The link between Guillain-Barré Syndrome and Zika, revelations about mimiviruses, and why obesity might raise the risk of colon cancer. This week in Abstract Science.
(The Lancet, 2/29/2016, Van-Mai Cao-Lormeau, et. al)
Scientists have suspected for awhile now that the mosquito-borne Zika virus is the culprit responsible for a rash of cases of Guillain-Barré Syndrome in French Polynesia. Now, for the first time, a case-control study provides evidence that the virus caused the strange autoimmune condition. The study, which appeared online, found that all but one of 42 patients diagnosed with Guillain-Barré Syndrome had neutralizing antibodies against Zika compared to just 54 of a matched group of 98 controls. The study was led by the Institut Pasteur’s Emerging Diseases Epidemiology Unit in Paris. Authors of the study said that because Zika virus is spreading rapidly across the Americas, “at risk countries need to prepare for adequate intensive care beds capacity to manage patients with Guillain-Barré syndrome.”
(Nature, 2/29/2016, Ewen Callaway)
The discovery of a working immune system in a mimivirus —viruses large enough to be seen under a microscope and with genomes larger than most bacteria—strengthens the claim that the giant viruses represent a new branch in a tree of life, researchers from Aix-Marseille University in France reported this week in Nature. The research team says that mimiviruses fend off invaders using defenses similar to the CRISPR gene-editing system. Mimiviruses are distantly related to viruses that include smallpox, but unlike most viruses, they have genes to make amino acids, DNA letters and complex proteins.
(Nature, 3/2/2016, Heidi Ledford)
It’s widely known that obesity raises the risk of colon cancer. A study conducted in obese mice could explain why. After feeding overweight mice a high-fat diet for over a year, researchers from the Koch Institute for Integrative Cancer Research at the Massachusetts Institute of Technology (MIT) in Cambridge and the Whitehead Institute, also in Cambridge, discovered that the diet activated PPAR-δ, which regulates metabolism, and stimulated the proliferation of intestinal stem cells that are more likely to give rise to tumor cells. The team also tested the response of intestinal cells grown in three-dimensional cultures called ‘organoids’, to fatty acids found in the high-fat chow. Those cells also activated PPAR-δ, suggesting that the fatty acids may have been acting directly on its expression.
—Compiled by Senior Scientific Writer Regina McEnery