Tracking foodborne outbreaks with whole genome sequencing

The Centers for Disease Control and Prevention (CDC) has expanded the use of
whole genome sequencing to track foodborne illness caused by Listeria,
Salmonella, Campylobacter and E. coli to 38 states and two cities and will be
reporting this information on their Antibiotic Resistance Investment Map. The
CDC has been using whole genome sequencing since 2013 to originally track
Listeria outbreaks in a pilot project which has been successful in identify new food sources and more instances of Listeria outbreaks. The uses of whole genome
sequencing to track Salmonella, Campylobacter and E. coli outbreaks are relatively
new being only implemented in some state in 2017. However, from the whole
genome sequencing pilot project tracking Listeria the CDC was able to rapidly
identify the strain of bacteria causing the Listeria outbreaks as well as track the
spread by linking patients with the same strain of bacteria together. Once the
specific strain is identified, the CDC was in a position to use this information to
identify possible food sources and prevent the spread of Listeria by locating its
origin.

See here for the CDC announcement, here for how the CDC uses of whole
genome sequencing, and here for the Listeria Whole Sequencing Project.


-Kristen Tuosto

Axolotl genome sequenced!

Scientists have just announced that they have sequenced the genome of the axolotl! Unlike humans, these small amphibians have the unique ability to regenerate injured limbs and organs. So far, researchers have learned that developmental genes are under constraint, and that regeneration properties are possibly due to species-restricted genes. The ultimate significance is that work done to understand the genomic mechanisms underlying axolotl regenerative properties may just provide us insight into healing human injuries. All hail the Mexican salamander!

See here for the Nature article and here for the IFL pop-science article.

- Elizabeth (Liz) Tapanes

"Sequencing the World" and how to pay for it

The Economist has a nice summary of the Earth BioGenome Project (EBP) - which would like to sequence all 1.5m known eukaryote species within a decade - and the Amazon Bank of Codes -an initiative to generate an open library of the Amazon’s biological/sequence data. Their proponents are using the current World Economic Forum’s meeting at Davos to drum up support and, most importantly, money money money. BGI suggests that the cost of sequencing would be ~$100 / genome. A bargain!

https://www.economist.com/news/21735546-how-map-dna-all-known-plants-and-animal-species-earth-sequencing

The Origin of Species: Homo sapiens Style

New DNA analysis of 2000 year old bones in South Africa points to an earlier emergence of Homo sapiens, from around 350-260kya, much earlier than the previously estimated 200kya. Through the use of mitochondrial DNA, researchers were able to use this data, along with a revised human mutation rate of 1.25e-8 per base pair per generation, to more accurately estimate the split of the Homo sapiens species. This analysis coincides with findings from another study conducted at the Jebel Irhoud site on fossil remains that estimated the origin of Homo sapiens to be ~300kya.



https://www.sciencenews.org/article/ancient-boys-dna-pushes-back-date-earliest-humans

You Can Now Blame Paranthropus Boisei for Genital Herpes

Researchers Underdown, Kumar, and Houldcroft have proposed in a recent study that the robust australopithecine known as Paranthropus boisei might be the reason why genital herpes exists in the human population today.  Genetic analysis done by early researchers revealed that the virus that causes genital herpes, HSV2, is closer to the chimpanzee herpes variant, ChHV2, than it is to its counterpart HSV1 (cold sores).  Using that data, researchers hypothesized that HSV2 was not passed along to hominins from the last common ancestor of humans and chimpanzees, but across species lines later down in evolutionary history between 3 and 1.4 million years ago.  What Underdown, Kumar, and Houldcroft conclude, using the statistical analysis of temporal and spatial relationships between early hominins and ancestral chimpanzees, is that Paranthropus boisei represents the most important, and most plausable intermediate transmitter of the HSV2 into hominin populations.  You can, therefore, blame Zinj giving humans genital herpes.

https://www.eurekalert.org/pub_releases/2017-10/uoc-mth092717.php

Amanda Kunkle

The Genetics of Staying in School

The article “The Genetics of Staying in School” from The Atlantic discusses a GWAS study done on 294,000 individuals from different areas of the world. The study found 74 gene variants that are associated with educational attainment. In other words, the people who have the variants, on average compete more formal schooling than individuals who do not have the variants. The Manhattan plot showed that there were big statistical differences on chromosomes 2, 3, 6, 9, 13, and 15, as well as some smaller differences on a few others. These kinds of studies can create a lot of public backlash, which is exactly what happened. Thus, the researchers also published a “Frequently Asked Questions” article discussing what the GWAS study really meant. The researchers explained that the 74 gene variants only accounted for 3 percent of the differences in education levels across the whole population. Thus, there are many other factors that affect educational attainment, and that nurture and nature go hand in hand when discussing educational success. However, this study will be helpful to social scientists who want to do educational studies about different styles of schooling in different populations.

https://www.theatlantic.com/science/archive/2016/05/the-genetics-of-staying-in-school/482052/

https://www.nature.com/nature/journal/v533/n7604/full/nature17671.html

http://ssgac.org/documents/FAQ_74_loci_educational_attainment.pdf

Flu Season: Could a Protein Be Our Protection?

A recent study done at the University of Maryland School of Medicine discovered the potential ability of a protein known as RC-101 to protect against influenza and other diseases. RC-101 has been previously identified as a protective agent against disease in the animals in which it is found, such as Orangutans. Although the protein was lost in recent primate evolution and is not found in humans, researchers found similar benefits of viral protection when they studied the protein in the context of human immune cells as well as in mice. In human immune cells, they discovered that the protein not only blocked the virus from entering the target cell, but also stopped the inflammation that is responsible for symptoms associated with the flu, such as fever, lethargy, and pain. In mice, they studied two different groups: both groups received a dose of lethal influenza, but only the first group received the RC-101 protein. As a result, only 20% of mice in the first group died, whereas 90% of mice in the control group died. Ultimately, the flu is an ongoing issue causing thousands of deaths annually, despite the existence of vaccines. Based on the findings of this study, researchers now hope to incorporate this unique double function of RC-101 in making medicine for protection not just from the flu, but also a multitude of viral infections that stem from inflammation.

-Julie Thomasian 

Source: Eurkalert, Published 09/29/2017

https://www.eurekalert.org/pub_releases/2017-09/uoms-rip092917.php