The Ebola Virus: An overview
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Published: Fri, 05 May 2017
In the Cote d’Ivoire, also called the Ivory Coast, is where my step-mother was raised as a child. She remembers the horrifying stores stories of blood-eyed village man that turned to liquid. She has never experienced an Ebola outbreak, but always feared its coming. The name Ebola is one that strikes fear in the hearts of many and conjures images of people with blood coming out of all orifices of the body. Fueled by the cult classic movie Outbreak, featuring Dutsin Hoffman and Morgan freeman, the public opinion on the Ebola-like virus called Motaba, is one of fear and little actual knowledge. Although as deadly as most people believe, there are several different strains of Ebola, one of which does not even cause disease in humans. The Ebola virus was named after a river in the Zaire, now called the Democratic Republic of Congo, Africa. The Ebola virus belongs to the same family as the Marbug virus.
Apart of the Filoviride family, Ebolavirus genus, and Mononegavirales order, the Ebola virus is a negative-sense, single-stranded, nonsegmented RNA virus, belonging to the V group in Baltimore classification. There are five species, also called subtypes, named for the region where there was documented human or animal disease; they include the Zaire ebolavirus (ZEV), Sudan ebolavirus (SEV), Ivory Coast or Cote d’Ivoire ebolavirus (CIEV), Bundibugyo ebolavirus (BEV), and Reston ebolavirus (REV)- not known to cause disease in humans. (Global Alert and Response) Ebola viruses are generally tubular-like shaped, but vary among virions. There is a classical shaped typical of Ebola viruses called a shepherd’s crook or also known as an eyebolt, which is shaped like a U, 6, or coiled and sometimes branched. They are typically 80nm in diameter and composed of a lipid bilayer with virally encoded glycoprotein spikes on the surface, which are 10nm long and 10nm apart- composing the outer envelope that is derived from the host cell membrane. Generally, they are 800nm-1000nm long with a central nucleocapsid core. (CDC Special Pathogens Branch) The nucleocapsid core is formed by the viral genomic ssRNA with coding for 4 virion structural proteins: nucleoprotein (N), VP35, VP30, and polymerase protein (L), and 3 membrane associated proteins: VP24, VP40, and glycoprotein (GP) – in secreted and non-secreted forms. The matrix space, between the nucleocapsid and envelope, is composed of viral proteins VP24 and VP40. (CDC Special Pathogens Branch) The genome consist of a linear negative-sense, single-stranded RNA molecule approximately 19,000 nucleotides in length. (“Global Alert and Response”) The 3 prime terminal end is not polyadenylated and the 5 prime end is not capped. Sections of the L and NP genes have been identified as endogeneous in the genomes of several small mammals. “Most Filovirus proteins are encoded in single reading frames; the surface GP is encoded in 2 frames (open reading frame [ORF]1 and ORF II) The ORFI (amino-terminal) of the gene encodes for a small (50-70kd), soluble, nonstructural secretory glycoprotein (sGP) that is produced in large quantities early in Ebola infection” (King)
Even though the genomic material alone is not infectious, after infection of human and nonhuman primates, there is an early onset of rapid viral replication that is usually associated with lethal cases due to an ineffective immunological response. The life cycle and replication of the ebolavirus is still being investigated. For replication, the ebolavirus utilizes the host cell machinery and metabolism to convert its genomic ssRNA into multiple copies. Via endocytosis from host cell vesicles, the ebolavirus attaches through the host receptors located on the glycoprotein surface. (King) The virus membrane fuses with the host vesicle, releasing the nucleocapsid into the host cell cytoplasm. This virus encodes for its own RNA-dependent RNA polymerase that transcribes the negative-sense, ssRNA genome into several viral monocistronic positive-sense, ssmRNA that is then recognizable by host cell machinery. Additionally, the viral RNA-dependent RNA polymerase synthesizes viral progeny using this positive-sense ssRNA as a template. (CDC Special Pathogens Branch) During protein synthesis, the viral proteins are processes and a glycoprotein precursor (GP0) is cleaved into glycosylated GP1 and GP2. The first form heterodimers and then trimers. This trimeric complex binds the virus to endothelial cells lining the interior surface of blood vessels, causing interference of coagulation and eventually hemorrhagic manifestations that characterize the ebolavirus. (King) Secreted glycoprotein precursors are cleaved and secreted from the cell after lysis. It is believed that the expression of ebolavirus glycoprotein on target cells enhance viral entry. (Manicassamy, and Rong 79) After protein and viral assembly occur, at the host cell plasma membrane, budding occurs, resulting in lysis, destroying the host cell. The main targets of infection for ebolavirus include tropism for endothelial cells, immune cells like macrophage and dendritic cells, and hepatocytes. Thereby targeting immune response and resulting in immune suppression. Secreted glycoprotein (sGP) binds to and inhibits the activation of neutrophils. The ebolavirus selectively inhibits the host’s interferon response. “The sGP binds to neutrophil CD16b, a neutrophil-specific Fcg receptor III, and inhibits early neutrophil activation.” (King)
Equipped with the ability to target immune cells, the pathogenesis of the ebolavirus is what sets it apart from other viruses and gives it a notorious reputation. The incubation period of the ebolavirus is 2-21 days. (CDC Special Pathogens Branch) The mechanism of viral dispersion is from transmission by direct contact with blood, oral secretions, or other bodily fluids of an infected person, via contact with the corpse of a previously infected person, and for some strains, even through handling of infected chimpanzees, gorillas, antelopes, and cynomolgus monkeys. (“Global Alert and Response”) “African-derived Filovirus infections are characterized by transmission from an unknown host (possibly bats) to humans or nonhuman primates, presumably via direct contact with body fluids such as saliva or blood or other infected tissues. (Leroy, Kumulungui, Pourrut,Rouquet, and Hassanin 575-576) Evidence in nonhuman primates indicates that Sudan ebolavirus and Zaire ebolavirus may be transmitted by contact with mucous membranes, conjunctiva, pharynx and gastrointestinal surfaces, small breaks in the skin, and, at least experimentally, by aerosol.” (King) Ebola virus infections are acute with no carrier state. Ebola hemorrhagic fever (EHF) is characterized by the onset of several symptoms including fever, malaise, weakness, joint and muscle pains, headaches, stomach pain and sore throat. This is usually followed by severe diarrhea, vomiting, rash, red eyes, hiccups, impaired liver and kidney function. In some cases, the infected person may exhibit internal and external bleeding. Long term consequences of can include death. It is currently unknown why some patients can recover from EHF while others die. (“Global Alert and Response”) However it is documented that those who die could not mount a significant immune response to the ebolavirus, and no proinflammatory cytokines were detectable.
As a result of viral clearance by the immune system, there are alterations in immune cell functions and severe focal necrosis occurs as a result of rapid viral replication in all tissues, causing body fluids to become highly infectious. Necrosis of the liver and kidneys is related to the formation of councilman-like bodies. Viral particles and cell damage caused by lysing of host cells after viral replication initiate the release of cytokines TNF-Î±, IL-1Î², IL-6, and IL-8. (King) Theses cytokines act as signaling molecules resulting in enhanced cell-mediated and humoral-mediated immune responses, including fever and inflammation. (CDC Special Pathogens Branch) Lymphopenia also occurs. The cytopathic effect caused by the ebolavirus is from viral infection in endothelial cells with the loss of vascular integrity. With the synthesis of GP, the loss of vascular integrity increases and decreased integrins that are used for cell adhesion to inter-cellular structures occur. (King) Along with ineffective coagulation, blood leaks through blood vessels causing internal and external bleeding characteristic of EHF.
Currently, there are no standardized treatments for patients diagnosed with EHF, yet they receive supportive therapy. This consists of “balancing the patient’s fluids and electrolytes, maintaining their oxygen status and blood pressure, and treating them for any complicating infections.” (CDC Special Pathogens Branch) There are currently no anti-Ebola viral agents that exist. “The nucleoside analogue inhibitors of S-adenosylhomocysteine hydrolase (SAH) have been shown to inhibit EBO-Z viral replication in adult BALB/c mice infected with mouse-adapted Ebola virus.” (King) The human case fatality rates are between 50-89%, depending on the species viral strain. The cause of death is usually shock or organ failure from internal bleeding. The most highly lethal species is the Zaire subgroup with a mortality rate up to 89%. There are currently no commercially available Ebola virus vaccines, although “a recombinant human monoclonal antibody directed against the envelope GP of Ebola has been demonstrated to possess neutralizing activity. This Ebola neutralizing antibody may be useful in vaccine development or as a passive prophylactic agent.” (King) Laboratory diagnosis includes serological testing of antigen capture ELISA testing, IgM-capture ELISA, PCR, virus isolation and observation via electron microscope, immunohistochemistry testing, IgG-capture ELISA, and RT-PCR. Since test sample pose an extreme biohazard risk, they should be handled in BSL-4 containment hood. Also, saliva and urine samples are used to test for the presence of the virus. Laboratory testing of manual cell differentials usually revel low white blood counts and low platelet counts, also elevated liver enzymes are typical among infected patients. (“Global Alert and Response”) In order to aid in the prevention of spread of the ebolavirus, containment of suspected patients should be followed with isolation from other patients and barrier nursing techniques used. Disinfecting techniques are required when handling any soiled linen of an infected patient. Disposable personal protective equipment should be utilized by health care and hospital workers. Additionally, people who have died from the Ebola virus should be buried quickly. Anyone that had contact with infected individuals should be placed under surveillance and monitored for Ebola-like symptoms. Tracking and following-up with people who may have been exposed, is important in containment of the Ebola virus. Quick prognosis of the disease is important; also accurate diagnosis is essential for necessary critical therapeutic care to begin. Because the natural reservoir for the Ebola virus is unknown, preventing future outbreaks is difficult. (Leroy, Kumulungui, Pourrut,Rouquet, and Hassanin 575-576) It has been postulated that the natural reservoir resides in the rain forest of the Africa continent or areas in the Western Pacific, and possible be fruit bats. Experimentally, fruit bats injected with the Ebola virus do not die. Humans are expected to be infected either directly from the natural reservoir or though a chain of transmission from the natural reservoir. (Leroy, Kumulungui, Pourrut,Rouquet, and Hassanin 575-576)
While mainly impacting sub-Saharan African countries, Ebola virus is not endemic to the United States. In the US, there have been human infections of the Reston strain of Ebola virus acquired by primate animal care workers. The Reston strain doses not have pathogenic effects in humans. There have been well documented outbreaks. About 1900 cases and approximately 1200 deaths have been documented since the Ebola virus was discovered. (“Global Alert and Response”) In 1967, the Ebola virus was first identified in the western province of Sudan and Zaire. There were 284 people infected in Sudan, 151 people died. Another outbreak occurred in Sudan in 1971 causing 22 deaths. In 1994, the first documented EHF case was detected in Gabon with 9 deaths in 1994 and 45 deaths in 1996. (CDC Special Pathogens Branch) Outbreaks of the Zaire subtype reported from 2001-2003 included 302 cases of infection with 254 deaths. Another large epidemic occurred in Kikwit, located in the Democratic Republic of the Congo, in 1995 with 315 cases and 250 deaths. (King) Due to the fact that most outbreaks have occurred in sub-Saharan Africa, most patients have been black, although the demographic of infection of the Ebola virus is not restricted to Africans alone. No sex predilection exists for the Ebola virus, although the way each sex is exposed to virus varies due to daily duties in the community. Risk factors for catching Ebola virus include close contact with infected individuals or infectious body fluids decreased knowledge on proper protection while dealing with infected patients. (CDC Special Pathogens Branch) Due to its high mortality rate, the Ebola virus is thought to be a possible bioterrist agent. Challenges exist in sub-Saharan regions of Africa during Ebola virus outbreaks. Due to social issues and low economical resources, during an outbreak the spread of the virus in healthcare facilities increases. Nosocomial transmission of the Ebola virus is common and lack of knowledge of proper isolation techniques and nurse barrier techniques are reasons for the increased spread in healthcare settings. Additionally, there is ongoing research to develop diagnostic tools to detect early EHF. (CDC Special Pathogens Branch) More knowledge of how the virus spreads and the exact natural reservoir for the virus is needed to prevent and contain outbreaks. (King) Epidemiological studies of the Ebola virus and its role in human hemorrhagic fevers include comparisons to the Marbug virus. Ebola virus is also lethal in cynomolgus macaques.
In conclusions, the Ebola virus could pose a possible bioterrist threat due to its high mortality rate. It is necessary to conduct further research on finding the actual natural reservoir for this virus and possible vaccination studies for this viruses. Additionally, medication to counteract the immune shut down sometimes caused by the viral replication of the Ebola virus should be researched and manufactured. Because this virus usually effected sub-Saharan African countries, programs should be implemented on the spread of Ebola and precautions to take while caring for infected individuals and proper burial of deceased loved ones. Ebola is an amazing virus and its ability to evade the host immune system is a mechanism that warrants future studies and more attention.
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