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Archive - Feb 24, 2015

MIT Scientists Develop Field-Usable Device Enabling 10-Minute Test to Detect & Differentiate Ebola, Yellow Fever, and Dengue Fever Viruses

In a February 24, 2015 release from the MIT News Office, it was announced that MIT scientists have developed a simple test that can detect and differentiate Ebola, yellow fever, and Dengue fever viruses. This is a major development with much practical promise. When diagnosing a case of Ebola, time is of the essence. However, existing diagnostic tests take at least a day or two to yield results, preventing health care workers from quickly determining whether a patient needs immediate treatment and isolation. The new test from MIT researchers could change that: the device, a simple paper strip similar to what is used for a pregnancy test, can rapidly diagnose Ebola, as well as other viral hemorrhagic fevers such as yellow fever and dengue fever. “As we saw with the recent Ebola outbreak, sometimes people present with symptoms and it’s not clear what they have,” says Dr. Kimberly Hamad-Schifferli, a visiting scientist in MIT’s Department of Mechanical Engineering and a member of the technical staff at MIT’s Lincoln Laboratory. “We wanted to come up with a rapid diagnostic that could differentiate between different diseases.” Dr. Hamad-Schifferli and Dr. Lee Gehrke, the Hermann L.F. von Helmholtz Professor in MIT’s Institute for Medical Engineering and Science (IMES), are the senior authors of a paper describing the new device in the journal Lab on a Chip. This article was published online on February 12, 2015 and is titles “Multicolored Silver Nanoparticles for Multiplexed Disease Diagnostics: Distinguishing Dengue, Yellow Fever, and Ebola Viruses.”

Analysis of 17 Million SNVs in 650 Tumors from Different Tissues Suggests Differential DNA Mismatch Repair Efficiency Underlies Mutation Rate Variation Across the Human Genome

Copying the large book that it is our genome without mistakes every time a cell divides is a difficult job. Luckily, our cells are well-equipped to proof-read and repair DNA mistakes. Now, two scientists from the EMBL-CRG Systems Biology Unit at the Centre for Genomic Regulation (CRG) in Barcelona, Spain, have published a study showing that mistakes in different parts of our genome are not equally well corrected. This means that some of our genes are more likely to mutate and, therefore, more likely to contribute to disease than others. The scientists analyzed 17 million “single nucleotide variants” (SNVs), i.e., mutations in just one nucleotide (letter) of the DNA sequence, by examining 650 human tumors from different tissues. These were so-called “somatic” mutations, meaning they are not inherited from parents or passed down to children, but, rather, accumulate in our bodies as we age. Such somatic mutations are the main cause of cancer. Many result from the impact of mutagens, such as tobacco smoke or ultraviolet radiation, and others come from naturally occurring mistakes that occur in the process of copying DNA as our tissues renew. Ben Lehner, Ph.D., Senior Group Leader, EMBL-CRG Systems Biology Unit, CRG, and his team had previously described that somatic mutations are much more likely in some parts of the human genome, thus damaging genes that may cause cancer. In a new paper, published online on February 23, 2015 in Nature, Dr. Lehner and his postdoc Fran Supek (photo), Ph.D., provide evidence that this is because genetic mistakes are better repaired in some parts of the genome than in others. This variation was generated by variation in the efficiency of a particular DNA repair mechanism called “mismatch repair,” a sort of a spell-checker that helps fix the errors in the genome after copying has taken place. Drs.