of the viral family Filoviridae. It is a negative-sense, enveloped RNA virus with 7 genes (Toner et al., 2014). The Ebola outbreak in 2014 is due to the Zaire strain of ebola virus. The virus was first transmitted to humans from wild animals, and is now predominantly spread through the human population via human-to-human interaction. Mortality rate of the disease is 50%, with the first cases arising in Central Africa. Currently, there are no approved Ebola vaccines. Two potential vaccine candidates are undergoing research (Dixon & Schafer, 2014).

Figure 1: The picture above shows the Ebola virus overlayed on a map of America. The picture represents the oncoming potential of the virus affecting individuals in America and causing mass deaths (Smith, 2014).

Ebola virus can be transferred from an animal reservoir to humans. Bats are thought to be the reservoir species, with other intermediary hosts acting in between (Toner et al., 2014).

The virus can be transferred to humans through contact with bodily secretions of infected wild wild animals, including; chimpanzees, gorillas, fruit bats, monkeys, forest antelope and porcupines found ill or dead in the rainforest (Dixon & Schafer, 2014). The ebola epidemic spreads widely mostly due to human-to-human contact of contaminated secretions. The virus is easily spread through traditional burial practises, where during the funeral the family would bathe, kiss, and embrace the body. Proper burial of bodies, and careful contact with infected patients is a vital asset in the prevention of the spread of ebola (Frieden et al., 2014).

In 1976 the first ever reported cases of Ebola were reported, but the cause of this virus is still unknown. A group of scientists looked at a group of more than a thousand small vertebrates between 2001 to 2003 to look and collect samples of Ebola. They looked in the areas of Gabon and the Republic of Congo, and found evidence of asymptomatic infection in three differing species of fruit bat. This could mean that the species could serve as a reservoir for the virus. Ebola outbreak in 2001 and 2005 were linked to analogous widespread deaths in gorilla and chimpanzee populations. To find the source of such infections 1,030 animals were captured, including 679 bats, 222 birds and 129 small terrestrial vertebrates. Of the infected species identified during these field collections, immunoglobulin G (IgG) specific for Ebola virus was detected in serum from three different bat species. The ebola virus specifically infected the liver and spleen of the animals, and the virus proliferated more rapidly in dry weather conditions (Leroy et al., 2005).

Figure 2: The diagram explains how the symptoms express in a patient infected by the virus (Center of Disease Control, 2014).

The symptoms of Ebola arise much like the common flu; with fever, fatigue, headache, sore throat and lethargic behaviour. The virus then moves into the gastrointestinal tract causing symptoms of vomiting, rash, impaired kidney and liver function and diarrhea. The infection affects all organs until the patient gets septic shock and suffers organ failure.

The following symptoms will occur in patients at varying rates dependent on immune function, and viral infection.

1. Early Stage Symptoms:

• 0-5 days after incubation period
• fever, fatigue, malaise, anorexia, headache, hiccups, abdominal pain
• These symptoms can often be overlooked and diagnosed as influenza if clinician isn't aware of an Ebola outbreak.

2. Mid-Stage Symptoms:

• Roughly after 5 days
• Severe watery diarrhea and vomiting

3. Late Stage Symptoms:

• Bleeding from eyes
• Septic Shock
• Death

(Toner et al., 2014)

The ebola virus (EV) first enters the host through the mucous membranes, breaks in the skin (including microabrasions), or punctures (Toner et al., 2014). The virus attacks and replicates in a wide variety of host cells, but initially targets immune cells such as the monocytes and macrophages at the site of inoculation, as well as dendritic cells (Walker & Paessler, 2013). Infected immune cells are responsible for the spread of the virus from the site of inoculation to the rest of the body (Martines et al., 2014). Infected cells travel through the lymphatic system to the regional lymph nodes where they enter the bloodstream to the liver and spleen (Martines et al., 2014). If left untreated, the virus then spreads to the rest of the body and is present in the skin and in all body fluids. The virus can thus cause cellular damage and leads to necrosis of many different organs.

The infection of human monocytes with ebola results in the activation of monocytes and increased release of pro-inflammatory cytokines and chemokines. The inflammation damages blood vessels, and causes leakage and internal bleeding of the host. Infected dendritic cells and macrophages result in impairment of T-cell maturation and proliferation, and thus compromises host immune system (Walker & Paessler, 2013). Additionally, the presence of ebola virus glycoproteins (GP) found on the transmembrane of the viral structure causes cell damage, and alters the release of cytokines important to inflammation and fever response. Additionally, the virus affects endothelial cells and causes damage to vascular integrity.

Figure 3: The pathogenesis of ebola virus. Initial entry into hostleads to increased inflammation, decreased immune response, damage to vasculature, and necrosis of different organs (Geisbert et al., 2003).

The onset of symptoms upon infection ranges between 2 to 21 days. An individual is not infectious until symptoms are shown. Laboratory tests will indicate high white blood cell and platelet counts and elevated liver enzymes.It is believed that that the Ebola virus works through glycoproteins found on the transmembrane of the structure. When the glycoprotein (GP) introduces its contents into monocytes or macrophages it causes cell damage that alters the release of cytokines important to inflammation and fever response, as well as affecting endothelial cells, causing damage to vascular integrity (Geisbert et al., 2003). The other glycoprotein released by the Ebola virus, sGP, may affect the human immune response by inhibiting neutrophil activation. The transmembrane GP may contribute the symptoms of hemorrhagic fever by localizing the virus to cells of the reticuloendothelial network and the lining of blood vessels (Frieden et al., 2014).

The ebola virus is covered in an glycoprotein envelope which allows the virus to bind to the host cell membrane and infect the cell. Within the envelope is the virus’ genome which consists of seven genes which are responsible for the production of proteins in transcriptional editing. Another protein termed sGP is responsible for the early stages of the infection. Its serves only as a structural protein and it does not adhere to the surface of the cell. The second protein, GP, contains a hydrophobic tail, and is present on the surface of the envelope, making it responsible for the infection of new cells. The human immune system works in preference of sGP over the GP protein. The goal of vaccine therapy is to create an antibody that targets the GP while ignoring sGP. Chemists have been better able to understand the structure of the virus to X-ray crystallography. GP is composed of 676 amino acids broken up into two sections by a cysteine disulphide bond. The first section is responsible for attachment to the host cell. The second subsection integrates the viral envelope into the host cell membrane. The most promising method for disrupting the virus life cycle involves the creation antibody that targets GP1 or GP2 (Geisbert et al., 2003).

Figure 4: The above diagram explains how glycoproteins found on the nuclear envelope of the virus cells attack macrophages. Once they attack macrophages, cytokines are leased that caused endothelial cell toxicity (Geisbert et al., 2003).

Rehydration with oral or IV fluids and treatment of specific symptoms improves chances of survival in symptomatic patients. Although there is no cure available for EVD, an arrange of potential treatments including blood products, immune therapies and drug therapies are currently being evaluated (Sullivan et al., 2000). The new treatments target the Zaire Ebola Virus Strain (ZEBOV), the strain observed in the current outbreak (Zeliadt, 2014). With over 50 million dollars in funding from the US National Institutes of Health, Thomas Geisbert’s lab at the University of Texas is conducting a big portion of this research along with scientists in Baltimore, Maryland and Canada’s Tekmira pharmaceuticals (Zeliadt, 2014).

This vaccine is being developed in Geisbert’s lab by using a recombinant vesicular stomatitis virus (rVSV). The vector expresses the Ebola glycoprotein in order to create immunity in rhesus macaques (Geisbert & Feldmann, 2011). Trials performed on macaque monkeys have shown that a single shot of the vaccine is enough to save them from a lethal dose of the virus (Meltzer et al., 2014). These observations were made twenty-eight days post infection (Geisbert & Feldmann, 2011). Furthermore, the vaccine has been shown to be effective when administered half an hour post infection (Geisbert & Feldmann, 2011). This vaccine is currently undergoing phase 1-safety trials in humans (Meltzer et al., 2014).

The newest treatment being developed in Geisbert’s lab is ZMapp. ZMapp is a monoclonal-antibody therapy consisting of the three monoclonal antibodies: c13C6, c2G4, and c4G7 (Qiu et al., 2014). Trials done on rhesus macaque monkeys have shown that ZMapp is effective in protecting macaque monkeys from a lethal dose of Ebola virus, with treatment starting as late as five days post infection (Qiu et al., 2014). When therapy was initiated, fever, leukocytosis, thrombocytopenia and viraemia were present in the majority of monkeys (Qiu et al., 2014). These symptoms and other physiological abnormalities were reversed and virus load was lowered after initiation of therapy (Qiu et al., 2014). The monkeys made a full recovery twenty-eight days after infection. However, it is unknown if ZMapp-treated survivors of Ebola are prone to reinfection (Qiu et al., 2014).

Recently, ZMapp was used compassionately for two American healthcare workers, Dr. Kent Brantly and Nancy Writebol, who were infected with Ebola virus (University of Texas, 2014). Overall, the two individuals responded well and are now virus-free (University of Texas, 2014). However, the efficiency of this therapy remains unknown as 45% of Ebola patients make a recovery without treatment (University of Texas, 2014).

This drug was developed by Canada’s Tekmira pharmaceuticals along with the Geisbert lab (Zeliadt, 2014). It involves RNA interference (RNAi) by targeting ZEBOV genes and silencing them (Zeliadt, 2014). The drug was observed to protect rhesus macaques from lethal doses of the Ebola virus; as long as it is administered within two days post infection (Zeliadt, 2014). It is now being tested in phase 1-safety human trials along with combinations of ZMapp and other antibodies. As the FDA continues to allow its development, TKM-Ebola may provide insights into the role of epigenetics in the Ebola outbreak (Zeliadt, 2014).

Human derived adenovirus has been used as a vector to develop vaccines for several pathogenic diseases (Stanley et al., 2014). In fact, a vaccine using the human derived adenovirus type 5 vector (rAd5) has been observed to protect macaque monkeys against ZEBOV (Stanley et al., 2014). However the main limitation to human derived adenovirus vectors is pre-existing immunity to the vector due to previous exposure in the environment (Stanley et al., 2014).

In affiliation with the University of Texas, Nancy J. Sullivan of the National Institute of Allergy and Infectious Diseases Vaccine Research Center has developed a vaccine that uses a chimpanzee derived adenovirus type 3 vector (NIH, 2014). The vector expresses the Ebola glycoprotein in order to trigger an immune response in macaque monkeys (Stanley et al., 2014). Only two of the four macaques that were vaccinated were able to survive when given lethal doses of the ZEBOV ten months following immunization (Stanley et al., 2014). However, when a booster shot was provided eight weeks post initial vaccination, all four macaques survived when the ZEBOV was introduced ten months later (NIH, 2014). The booster shot was created from a different vector, a poxvirus, with Ebola glycoprotein expression (Stanley et al., 2014). This research suggests that CD8+ T-cells (also known as Killer T cells) as well as memory T cells are needed in high quantities so that the immune system can clear the virus from the host (Stanley et al., 2014). This vaccine is currently in phase 1-safety trials in Maryland (NIH, 2014).

Recently, it has been reported that the Health Science Department in Hamilton, Ontario will be an institution accepting individuals that could potentially have Ebola. They have provided a list of things that will be used. These involve:

• Hand sanitizer
• Equipment that covers the foot and extends to the knee
• Gown (prevents needles from entering)
• n95 mask(air filter)
• gloves

At the end of this process, another person will ensure there aren’t any openings (CHCH news, 2014).

Individuals in Hamilton should not worry. One of the reasons is that an individual doesn’t get Ebola that quickly from another person. It requires very close association with another person’s bodily fluids. Moreover, there aren’t flights heading from West Africa to Canada. Hence, this drastically decreases the possibility of Ebola coming to Canada. In addition, it does put fear in people since there isn’t a cure for it. There have been approximately 20 potential Ebola cases but they have all been negative (Carter, 2014).

An individual named Sawyer arrived to Nigeria on July 20th. Sawyer was extremely ill and had recently come back from his sister’s funeral in Liberia. Sawyer was taken to the hospital and he past away (Macharia, 2014).

The steps taken that allowed Nigeria to contain Ebola from spreading rapidly:

Firstly, there was immediate documentation: Sawyer was the first individual to be diagnosed with Ebola and was taken to the hospital immediately. Secondly, there was excellent support from the government. Was able to provide the necessary resources such as funds to solve the situation. Thirdly, the virology laboratory equipment is advanced which allows determination of potential Ebola situations much easier. Fourthly, the campaigns are effective. Lastly, they were able to determine the 20 individuals and families that came into contact with Sawyer at the Hospital. In addition, they concluded that there was about 898 individuals that the 20 people came into contact. They were all checked for symptoms regarding Ebola for a period of 21 days (Macharia, 2014).

Ebola is a very contagious and deadly disease. The best way to prevent infection is to avoid contact with sick individuals and avoid handling human remains of sick individuals. Additionally, avoid areas with known outbreaks. Wash hands frequently to avoid spread and infection of ebola. Avoid bush meat in specific areas of Africa. Most importantly, when in contact with individuals who are infected, follow CDC protocol for infection control (Meltzer et al., 2014).

The CDC is predicting 1.2 million Ebola cases by January 2015. However, the recent eradication of Ebola in Nigeria gives hope that, when proper preventative and control measures are taken, Ebola can be contained and the outbreak can be brought to an end. Worldwide efforts are needed in order to stop the spread of Ebola to other countries. Financial and healthcare support needs to continue to be sent to areas currently dealing with outbreaks. Initial control efforts in certain regions were hindered because there was disbelief that an Ebola outbreak was real and something to be concerned about. To ensure that citizens are willing to comply with and join control measures issued by governments and health agencies, we all need to be spreading awareness of the significance of Ebola but at the same time prevent unnecessary anxiety and false information from being passed on. Regardless of where you live, by everyone knowing how to recognize the signs of Ebola and what to do in case of an outbreak would greatly reduce the chance of an Ebola in other parts of the world. Humanity needs to join together and we all need to do what we can to help those who are effected and prevent others from being effected (Toner et al., 2014).

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