One Group With Live Ebola Virus example essay topic

Each outbreak of Ebola has been traced to an index case, the first infected person who came in contact with the disease host. 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 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).