Ebola Virus You think you have a case of the flu coming on. Nothing a few good nights’ rest won’t cure, you think. The next morning, your head throbs. Your skin aches. You feel feverish, and your chest hurts. You can’t get out of bed.
In the new few days, your fever skyrockets. You are disoriented and delirious. You throw up and notice the vomit is laced with blood. Next, you feel a liquid trickle out of your ears. With horror, you realize that it’s more blood. Soon blood is seeping from your nose, gums, and eyes.
The pain is excruciating. Inside your body, an army of microorganisms eats away at your veins and arteries and turns your organs into a sort of bloody cottage cheese. In 36 hours, you’re gone. You die in a pool of blood that has oozed out of every part of your body. That is what can happen to someone who contracts Ebola–one of the deadliest, most contagious viral diseases in the world. Ebola is a death sentence for up to 90 percent of those infected. (Peters, p.
1545) Few viruses are as deadly as Ebola. Its victims bleed to death, sometimes within days of infection. Researchers are just starting to learn how the virus kills. The first symptoms of infection with the Ebola virus–sore throat, headache, muscle pain–are deceptively mild harbingers of the horrors to come. After a few days the virus’s victims begin vomiting blood and bleeding profusely, both internally and from the nose, eyes, and gums. Between 50 and 90 percent of them die within two weeks–some within days–from blood loss and shock. There is no cure for Ebola and no vaccine.
The Essay on Ebola Zaire Virus Building Book
... microscope. To their surprised it looked very similar to the Ebola Zaire virus. They became frightened because they had been exposed to ... Nairobi. During the flight to Nairobi Charles found himself vomiting blood with a black liquid. Charles finally reached the hospital only ... went to a large cave called Kit cum cave. Three days after his return home, Charles began to have a headache. ...
A 1995 epidemic in the former Zaire, for example, left 245 dead; at least 44 more died in Gabon in 1996 and 1997. (Garrett, p. 57) The disease was first identified in 1976 in Sudan and Zaire (now Democratic Republic of the Congo).
The disease killed 397 of the 602 people infected. Since then, there have been outbreaks of Ebola in Ivory Coast and Uganda. This is the fourth time in seven years that the disease has struck Gabon. The WHO estimates that more than 800 people have died from Ebola, for which there is no cure or vaccine. One of the biggest challenges facing WHO workers in Gabon is educating villagers about the disease. “It’s difficult to ask much of villagers, many of whom are illiterate and who traditionally help their sick and transport the bodies of their dead,” said WHO director Victor Obiang.
(Garrett, p. 88) Common burial practices in the region include washing and dressing the dead before their journey to the afterlife. Burial practices often go on for several days, in part, to ensure that a person is really dead. When an outbreak in Uganda in 2000 killed 224 people, villagers came to fear local health officials and WHO workers, who sterilized corpses with bleach while wearing protective suits and then buried the dead far away from the living. “There was some propaganda that we were burying people alive, that we sold bodies,” said Lt. Col.
Walter Ochora, an official in Gulu, Uganda. “So people started hiding bodies.” (Garrett, p. 112) As WHO workers try to contain the recent Ebola outbreak, doctors and scientists around the world are trying to better understand the killer disease. Scientists don’t know what causes Ebola or where the virus lives in between outbreaks. There is no way of knowing when outbreaks will occur. Scientists suspect an animal or an insect carries the virus and that the first patient becomes infected through contact with an infected animal.
An early inquiry into the Gabon outbreak suggested that victims might have eaten the meat of an infected monkey they found dead in the jungle. For now, Ebola remains as mysterious as it is deadly. “What we don’t understand is how the virus lives in nature. All we know is that it’s out there, ready to attack another day,” said Mike Ryan, WHO’s outbreak coordinator. “It’s in there in the forest.” (Garrett, p. 125) Each outbreak of Ebola has been traced to an index case, the first infected person who came in contact with the disease host.
The Essay on Ebola Virus First Disease
... to cure the remaining people who had been infected with the virus. According to the movie, the first case of Ebola was in Germany ... and forty-two of the three hundred and fifteen people infected, died. A previous outbreak occurred in the same area 19 years earlier, ... doctors disagreed because the could not test for the multiple diseases that the blood could also contain. They were also not ...
Of all the disease-causing human refuses, only Ebola and a similar virus called Marburg, are the only ones remaining for which the host and cycle of transmission are not known. According to the World Health Organization (WHO), different theories have been developed to explain the origin of Ebola outbreaks. Initially, rodents were suspected. Laboratory studies suggest that bats infected with Ebola do not die, raising speculation that they may play a role in maintaining the virus in tropical forests. How does Ebola induce such massive hemorrhaging, and why do so few people fight it off? Researchers are only now providing the first clues to Ebola’s virulence. Surprisingly, this preliminary work has already led to an experimental vaccine that, in guinea pigs at least, seems to thwart the virus. One of the few things known about Ebola was that during the initial stages of infection, the virus floods the bloodstream with a glycoprotein–a protein with sugars attached. No one really knew what the glycoprotein’s role was in the viral assault, but its overwhelming presence suggested it meant bad news.
Researchers at the University of Michigan and at the Centers for Disease Control in Atlanta, however, have recently learned that the glycoprotein is part of a two-pronged attack on the body that leaves the victim bleeding and defenseless. (Jacobson, p. 80) There are actually two forms of the glycoprotein. The virus releases one into the bloodstream. The other–a larger version of the same glycoprotein–remains attached to the virus. Gary Nabel, a molecular virologist at the University of Michigan, has found that the free form fastens onto a type of white blood cell called a neutrophil.
These cells are the immune system’s frontline troops. They engulf and destroy invading viruses and bacteria. Neutrophils also signal the other fighters of the immune system: the B cells that make antibodies and the T cells that kill virus-infected cells. Nabel suspects that by binding to the neutrophils, Ebola’s free glycoprotein hobbles them so they can’t combat the invader or signal other cells. This frees the virus to attack the body’s blood vessels, using the attached glycoprotein as a key to enter endothelial cells–the cells that line the interiors of our veins and arteries. It seems that as Ebola invades and subverts the cells’ genetic machinery to make more of itself, it also damages the endothelial cells, making blood vessels leaky and weak.
The Essay on The Ebola Virus Cell Blood Host
The Ebola Virus History of, Occurrences, and Effects of Ebola, a virus which acquires its name from the Ebola River (located in Zaire, Africa), first emerged in September 1976, when it erupted simultaneously in 55 villages near the headwaters of the river. It seemed to come out of nowhere, and resulted in the deaths of nine out of every ten victims. Although it originated over 20 years ago, it ...
The patient first bleeds and then goes into shock as failing blood pressure leaves the circulatory system unable to pump blood to vital organs. Long before their immune systems can mount an antibody response–a process that can take weeks–most Ebola victims bleed to death. (Jacobson, p. 77) This understanding of Ebola’s deadly one-two punch may help Nabel further develop a prototype vaccine that has shown promising results in guinea pigs. The vaccine consists of the gene that codes for either type of Ebola’s glycoprotein spliced into a plasmid–a harmless piece of DNA from a bacterium. Nabel injected the vaccine into two groups of guinea pips. Two months later, he infected one group with live Ebola virus.
After four months lie infected the second group. (Guinea pigs suffer the same hemorrhagic response to Ebola as humans do.) The animals in the first group not only produced T cells and antibodies against Ebola but remained entirely healthy; most of the animals in the second group also survived the attack. Evidently, the vaccine gave the guinea pigs enough time to muster an immune response to counter Ebola. Nabel hopes his experimental vaccine will one day protect high-risk populations living in the virus’s home turf in sub-Saharan Africa, as well as the doctors and nurses who attend Ebola patients and the animal handlers in laboratories. Although Nabel is optimistic about the prospects for his vaccine, he points out that diseases often thwart the best efforts of medical research: “Viruses have a way of mutating and adapting.” (Jacobson, p. 25) Words Count: 1, 364.
Bibliography:
Garrett, L. The Coming Plague.
USA: HarperCollins, 2002. Jacobson, A. (1999.) Emerging and re-emerging viruses: An essay. www.uct.ac.za/microbi ology/ebola.html. Peters, C.J. 1995. Filoviridae: Marburg and Ebola virus hemorrhagic fevers.
The Term Paper on Ebola And Marburg Viruses
Ebola and Marburg Viruses Ebola and Marburg Viruses: Description Ebola is a member of negative-stranded RNA virus family Filoviridae. Ebola and Marburg viruses (filoviruses) are very similar in density, morphology, and odium dodecyl sulfate - polyacrylamide gel electrophoresis (SDS-PAGE) profile. As far as these particles are pleomorphic, it means that they can exist in many shapes. The Marburg ...
In Mandell, Douglas and Bennett’s principles and practice of infectious diseases, ed. G.L. Mandell, J.E.Bennett, R.Dolin, pp. 1543-46. New York: Churchill Livingstone..
