You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT JAMA
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 284 No. 11, September 20, 2000 TABLE OF CONTENTS
  JAMA
  •  Online Features
  Health Agencies Update
 This Article
 •Extract
 •PDF
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Contact me when this article is cited
 Related Content
 •Similar articles in JAMA
 Topic Collections
 •Bioterrorism
 •Alert me on articles by topic

Ebola's Killer Protein Identified

Joan Stephenson, PhD

JAMA. 2000;284:1371.

Scientists at the National Institutes of Health (NIH) have identified a protein that appears to be the key to the uncontrollable bleeding that is a hallmark of Ebola virus infection (Nat Med. 2000;6:886-889).

The investigators found that one of Ebola virus's seven gene products, a glycoprotein (GP) that extends out from the surface of the virus, is apparently responsible for the virus's toxic effects. In studies of isolated blood vessels, GP caused the vessels to become leaky because of massive loss of the endothelial cells that line them. However, GP from a monkey strain of Ebola virus that does not cause illness in humans destroyed only monkey blood vessels, not human ones.

Further study revealed that a specific region of the GP is responsible for its toxic effects. When the investigators tested synthetic forms of GP lacking this region, the protein no longer ravaged blood vessels.

The researchers suggest that GP-inhibiting drugs might be able to help counter the deadly effects of Ebola infection, which kills up to 90% of the people it infects.







HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 2000 American Medical Association. All Rights Reserved.