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From:
Haruna Darbo <[log in to unmask]>
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The Gambia and related-issues mailing list <[log in to unmask]>
Date:
Thu, 7 Aug 2008 15:01:00 EDT
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I am looking for a "good virus" or good Jinn. No luck yet. If you find one,  
lemme know. Meantime enjoy this new discovery. Haruna.
 
In a breakthrough that could eventually help tame one of the deadliest  
viruses known to man, researchers have laid bare the key to _Ebola's power_ 
(http://www.sciam.com/article.cfm?id=new-clues-to-ebolas-feroc) : a lone protein that 
resides on its  surface. The discovery paves the way for new treatments that 
target and destroy  the designated culprit, rendering impotent a virus that, 
though rare, can kill  up to 90 percent of the people it infects.

The so-called Ebola virus  glycoprotein, or "spike protein," was first 
discovered a decade ago and has been  a target for scientists attempting to _design 
vaccines_ (http://www.sciam.com/article.cfm?id=an-uncertain-defense)  and 
therapies to prevent it from  infecting cells. But, until now, researchers did not 
understand the protein's  structure—and thus, the best way to attack it.

"It's the only thing that  the virus puts on its surface that is absolutely 
critical for attaching to a  host and driving into that host for infection," 
says Erica Ollmann Saphire, an  immunologist at The Scripps Research Institute 
in La Jolla, Calif., and a  co-author of the study appearing today in _Nature_ 
(http://www.nature.com/nature/journal/v454/n7201/full/nature07082.html) .

Researchers discovered that the  compound is wrapped in benign carbohydrates 
that mask the virus's deadliness,  allowing it to elude immune system scouts. 
(The human immunodeficiency virus,  HIV, that causes AIDS also has this 
trait.) The good news: the discovery could  pave the way for drugs designed to see 
through that protective coating—and  trigger the immune system to attack.

"The structure of the glycoprotein  shows us the very few sites on its 
surface that are not cloaked by  carbohydrate," Ollmann Saphire explains. "These 
[sites] are the chink in the  armor, or the Achilles' heel, that we can target 
antibodies against."

"We  now have a much better handle on how in the world this virus gets into 
cells,"  Ollmann Saphire says. "We also have new maps we can use to develop 
strategies to  fight against it."

_Ebola_ (http://www.sciam.com/article.cfm?id=shaking-the-ebola-tree)  is an 
incurable disease that was first discovered  in 1976 in western Sudan and the 
eastern part of the Democratic Republic of the  Congo (then known as Zaire). It 
_seems to have arisen_ 
(http://www.sciam.com/article.cfm?id=experts-where-did-viruses-come-fr)  in the _rain forests of Africa_ 
(http://www.sciam.com/article.cfm?id=ebola-epidemic-wiping-out)  and parts of the western  Pacific. A 
person acquires the virus through contact with the bodily fluids of  someone 
already infected. It can take from two days to three weeks for symptoms  of Ebola 
to appear. The disease presents itself with a fever, muscle aches and a  cough 
before progressing to severe vomiting, diarrhea and rashes, along with  
kidney and liver problems. Death generally occurs as the result of either one or  a 
combination of:dehydration, massive bleeding due to leaky blood vessels,  
kidney and liver failure. The World Health Organization has documented 1,850  
cases of Ebola (mostly in sub-Saharan Africa) since its discovery; only 600 (32  
percent) of the victims survived.

Researchers made their latest finding  by studying the bone marrow of a lucky 
survivor of a 1995 Ebola outbreak in  Kikwit, a city in the southwestern part 
of the Democratic Republic of the Congo.  They found the glycoprotein 
attached to an antibody (a protein unleashed by the  immune system to fight viruses) 
in the marrow, the soft core of bones where red  blood cells are manufactured.

According to Ollmann Saphire, there is a  receptor located deep in the 
bowl-shaped structure of Ebola's glycoprotein that  latches onto the surface of host 
cells and tricks a protein there into granting  the virus entry. Once inside 
the cells, the fast-acting Ebola co-opts their  machinery to make millions of 
copies of itself and floods the person's  bloodstream.

Judith White, a microbiologist at the University of  Virginia, says that 
arming researchers with the protein structure that Ollmann  Saphire's group has 
described will allow them to "nip [the virus] in the bud,"  by beating down 
Ebola before it enters its host. (Most antivirals target viruses  such as HIV 
after they're already inside a host cell.)

"For those of us  in the trenches trying to study the virus entry, and the 
immune reactions to the  virus, and how to prevent virus entry, and how to come 
up with better immune  therapies," she says, "this gives us all new eyes to 
[solving] those  problems."



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