Eradicating Ebola: In U.S. Biomedical Research, We Trust

BSL-4 environment

Caption: Researcher inside a biosafety level 4 laboratory, which provides the necessary precautions for working with the Ebola virus.
Credit: National Institute of Allergy and Infectious Diseases, NIH

Updated August 28, 2014: Today, the National Institutes of Health (NIH) announced plans to begin initial human testing of an investigational vaccine to prevent Ebola virus disease. Testing of the vaccine, co-developed by NIH’s National Institute of Allergy and Infectious Diseases (NIAID) and GlaxoSmithKline, will begin next week at the NIH Clinical Center in Bethesda, MD.

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As the outbreak of Ebola Virus Disease continues to spread in West Africa, now affecting four countries in the region, I am reminded how fragile life is—and how important NIH’s role is in protecting it.

NIH research has helped us understand how Ebola initially infects people and how it spreads from person to person. Preventing this spread is currently our greatest defense in fighting it. Through research, we know that the Ebola virus is transmitted through direct contact with bodily fluids and is not transmitted through the air like the flu. We also know the symptoms of Ebola and the period during which they can appear. This knowledge has informed how we manage the disease. We know that the virus can be contained and eradicated with early identification, isolation, strict infection control, and meticulous medical care.

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Cool Videos: Alzheimer’s Disease

NIH logo, surrounded by a filmstrip border

To keep everyone energized during the hot, hazy days of summer, I’ve decided to start a new series called Cool Videos. This virtual mini-film fest will feature a variety of videos—some even produced by researchers themselves—in which biomedical science plays a starring role.

Throughout August, you’ll have a chance to screen some of the winners of a recent video competition celebrating the Tenth Anniversary of the NIH Common Fund. These short clips, created by NIH-funded researchers, include a parody of “Breaking Bad,” some underwater camerawork reminiscent of Jacques Cousteau, and even a rap video.

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PubMed Commons: Catalyzing Scientist-To-Scientist Interactions

LogoToday’s scientists find it tough to keep up with all of the latest journal articles, innovative methods, and interesting projects of colleagues in their fields. That’s understandable, because there are tens of thousands of journals, hundreds of conferences in major fields, dozens of emerging technologies, and huge geographic distances separating researchers who may share common interests. But science is increasingly a team sport—and it’s important to provide scientists with as many avenues as possible through which to interact, including commenting on each other’s work.

To encourage such exchanges, NIH’s National Center for Biotechnology Information (NCBI) recently developed PubMed Commons, a resource that gives researchers the opportunity to engage in online discussions about scientific publications 24/7. Specifically, this service allows scientists with at least one publication to comment on any paper in PubMed—the world’s largest searchable database of biomedical literature, with more than 3 million full-text articles and 24 million citations.

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Snapshots of Life: Wild Outcome from Knocking Out Mobility Proteins

Spiky fibroblast cell

Credit: Praveen Suraneni and Rong Li, Stowers Institute for Medical Research

When biologists disabled proteins critical for cell movement, the result was dramatic. The membrane, normally a smooth surface enveloping the cell, erupted in spiky projections. This image, which is part of the Life: Magnified exhibit, resembles a supernova. Although it looks like it exploded, the cell pictured is still alive.

To create the image, Rong Li and Praveen Suraneni, NIH-funded cell biologists at the Stowers Institute for Medical Research in Kansas City, Missouri, disrupted two proteins essential to movement in fibroblasts—connective tissue cells that are also important for healing wounds. The first, called ARPC3, is a protein in the Arp2/3 complex. Without it, the cell moves more slowly and randomly [1]. Inhibiting the second protein gave this cell its spiky appearance. Called myosin IIA (green in the image), it’s like the cell’s muscle, and it’s critical for movement. The blue color is DNA; the red represents a protein called F-actin.

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Autism Architecture: Unrolling the Genetic Blueprint

An array of childrenWe know that a combination of genetic and environmental factors influence a child’s risk of autism spectrum disorder (ASD), which is a diverse group of developmental brain conditions that disrupt language, communication, and social interaction. Still, there remain a great many unknowns, including the crucial issues of what proportion of ASD risk is due to genes and what sorts of genes are involved. Answering such questions may hold the key to expanding our understanding of the disorder—and thereby to devising better ways to help the millions of Americans whose lives are touched by ASD [1].

Last year, I shared how NIH-funded researchers had identified rare, spontaneous genetic mutations that appear to play a role in causing ASD. Now, there’s additional news to report. In the largest study of its kind to date, an international team supported by NIH recently discovered that common, inherited genetic variants, acting in tandem with each other or with rarer variants, can also set the stage for ASD—accounting for nearly half of the risk for what’s called “strictly defined autism,” the full-blown manifestation of the disorder. And, when the effects of both rare and common genetic variants are tallied up, we can now trace about 50 to 60 percent of the risk of strictly defined autism to genetic factors.

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