Ebola Virus Disease – Uncommon and Dangerous Illness

Ebola Virus Disease (EVD) is an uncommon and dangerous illness, most commonly affecting humans and nonhuman primates (monkeys, gorillas, and chimpanzees). It is caused by an infection with five categories of viruses within the genus Ebolavirus: Taï Forest virus (species Taï Forest ebolavirus, formerly Côte d’Ivoire ebolavirus), Bundibugyo virus (species Bundibugyo ebolavirus), Ebola virus (species Zaire ebolavirus), Sudan virus (species Sudan ebolavirus), Reston virus (species Reston ebolavirus), and Bombali virus (species Bombali ebolavirus). Of these, only four (Ebola, Sudan, Taï Forest, and Bundibugyo viruses) are known to cause illness in humans.

Reston virus is known to cause illness in nonhuman primates and pigs, but not in humans. It is unknown if Bombali virus, which was recently identified in bats, causes illness in either animals or humans.

Ebola virus was first discovered in 1976 near the Ebola River in what is now the Democratic Republic of Congo. Since then, the virus has been infecting people intermittently, leading to outbreaks in several African countries. Scientists do not know where the Ebola virus comes from. However, based on the nature of similar viruses, they believe the virus is animal-borne, with bats being the most likely source. The bats carrying the virus can transmit it to other animals, like gorillas, monkeys, duikers, and humans.

Ebola Virus Disease spreads to people through direct contact with the bodily fluids of another human who is ill with or has already died due to EVD. This can occur when a person makes contact with the infected body fluids (or objects that are contaminated with them), and the virus breaches the body through broken skin or mucous membranes in the mouth, eyes, or nose. The virus can also spread to people through direct contact with the blood, bodily fluids, and tissues of infected fruit bats or primates. People can contract the virus through sexual contact as well.

Ebola survivors may experience difficult side effects after their recovery, such as fatigue, muscle aches, eye and vision problems, and stomach pains. Survivors may also face stigma as they reintegrate into their previous homes and communities.

What Are the Signs and Symptoms of Ebola?

Symptoms of Ebola Virus Disease (EVD) include fever, severe headache, muscle pain, weakness, fatigue, uncontrollable diarrhea, violent vomiting, abdominal pain, and unexplained hemorrhage (bleeding and/or bruising). Side effects may show up anywhere from 2 to 21 days after contact with the infection, with an average of 8 to 10 days. Numerous illnesses can have these same symptoms, including flu (influenza) or malaria. Dr. William Schaffner, an infectious disease expert at Vanderbilt University states, “The supportive care that we’re able to provide in the United States is so much better, so much more sophisticated, than what’s available in West Africa. … So we can move that needle of survival way down. Even Doctors Without Borders in West Africa are moving the fatality rate from 50 percent down to 30 percent. I bet we can do substantially better than that here” (Tognotti, 2018).

In some cases, internal and external bleeding may occur. This usually begins 5 to 7 days after the onset of symptoms. All infected individuals show some decreased blood clotting. Bleeding from mucous membranes or from locations of needle punctures has been reported in 40% to 50% of cases. This may cause vomiting blood, coughing up of blood, or blood in stool. Bleeding into the skin may cause petechiae, hematomas, ecchymoses, or purpura (especially around needle injection sites). Bleeding into the whites of the eyes, seeping from the gums, and blood in stool may also occur. Severe bleeding is rare; if it occurs, it is most likely in the gastrointestinal tract. The incidence of bleeding into the gastrointestinal tract has decreased since previous epidemics and is now estimated to be around 10%, with improved prevention of disseminated intravascular coagulation. Laboratory findings include low white blood cell and platelet counts, and elevated liver enzymes (EBV, 2016).

What Is the Cause?

Ebolaviruses contain single-stranded, non-segmented RNA genomes. This genome includes seven genes: 3′- UTR-NP-VP35-VP40-GP-VP30-VP24-L-5′- UTR. The genomes of the five diverse ebolaviruses (EBOV, SUDV, RESTV, BDBV, and TAFV) contrast in sequence and the number and location of gene overlaps.

As is the case with all filoviruses, ebolavirus virions (the complete, infective form of a virus outside a host cell, with a core of RNA or DNA and a capsid) are filamentous particles. They may take the form of a shepherd’s hook, a “U”, or a “6”, and they may be coiled, toroid, or branched. On average, ebolavirions are 80 nanometers in width and up to 14,000 nanometers in length.

The life cycle of the virus is believed to start with a virion joining to specific cell-surface receptors, such as C-type lectins, DC-SIGN, or integrins (proteins that function both mechanically, by attaching the cell cytoskeleton to the extracellular matrix (ECM), and biochemically, by sensing whether adhesion has occurred). This is followed by fusion of the viral envelope with cellular membranes.

The virions taken up by the cell then travel to acidic endosomes and lysosomes where the viral envelope glycoprotein GP is cleaved. This processing appears to enable the virus to bind to cellular proteins, prompting it to fuse with inner cellular membranes and release the viral nucleocapsid. The Ebolavirus structural glycoprotein, known as GP1,2, is responsible for the virus’s ability to bind to and infect targeted cells.

The viral RNA polymerase, encoded by the L gene, partially uncoats the nucleocapsid and translates the genes into positive-strand mRNAs. These are then translated into structural and non-structural proteins. The most abundant protein produced is the nucleoprotein. Its concentration in the host cell determines when L switches from gene translation to genome replication.

Replication of the viral genome results in full-length, positive-strand antigenome copies which are then transcribed into genome replicas for negative-strand virus progeny. Newly synthesized structural proteins and genome replicas assemble near the cellular membrane. Virions bud off from the cell and acquire their envelopes from the cellular membrane at the site of budding. The mature progeny particles then infect other cells to continue the cycle.

Studying the genetics of the Ebola virus is challenging due to EBOV’s virulent characteristics (Hotez, 2014).

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