Debunking myths on genetics and DNA

Sunday, May 15, 2016

To all of you who think New Mexico is all desert ...

... think again! ;-)
The Jemez mountains are covered in ponderosa pines and rivers like Rio Puerco give rise to the beautiful waterfalls we scouted with some photographer friends this past week-end. Enjoy!

© Elena E. Giorgi

© Elena E. Giorgi

© Elena E. Giorgi

© Elena E. Giorgi


Friday, May 13, 2016

Using Supercomputers to Probe the Early Universe

Artist's depiction of the WMAP satellite gathering data to understand the Big Bang. Source: NASA.

For decades physicists have been trying to decipher the first moments after the Big Bang. Using very large telescopes, for example, scientists scan the skies and look at how fast galaxies move. Satellites study the relic radiation left from the Big Bang, called the cosmic microwave background radiation. And finally, particle colliders, like the Large Hadron Collider at CERN, allow researchers to smash protons together and analyze the debris left behind by such collisions.

Physicists at Los Alamos National Laboratory, however, are taking a different approach: they are using computers. In collaboration with colleagues at University of California San Diego, the Los Alamos researchers developed a computer code, called BURST, that can simulate a slice in the life of our young cosmos.

While BURST is not the first computer code to simulate conditions during the first few minutes of cosmological evolution, it can achieve better precision by a few orders of magnitude compared to its predecessors. Furthermore, it will be the only simulation code able to match the precision of the data from the Extremely Large Telescopes currently under construction in Chile. These new telescopes will have primary mirrors that range in aperture from 20 to 40 meters, roughly three times wider than the current very large telescopes, and an overall light-collecting area up to 10 times larger.

A few seconds after the Big Bang, the universe was composed of a thick, 10-billion degree "cosmic soup" of subatomic particles. As the hot universe expanded, these particles' mutual interactions caused the universe to behave as a cooling thermonuclear reactor. This reactor produced light nuclei, such as deuterium, helium, and lithium — all found in the universe today. "Our code, developed with Evan Grohs, who at the time was a graduate student at UCSD, looks at what happened when the universe was about 1/100 of a second old to a few minutes old," says Los Alamos physicist Mark Paris of the Theoretical Division. "By determining the amount of helium, lithium and deuterium at the end of those first few minutes of life, BURST will be able to shed light to some of the existing puzzles of cosmology."

One such puzzle is dark matter: physicists know that such matter exists because of the way galaxies rotate, but they haven't been able to detect it because it does not radiate in any known spectrum. Physicists have theorized that dark matter is made of so-called "sterile neutrinos", which do not interact with any other particle and are responsible for these unobservable interactions. "Once we start getting data from the Extremely Large Telescopes," Paris explains, "we will model sterile neutrinos into the BURST code. If we get a good description, we will be able to prove their existence."

Measurements of the cosmic microwave background radiation have led physicists to theorize "dark radiation," a speculative form of energy that may have acted in the early universe. BURST could possibly reveal whether or not dark radiation is real and caused by sterile neutrinos. "The universe is our laboratory," Paris enthusiastically concludes. "BURST will help us answer questions that are currently very difficult to address with particle colliders like the one at CERN."

Ongoing support for the project is provided by the National Science Foundation at UCSD and the Laboratory Directed Research and Development program through the Center for Space and Earth Sciences at Los Alamos. BURST will be running on the supercomputing platforms at Los Alamos National Laboratory.

Reference
Grohs, E., Fuller, G., Kishimoto, C., Paris, M., & Vlasenko, A. (2016). Neutrino energy transport in weak decoupling and big bang nucleosynthesis Physical Review D, 93 (8) DOI: 10.1103/PhysRevD.93.083522

ResearchBlogging.org

Wednesday, May 4, 2016

May IWSG: Spring is finally here!


This is a monthly event started by the awesome Alex J. Cavanaugh and organized by the Insecure Writer's Support Group. Click here to find out more about the group and sign up for the next event. You can also sign up for the newsletter.

First off a big announcement: the IWSG anthology, titled Parallels: Felix Was Here, is here! Featuring 10 stories from ISWG authors, hand-picked by a panel of agents and writers, you can now get it from Amazon and other retailers. Complete list of purchasing links here.


It's May already, can you believe it? How was your month of April, did you do the A-Z challenge? Already making plans for the summer?

My April wasn't too bad: I'm wrapping up a project at work and I finished a short story which will be the prequel to a new world I'm creating. It's a space opera and I'm very excited about it mostly because... I've never written space opera before! :-) Here's a question for you: would you release a prequel as soon as it's ready or would you wait until the first installment in the series is ready to be released too?

In other news, we've had some very much needed moisture in Northern New Mexico and so I took the chance and shot some droplet macros. :-) Happy May everyone!



Friday, April 29, 2016

Hunting For The Signatures of Cancer

Signatures of Mutational Processes Extracted from the Mutational Catalogs of 21 Breast Cancer Genomes. Credit:http://dx.doi.org/10.1016/j.celrep.2012.12.008

Cancer is the second leading cause of death worldwide, with approximately 14 million new cases and 8.2 million cancer related deaths each year (Source: WHO). A family history of cancer typically increases a person's risk of developing the disease, yet most cancer cases have no family history at all. This suggests that a combination of both genetics and environmental exposures contribute to the etiology of cancer. In this context, "genetics" means the genetic make-up we are born with and inherited from our parents. For example, women born with specific mutations in the BRCA1 and BRCA2 genes are known to have a much higher risk of developing breast cancer later in life.

However, besides the genetic make-up we carry from birth, there are many geographical and environmental factors that contribute to the risk of cancer. For example, the incidence of breast cancer is over 4 times higher in North and West Europe compared to Asia and Africa (Source: WHO). Stomach cancer, on the other hand, is much more prevalent in Asia than the US. If you think that this may be linked to the genetic differences across ethnicities, think again. The National Cancer Institute published a summary of several studies that compared the incidence of first and second generation immigrants in the US with the local population. They found that:
"cancer incidence patterns among first-generation immigrants were nearly identical to those of their native country, but through subsequent generations, these patterns evolved to resemble those found in the United States. This was true especially for cancers related to hormones, such as breast, prostate, and ovarian cancer and neoplasms of the uterine corpus and cancers attributable to westernized diets, such as colorectal malignancies."
According to the World Health Organization (WHO),
"around one third of cancer deaths are due to the 5 leading behavioral and dietary risks: high body mass index, low fruit and vegetable intake, lack of physical activity, tobacco use, alcohol use."
Cancer is the result of a series of cellular mechanisms gone awry: every time a cell divides, somatic mutations accumulate in the cell's genome. These are not mutations we are born with, inherited from our parents. Rather, these are changes that accumulate in certain cells as we grow old and are not  the same across all cells in the body. Many environmental exposures contribute to this process and affect the rate at which these mutations accumulate. However, cells have various mechanisms that are normally able to repair harmful mutations or, when the damage is beyond repair, to trigger cell death. The immune system is also "trained" to recognize cancer cells and destroy them.

When all these defense mechanisms fail, cancer cells start dividing uncontrollably.

As a result, all cancer cells carry a number of somatic mutations that set them apart from healthy cells, and some tend to be the same across different cancer patients: for example, specific mutational patterns found in lung cancer have been attributed to tobacco exposure and were indeed reproduced in animal models. Another set of mutations has been attributed to UV exposure and has been found in skin cancers [1, 2].

This prompts the ambitious question: can we find common mutations across individuals with the same cancer? And how many of these mutational patterns that are common across individuals can we attribute to particular exposures and/or biological processes? Distinguished postdoctoral researcher Ludmil Alexandrov, from the Los Alamos National Laboratory, has been working on this problem since his he was a PhD student at the Wellcome Trust Sanger Institute.

"It's like lifting fingerprints," Alexandrov explains. "The mutations are the fingerprints, but now we have to do the investigative work and find the 'perpetrator', i.e., the carcinogens that caused them." During his graduate studies, under the supervision of Mike Stratton of the Wellcome Trust Sanger Institute, Alexandrov developed a mathematical model that, given the cancer genomes from a number of patients, is able to pick the "common signals" across the patients -- i.e. mutation patterns that are common across the patients -- and classify them into "signatures."

"When formulated mathematically," Alexandrov explains, "the question can be expressed as the classic 'cocktail party' problem, where multiple people in a room are speaking simultaneously while several microphones placed at different locations are recording the conversations. Each microphone captures a combination of all sounds and the problem is to identify the individual conversations from all the recordings." Taking from this analogy, each cancer genome is a "recording", and the task of the mathematical model is to reconstruct each conversation, in other words, the mutational patterns. These are sets of somatic mutations that are the observed across the cancer genomes and that characterize certain types of cancers.

In 2013, Alexandrov and colleagues analyzed 4,938,362 mutations from 7,042 patients, spanning 30 different cancers, and extracted more than 20 distinct mutational signatures [2]. "Some patterns were expected, like the known ones caused by tobacco and UV light," Alexandrov says. "Others were completely new."

Of the new signatures found, many are involved in defective DNA repair mechanisms, suggesting that drugs targeting these specific mechanisms may benefit cancers exhibiting these signatures [3]. But the most exciting part of this research will be finding the 'perpetrator' or, as Alexandrov explains, the mutations triggered by carcinogens like tobacco, UV radiation, obesity, and so on. The challenge will be to experimentally associate these mutational patterns to the exposures that caused them. In order to do this, the scientists will have to expose cultured cells and model organisms to known carcinogens and then analyze the genomes of the experimentally induced cancers.

In the meantime, the signatures found so far are only the beginning: Alexandrov and colleagues have teamed up with the Los Alamos High Performance Computing Organization in order to analyze the genomes of almost 30,000 cancer patients.

"The amount of data we will have to handle for this task is enormous, on the order of petabytes," Alexandrov says. "Few places in the world have the capability to handle this many data. Under normal circumstances, it takes months to answer a question on 10 petabytes of data. The supercomputing facility at Los Alamos can provide an answer within a day."

Because of his research, in 2014 Alexandrov was listed by Forbes magazine as one of the “30 brightest stars under the age of 30” in the field of Science and Healthcare. In 2015 he was awarded the AAAS Science & SciLifeLab Prize for Young Scientists in the category Genomics and Proteomics [2] and the Weintraub Award for Graduate Research. He is now the recipient of the prestigious Oppenheimer fellowship at Los Alamos National Laboratory.

References
Siegel, R., Miller, K., & Jemal, A. (2015). Cancer statistics, 2015 CA: A Cancer Journal for Clinicians, 65 (1), 5-29 DOI: 10.3322/caac.21254

[1] Alexandrov LB (2015). Understanding the origins of human cancer. Science (New York, N.Y.), 350 (6265) PMID: 26785464

[2] Alexandrov LB, Nik-Zainal S, Wedge DC, Aparicio SA, Behjati S, Biankin AV, Bignell GR, Bolli N, Borg A, Børresen-Dale AL, Boyault S, Burkhardt B, Butler AP, Caldas C, Davies HR, Desmedt C, Eils R, Eyfjörd JE, Foekens JA, Greaves M, Hosoda F, Hutter B, Ilicic T, Imbeaud S, Imielinski M, Jäger N, Jones DT, Jones D, Knappskog S, Kool M, Lakhani SR, López-Otín C, Martin S, Munshi NC, Nakamura H, Northcott PA, Pajic M, Papaemmanuil E, Paradiso A, Pearson JV, Puente XS, Raine K, Ramakrishna M, Richardson AL, Richter J, Rosenstiel P, Schlesner M, Schumacher TN, Span PN, Teague JW, Totoki Y, Tutt AN, Valdés-Mas R, van Buuren MM, van 't Veer L, Vincent-Salomon A, Waddell N, Yates LR, Australian Pancreatic Cancer Genome Initiative, ICGC Breast Cancer Consortium, ICGC MMML-Seq Consortium, ICGC PedBrain, Zucman-Rossi J, Futreal PA, McDermott U, Lichter P, Meyerson M, Grimmond SM, Siebert R, Campo E, Shibata T, Pfister SM, Campbell PJ, & Stratton MR (2013). Signatures of mutational processes in human cancer. Nature, 500 (7463), 415-21 PMID: 23945592

[3] Alexandrov LB, Nik-Zainal S, Siu HC, Leung SY, & Stratton MR (2015). A mutational signature in gastric cancer suggests therapeutic strategies. Nature communications, 6 PMID: 26511885

ResearchBlogging.org

Friday, April 22, 2016

Digging For Clues About Climate Change

Guest post by Rebecca McDonald, science writer

Photo Credit: LeRoy N. Sanchez

While many scientists who study climate change look up to the sky for clues about the Earth’s future, one researcher has spent her career looking down—at the abundance of life in the soil below. Innumerable microorganisms such as bacteria and fungi live in harmony with plant roots, decomposing fallen leaves and dead animals. In addition to acting as the ultimate recyclers, they also stabilize the soil and help to retain water. 

Cheryl Kuske, a microbiologist at Los Alamos National Laboratory, has focused the last two and a half decades on studying this microbial environment. “By decomposing organic matter,” she explains, “microorganisms help cycle carbon and nitrogen through the ecosystem.” Some of the carbon and nitrogen released from the organic matter goes into the soil and is assimilated into roots to help new plants grow—the carbon is incorporated into sugars, and the nitrogen atoms are used to build proteins. But some of these molecules are also released as CO2 and N2 gases into the atmosphere.

The soil ecosystem functions in a delicate balance. Although some organisms release gases into the air, others—including certain bacteria and leafy plants—remove harmful CO2 from the atmosphere for food production.

Kuske and her colleagues at Los Alamos National Laboratory have been investigating the roles of these microbes in carbon and nitrogen cycling to help make better predictions about terrestrial ecosystem responses to climate change. Using a technique called metagenomics to sequence the DNA of all the microbes at once, the team can study the organisms’ genes and the enzymes they produce.

These microrganisms’ lifecycles are so intertwined that their single genomes cannot be isolated for sequencing. However, analyzed jointly, they yield important clues about their collective functions in the environment. Scientists can identify things such as which bacteria or fungi are responsible for fixing nitrogen or carbon, the ratio of bacteria to fungi in the soil, and which microbes are closely associated with root health or plant growth. The researchers can even figure out which enzymes are currently being used through a technique called meta-transcriptomics; this approach sequences only the transcripts of genomic data that are actively being made and used for protein synthesis.

Photo courtesy of Cheryl Kuske

By sampling microbes from various soil environments over long periods of time, Kuske’s team and collaborators are able to understand what happens under the surface when things change aboveground. For instance, in a recent long-term study in Utah, the scientists discovered that slight changes in the summer precipitation pattern, combined with a 2°C rise in soil temperature, resulted in significant changes in the population of microbes below: the types of organisms completely changed, thus altering their overall role in the environment. For example, cyanobacteria—bacteria that create energy through photosynthesis—were no longer present. As a consequence, the new population of microbes no longer had the ability to pull carbon out of the air and had a decreased capacity for fixing nitrogen for protein synthesis.

Increased nitrogen from industrial runoff or fertilizer from agriculture can also have significant effects on the composition of organisms in the soil, as nitrogen is an essential molecule for the growth of both plants and bacteria. A comparison of 15 recent field experiments where nitrogen deposition was measured showed that in an arid environment, an increase in nitrogen had a positive effect on soil health at low concentrations, but too much was toxic to the soil community [1]. In a field experiment in Nevada, higher nitrogen concentrations changed the species composition of bacteria—but not fungi—leading to a fungi-dominated community [2,3].

Although the ramifications of these changes to the microbial world are not yet completely understood, Kuske’s team is continuing their studies, both in the laboratory, under controlled conditions, as well as at various field sites in the American Southwest. What they do know is that the feedback loop is strong. Changes in the aboveground environment—such as rising temperatures, altered precipitation, and increased nitrogen runoff—lead to changes below ground that can have far-reaching consequences.

“The studies being conducted at Los Alamos provide an understanding of the interactive biological processes that are inherent in all types of terrestrial ecosystems and that tightly control carbon and nitrogen fluxes to the atmosphere,” says Kuske. Climate warming and altered weather patterns will disrupt this balance. When the diversity of soil microbes change, the feedback loops that ensue could have lasting effects on the amounts of carbon and nitrogen in the soil and the atmosphere.

Rebecca McDonald is a science writer at Los Alamos National Laboratory specializing in the communication of bioscience research. She has also worked as a freelance writer, and volunteers her time as a communications consultant for a science education non-profit.

Disclaimer: Elena E. Giorgi is a computational biologist in the Theoretical Division of the Los Alamos National Laboratory. She does not represent her employer’s views. LA-UR-16-22406.


[1] Steven B, Kuske CR, Gallegos-Graves LV, Reed SC, & Belnap J (2015). Climate change and physical disturbance manipulations result in distinct biological soil crust communities. Applied and environmental microbiology, 81 (21), 7448-59 PMID: 26276111

[2] Sinsabaugh RL, Belnap J, Rudgers J, Kuske CR, Martinez N, & Sandquist D (2015). Soil microbial responses to nitrogen addition in arid ecosystems. Frontiers in microbiology, 6 PMID: 26322030

[3] Mueller RC, Belnap J, & Kuske CR (2015). Soil bacterial and fungal community responses to nitrogen addition across soil depth and microhabitat in an arid shrubland. Frontiers in microbiology, 6 PMID: 26388845

ResearchBlogging.org

Friday, April 8, 2016

The Antibacterial Resistance Threat: Are We Heading Toward a Post-Antibiotic Era?

Source: PEW Charitable Trusts

The above graphic, from the Antibiotic Resistance Project by the PEW charitable trusts, summarizes how alarming the emergence of drug resistant bacterial strains has gotten over the past few decades. According to data from the Center for Disease Control (CDC), every year 2 million Americans acquire drug-resistant infections [1], in other words infections that do not respond to treatment with ordinary antibiotics. Not only do drug-resistant infections require much stronger drugs, but, when not deadly, they often leave patients with long-lasting complications.

One of the scariest threats is carbapenem-resistant Enterobacteriaceae (CRE), bacteria that are resistant to several kinds of antibiotics. In 2001, only North Carolina, out of all 50 states had reported one CRE infection. Last year, in 2015, 48 states reported CRE infections to the CDC. And while drug-resistant strains emerge rapidly, the discovery of antimicrobial substances has stalled: in the last decade, only 9 new antibiotics were approved, compared to 29 discovered in the 1980s and 23 in the 1990s. We are fighting a new war, and we are running out of weapons.

How does drug resistance emerge?

Bacteria constitute an irreplaceable building block of our ecosystem: they are found in soil, water, air, and in every living organism. In humans, it's estimated that they outnumber our cells by 3:1, and numerous studies have shown that not only do they help us digest and produce enzymes that our body wouldn't otherwise be able to break down, but they can also influence gene expression and certain phenotypes (see some of my past posts for more information).

They live in symbiosis with us, yet some bacteria can be highly pathogenic. The overall mortality rate from infectious diseases in the US fell by 75% over the first 15 years following the discovery of antibiotics [3], and researchers estimate that antibiotics have increased our lifespan by 2 to 10 years [4] by enabling us to fight infections that would otherwise be deadly.

However, evolution has taught bacteria to fight back.

Bacteria develop drug resistance through the acquisition of genetic mutations that either modify the bacteria's binding sites (and therefore the drug can no longer enter the membrane), or reduce the accumulation of the drug inside the bacterium. The latter happens through proteins called "efflux pumps", so called because their function is to pump drugs and other potentially harmful chemicals out of the cell. Once these advantageous mutations appear in the population, they spread very quickly, not only because they are selected for, but also thanks to bacteria's ability to transfer genes: the drug-resistant genes form a circular DNA unit called plasmid, and the unit is passed on to nearby bacteria so that they, too, can become drug resistant.

These mechanisms are not new to bacteria, however, what's new is the increasing overuse of antibiotics and antimicrobial chemicals in our modern lifestyle. The antimicrobial agent called triclosan, for example, can be found in all antibacterial soaps, toothpaste, mouthwash, detergents, and even toys and kitchen utensils. Because of its wide use in household and hygiene products, triclosan has been found in water, both natural streams and treated wastewater, as well as human samples of blood, urine, and breast milk. As though that alone wasn't enough to alert consumers, a study published on the Proceedings of the National Academy of Sciences [5] claims that triclosan, which can be absorbed through the skin, can impair the functioning of both skeletal and cardiac muscle. The researchers confirmed these findings both in vitro and in animal models.

Resistance is also spread through the use of antibiotics in industrial farming. In the US alone, the daily consumption of antibiotics amounts to 51 tons, of which around 80% is used in livestock, a little under 20% is for human use, and the rest is split between crops, pets, and aquaculture [3]. A meta-analysis published last year in PNAS [6] found that between 2000 and 2010 the global use of antibiotic drugs increased by 36%, with 76% of the increase coming from developing countries. The researchers projected that worldwide antibiotic consumption would rise by 67% by 2030 due to population growth and the increase in consumer demand.

These frightening statistics prompted CDC director Tom Frieden to issue a warning: “If we are not careful, we will soon be in a post-antibiotic era.” An era when common infections are deadly again.

"We need to be very careful in using antimicrobial agents for everything from hand washing to toothpaste," Harshini Mukundan, microbiologist at Los Alamos National Laboratory, explains. "Increased selection of drug resistant organisms means that future generations will be helpless in fighting even the most common bacterial infections."

Mukundan and her colleagues have been working on biosurveillance and tracking the emergence of drug resistant strains in high disease burden populations where emerging antibiotic resistance is a huge concern. In collaboration with the Los Alamos National Laboratory metagenomics group, and Los Alamos scientists Ben McMahon and Norman Doggett, the team is working on developing new assays for faster diagnosis of drug resistant infections. Another approach to fight drug resistance is trying to understand how bacterial efflux pumps work at excreting the drug out of the bacterium. Gnana Gnanakaran, a computational biologist at Los Alamos National Laboratory, and his team have developed mathematical models to describe the structure of these pumps [7] and find a way to deactivate them.

While this research is highly promising and exciting, we all need to step up and do our part before it's too late: the CDC published a series of recommendations for patients to follow at the doctor's office, and there are smart choices we can make at home, too. In a recent report, the Food and Drug Administration (FDA) claims that there is no evidence that antibacterial soaps do a better job at preventing infections than ordinary soap, and that in fact:
"New data suggest that the risks associated with long-term, daily use of antibacterial soaps may outweigh the benefits."
In its 2011 policy paper, the Infectious Diseases Society of America (IDSA) recommended a substantial reduction in the use of antibiotics for growth promotion and feed efficiency in animal agriculture, and encouraged the FDA to complete and publish risk assessments of antibiotics currently approved for non-therapeutic use.

Just like any other precious resource, antibiotics (and antimicrobial drugs in general) need to be used with parsimony.

Resources:
[1] Antibiotic Resistance Threats in the United States, 2013 (CDC)

[2] PEW Antibiotic Resistance Poject

[3] Armstrong GL, Conn LA, & Pinner RW (1999). Trends in infectious disease mortality in the United States during the 20th century. JAMA, 281 (1), 61-6 PMID: 9892452

[4] Hollis, A., & Ahmed, Z. (2013). Preserving Antibiotics, Rationally New England Journal of Medicine, 369 (26), 2474-2476 DOI: 10.1056/NEJMp1311479

[5] Cherednichenko, G., Zhang, R., Bannister, R., Timofeyev, V., Li, N., Fritsch, E., Feng, W., Barrientos, G., Schebb, N., Hammock, B., Beam, K., Chiamvimonvat, N., & Pessah, I. (2012). Triclosan impairs excitation-contraction coupling and Ca2+ dynamics in striated muscle Proceedings of the National Academy of Sciences, 109 (35), 14158-14163 DOI: 10.1073/pnas.1211314109

[6] Van Boeckel, T., Brower, C., Gilbert, M., Grenfell, B., Levin, S., Robinson, T., Teillant, A., & Laxminarayan, R. (2015). Global trends in antimicrobial use in food animals Proceedings of the National Academy of Sciences, 112 (18), 5649-5654 DOI: 10.1073/pnas.1503141112

[7] Resisting Bacterial Resistance, by Rebecca McDonald, 1663 Magazine.

ResearchBlogging.org

Wednesday, April 6, 2016

April IWSG roundup


This is a monthly event started by the awesome Alex J. Cavanaugh and organized by the Insecure Writer's Support Group. Click here to find out more about the group and sign up for the next event. You can also sign up for the newsletter.

I know many of you are busy doing the A-Z challenge this month, so I'll keep it short.

As you know, I'm working on two projects at the same time, which is something I never did before. This results in both projects being slower but I fear that if I miss the spontaneity of the moment and put wither one aside, when I'll get back to it later on the voice won't sound half as good. Or at least that's what I tell myself, haha. :-)

I explain this process in a podcast interview with two good friends of mine, and awesome writers, Jason Anspach and Kevin G. Summers. Kevin and Jason started the Literary Outlaws podcast this year and they've already interviewed some pretty cool people. If you have time during your commute to work, I highly recommend you check them out. :-)

That's all folks, hope all is well with your writing, hope you're not sneezing too much this spring but instead enjoying the outdoors and warmer temperatures. And if you are in the southern hemisphere, enjoy the beauty of fall.

Friday, April 1, 2016

Allergies: Can Too Much Hygiene Actually Harm Us?


It's that time of the year again. You step out of the house and your eyes itch, your nose starts running and your head feels like an empty balloon. Yes, it's allergy season again. Even the resilient ones, give them enough time and eventually they will develop some form of allergic reaction.

But what are allergies and why do so many people suffer from them?

Allergies are a glitch in our immune system. The immune system is built to recognize and destroy pathogens -- potential threats like viruses and harmful bacteria. Unlike pathogens, allergens are substances that, despite being harmless to the body, still trigger a response from the immune system. As soon as the allergen is detected, the immune system releases a class of antibodies called IgE. These antibodies signal the cells to release histamine, a neurotransmitter that triggers all the pesky symptoms typical of an allergic reaction: wheezing, watery eyes, running nose, coughing, and all the like.

Spring is a particularly dreaded time of the year for allergy sufferers because of all the pollen released in the air. Global warming has impacted the duration and spread of pollen allergies: shorter winters and warmer temperatures translate into longer pollen seasons, which in turn increase the duration and severity of symptoms for allergy sufferers. In addition, they also increase the exposure and possible sensitization of people who don't suffer from allergies ... yet [1].

Are allergies on the rise?

In his 2015 review [2], Thomas Platts-Mills, of the University of Virginia School of Medicine, looks at the prevalence over the past five decades of asthma, hay fever, and peanut allergy, and reports a progressive increase in pediatric asthma, as well as a "dramatic" increase in food allergies. Allergies are more prevalent in developed countries, and particularly in urban settings, suggesting that something in the industrialized lifestyle may have triggered the increase. However, given the many drastic changes introduced in these countries over the past century, it's hard to pin-point one specific cause. Several factors have been suggested as possible explanations: changes in hygiene, for example, together with a decrease in outdoor life, smaller families and no more exposure to farm animals, have significantly reduced our exposure to bacteria; the progressive use of antibiotics and antimicrobial products have also reduced such exposure; less outdoor time also means less physical activity, more exposure to indoor allergens, and an increase in body mass.

First proposed in 1989 [3], the "hygiene hypothesis" -- the theory that the rise in allergic reactions is caused by a decrease in childhood exposure to harmless bacteria -- has grown to encompass many other disorders, not just allergies. The theory originally spurred from the observation that children with a higher number of siblings had a lower risk of developing asthma, something that led researchers to think that this was due to a higher exposure to bacteria.

The human microbiome is the set of all bacteria coexisting in our body. They are estimated to outnumber our cells by 3:1 and the vast majority of these organisms are not only harmless, they actually play an important role in our health. For example, by modulating the concentration of chemicals that are precursors of important neurotransmitters, they can affect our mood and mental health [4]. They can also influence our propensity to certain phenotypes such as leanness or obesity by affecting gene expression in our guts [5].

Scientists have used a mouse model to show that by transferring gut micriobiota from allergic mice to resistant mice they could actually transfer the food allergy to the latter [6], proving a correlation between the two. Tolerance to food is acquired during infancy thanks to the interaction between the immune system and the gut microbiota, and therefore, early development of the gut microbiome is believed to play a fundamental role in the predisposition to allergies and other diseases later in life. Indeed, in the industrialized countries that are experiencing an increase in allergies, scientists have observed a delayed gut colonization after birth, less biodiversity in the gut microbiome, and reduced turnover of gut bacterial strains in infants [6].

Three major factors could be responsible for this: (i) natural birth versus C-section (a C-section deprives the newborn of beneficial exposure to commensal bacteria residing in the birth canal); (ii) breast-feeding versus formula; (iii) early exposure to antibiotics. All three practices -- C-section, formula feeding, and the use of antibiotics and antimicrobial products -- have been increasingly used in developed countries, and all three affect the development of the gut microbiome of infants. While studies that have looked at possible associations between any one of them and the risk of allergies so far have not yielded conclusive results, the differences in microbiomes between healthy people and those with asthma and allergies are an indication that early exposure to bacteria may protect against these conditions [7].

Is there such a thing as too much protection?

These observations don't mean that we should all stop washing our hands and start living filthy. They do, however, point to a trend in overuse of antimicrobial household products (soaps, laundry detergents, kitchen cleaners, etc.). These products should be used with care and only when truly needed. In most instances, natural substitutes like vinegar to clean surfaces are a better choice, as they keep your kitchen clean without killing microorganisms that are actually beneficial to our health. As much as we strive to protect our little ones, remember that childhood exposure to pathogens makes your child's immune system grow stronger and well trained to recognize bigger dangers. (On a side note, vaccines equally stimulate the immune system without the hassle of all the symptoms.) Finally, global measures like recycling gray water can benefit both the planet and our own health, as it saves gallons of drinking water from being used in landscaping and farming, while restoring important bacteria into the soil and back into our environment.

References

[1] Ziska, L., Knowlton, K., Rogers, C., Dalan, D., Tierney, N., Elder, M., Filley, W., Shropshire, J., Ford, L., Hedberg, C., Fleetwood, P., Hovanky, K., Kavanaugh, T., Fulford, G., Vrtis, R., Patz, J., Portnoy, J., Coates, F., Bielory, L., & Frenz, D. (2011). Recent warming by latitude associated with increased length of ragweed pollen season in central North America Proceedings of the National Academy of Sciences, 108 (10), 4248-4251 DOI: 10.1073/pnas.1014107108

[2] Platts-Mills, T. (2015). The allergy epidemics: 1870-2010 Journal of Allergy and Clinical Immunology, 136 (1), 3-13 DOI: 10.1016/j.jaci.2015.03.048

[3] Strachan DP (1989). Hay fever, hygiene, and household size. BMJ (Clinical research ed.), 299 (6710), 1259-60 PMID: 2513902

[5] Ridaura VK, Faith JJ, Rey FE, Cheng J, Duncan AE, Kau AL, Griffin NW, Lombard V, Henrissat B, Bain JR, Muehlbauer MJ, Ilkayeva O, Semenkovich CF, Funai K, Hayashi DK, Lyle BJ, Martini MC, Ursell LK, Clemente JC, Van Treuren W, Walters WA, Knight R, Newgard CB, Heath AC, & Gordon JI (2013). Gut microbiota from twins discordant for obesity modulate metabolism in mice. Science (New York, N.Y.), 341 (6150) PMID: 24009397

[4] Li, Q., & Zhou, J. (2016). The microbiota–gut–brain axis and its potential therapeutic role in autism spectrum disorder Neuroscience DOI: 10.1016/j.neuroscience.2016.03.013

[6] Molloy, J., Allen, K., Collier, F., Tang, M., Ward, A., & Vuillermin, P. (2013). The Potential Link between Gut Microbiota and IgE-Mediated Food Allergy in Early Life International Journal of Environmental Research and Public Health, 10 (12), 7235-7256 DOI: 10.3390/ijerph10127235

[7] Riiser, A. (2015). The human microbiome, asthma, and allergy Allergy, Asthma & Clinical Immunology, 11 (1) DOI: 10.1186/s13223-015-0102-0

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Wednesday, March 23, 2016

We Agree to Disagree: The Science of Why Your Political Posts Won’t Make Anyone Change Their Mind


In today's heated political stage, where everyone has a soapbox thanks to outlets like Facebook, Twitter, Instagram and all the personal blogs, I've tried my best not to share my political views publicly. And I've miserably failed. I use my own Facebook page and profile to talk about science, books and photography, but then I can't resist browsing other people's posts. Most of my friends are not as shy as me about making their political views heard and that's when I fall into the trap: I comment. And then someone replies. And I comment back. And on and on it goes until one of us drops out of the conversation because clearly we're not getting anywhere.

Science has taught me to be humble and rational. And yet I'm human, and every time I make a mistake in my line of work I feel something inside my brain stir and protest: "How's that possible? Surely they sent me the wrong data, or they didn't give me the correct information, or the world collapsed and my computer exploded, but there's no way I could've made that stupid mistake."

Apparently, I'm not unique. We all go through this kind of mental distress whenever we encounter an inconsistency between reality and our expectations, and between other people's opinions or choices and our own. It's called "cognitive dissonance." According to Wikipedia, social psychologist Leon Festinger described four ways our brain deals with this:
In an example case where a person has adopted the attitude that they will no longer eat high fat food, but eats a high-fat doughnut, the four methods of reduction are:

  • 1. Change behavior or cognition ("I will not eat any more of this doughnut")
  • 2. Justify behavior or cognition by changing the conflicting cognition ("I'm allowed to cheat every once in a while")
  • 3. Justify behavior or cognition by adding new cognitions ("I'll spend 30 extra minutes at the gym to work this off")
  • 4. Ignore or deny any information that conflicts with existing beliefs ("This doughnut is not high in fat")
What determines what choice we make?

In my case, I end up going back to my computer program. I typically find the bug (which I unknowingly introduced as I was coding), correct it, and rerun the analyses. Admitting my mistake costs me emotional distress, in addition to that nagging doubt at the back of my head -- will my boss still like me even though I made a stupid mistake? -- but in the long run it would cost me a lot more not to correct the error and hand the wrong analyses to our collaborators.

So why can't we do the same when we are heatedly debating politics or religion? Why do some of us even resort to insults rather than admitting that our own logic is faulty?

One possible reason is that there are no consequences to being disrespectful or even offensive when debating on line. After all, even when we use our real name, we are still hiding behind a shield of impersonality when typing our thoughts on an electronic device. On the other hand, if I hand out the wrong results and my collaborators publish them, there will be huge consequences for me. And frankly, trial and error is part of the scientific process: we all make mistakes, we correct them, and we repeat the process over and over again until we have clean and sensible results. Only then we publish a paper.

But in a political or religious debate the consequences can be far more costly if we suddenly admit that we may have been wrong all along. Changing our mind affects our self-esteem and may lead to self-blame, possibly disrupting the relationships around us. That's why our brain has a tendency to choose the easier path, which often coincides with reinvigorating present beliefs rather than shifting to new ones. As Nyhan and Reifler notice in a 2010 paper [1], there's a difference between being uninformed and being misinformed, as the latter is much harder to correct. In the paper, the authors claim that "humans are goal-directed information processors who tend to evaluate information with a directional bias toward reinforcing their pre-existing views," and conclude: "Indeed, in several cases, we find that corrections actually strengthened misperceptions among the most strongly committed subjects."

This behavior of reinforcing one's beliefs the more the contrasting evidence is presented, is called the "confirmation bias". Patterson et al. [2] define this bias as the tendency to favor certain explanations that conform to our own beliefs and/or emotional response, and classify it as "cognitive" or "emotional" depending on whether it reflects the former or the latter. It's a very familiar bias, as we've all seen it everywhere around us, whether it was to defend our favorite presidential candidate or to debate climate change. A little harder is to pin it down when we are engaging in this behavior ourselves -- but rest assured, we all do it at some point, although each one of us to different extents.

"Because of this mechanism," explains Robin S. Cohen, a Los Angeles based psychoanalyst, "not only are we biased to favor perceptions that are in line with our beliefs, but we are also very likely to organize our world in order to only experience things that conform to our own ideas. This makes it less likely to be confronted with alternative opinions. Our own beliefs are so thoroughly reinforced through this process that new perceptions gain very little traction."

Interestingly, as Leonid Perlovsky describes in a 2013 review [3], experiments have shown that music helps abate the stressful consequences of cognitive dissonance. So, maybe I could try playing a little music in the background next time I'm trying to convince a Trump supporter to find a better presidential candidate. What do you think? Mozart or Metallica?

[1] Nyhan, B., & Reifler, J. (2010). When Corrections Fail: The Persistence of Political Misperceptions Political Behavior, 32 (2), 303-330 DOI: 10.1007/s11109-010-9112-2

[2] Patterson, R., Operskalski, J., & Barbey, A. (2015). Motivated explanation Frontiers in Human Neuroscience, 9 DOI: 10.3389/fnhum.2015.00559

[3] Perlovsky, L. (2013). A challenge to human evolution—cognitive dissonance Frontiers in Psychology, 4 DOI: 10.3389/fpsyg.2013.00179

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Wednesday, March 16, 2016

An open letter to all science lovers who want to defend science ... please don't.



Last week I had an animated discussion on Facebook over an older post in which I describe some literature I dug out on possible (underline “possible”!) correlations with autism. True, my post is highly incomplete, but it was meant as a discussion starter to point at things that scientists have been looking at in an attempt to unravel what feels like a rise in autism. Is autism the new childhood plague of our modern society or has it always been around and we just became more aware of it? And if the rise is real, what caused it?

To me the most intriguing bit is that if you type 'autism gut microbiota' into the PubMed search field (for those not familiar with PubMed, it's a repository for medical literature), you find an incredible number of studies and reviews: apparently there is an association between autism and disruptions of the gut microbiota, but whether the two are truly correlated or the correlation is spurious is still unclear.

Before I go on analyzing the literature I found on this topic, let me open a parenthesis on the Facebook discussion because it's something I deeply care about. You might think that the animated discussion I got into was with anti-vaxxers who believe that vaccines cause autism. Instead, my post was criticized by pro-vaccine people who, with the same unflinching certainty typical of the anti-vaxxers, believe that the rise in autism is fiction invented by anti-vaxxers, that autism has always been around, and that any difference between gut microbiota of autistic children and non-autistic children has been disproved. "By whom?" I asked. By this one report:
"Children with autism have no unique pattern of abnormal results on endoscopy or other tests for gastrointestinal (GI) disorders, compared to non-autistic children with GI symptoms, reports a study in the Journal of Pediatric Gastroenterology and Nutrition."
Notice that this opening line is a bit misleading because here is the actual paper [1] whose conclusion, quoting from the abstract, are a bit more cautiously stated:
"This study supports the observation that children with autism who have symptoms of gastrointestinal disorders have objective findings similar to children without autism. Neither non-invasive testing nor endoscopic findings identify gastrointestinal pathology specific to autism, but may be of benefit in identifying children with autism who have atypical symptoms."
Notice also the difference from the abstract and the title of the report. You can tell which one was written by a scientist, right? Because when you do a search on PubMed using keywords autism and gut microbiota you find a long list of references and decades of research. So to me what this says is that the question is still open and we need to understand the issues better. It takes way more than one paper to disprove hypothesis-raising questions spurred from decades of research.

Now here's the mother of all problems: the Internet has made everyone (EVERYONE!) an expert. Today you no longer need a medical degree to speak authoritatively about vaccines, disease, and health. This has generated movements like the anti-vaxxers, but, even more unfortunate is the rise of groups that reply to the anti-vaxxers without a scientific mind-set: these people are doing even more damage to the community than the anti-vaxxers themselves. I found myself in a conversation that had the same one-ended arguments used by anti-vaxxers except these were people who are actually in favor of vaccines: for every paper on autism and gut microbiota I brought up they would dismiss it with another one that said the opposite, demonstrating no understanding of the difference between raising hypotheses and making a claim.

As a scientist, I can tell you that this behavior is the very opposite of scientific thinking. All the people who are in favor of science but DO NOT adopt a scientific attitude when counter-arguing non-scientific claims are hurting the scientific community. It's happening for vaccines, for evolution, and for global warming. For example, people who support intelligent design are mistaken about evolution because they don't understand the meaning of the word "theory" and they don't understand how scientific thinking works. We need to educate people on scientific thinking, not give bad examples of undebatable and absolute notions.

So, PLEASE, all science fans, I beg of you: support us by giving us a cheer, by always citing original papers, and by keeping an open mind because that's what a real scientist would do. We are raising hypotheses, not discussing the meaning of Bible verses. And if you know you can't do any of the above, then the best support you can give us is to shut up. Let real science speak for itself.

I'm fully aware that I'm preaching to the choir so I'll stop now and resume my discussion on autism and gut microbiota. As an additional side note, let me emphasize how difficult it is to discuss a topic like autism because of its extreme complexity: it's a relatively new diagnosis (first described in the early twentieth century), and even though no exact etiology has been found of date, the genetic studies conducted so far have implicated as many as 400 genes such that a malfunction in any of these genes could possibly result in autism [2].

Let's start from the facts: our body hosts more microbial cells than human cells, with the vast majority residing in the gut. These organisms, which we collectively call the "human microbiota" (and “gut microbiota” when referring to the ones residing in the gut) interact with our cells in symbiosis and in fact, some experiments have shown that they can affect our health and even gene expression (see this old post for a striking example of how genes expressed by gut bacteria can affect whether we are fat or lean). All this has been known for a long time, but it's only recently that, thanks to the advent of new DNA sequencing techniques that scientists have been able to look deeper into the composition and classification of the human microbiota. Metagenomic studies have found over 3 million distinct microbial genes (collectively called the "microbiome") in human stools, which is astonishing if you think that the human genome, in comparison, contains about 20-30 thousand genes. The gut microbiome is rich in enzymes without which our body would be unable to digest important nutrients. In fact, it's estimated that roughly 10% of our dietary energy intake comes from byproducts of fermentation from the gut bacteria.

That's all fine and dandy, but what does this have to do with behavior and brain health? A lot, actually, to the point that scientists coined the phrase "gut-brain axis" to denote the deep interaction between the nervous system and the gut microbiota. A 2011 PNAS study [3] used a mouse model to demonstrate how the gut microbiota affects mammalian brain development and behavior. This can happen in a number of ways, but one interesting hypothesis is that a healthy gut microbiome can help modulate the concentration of chemicals that are important for brain development as well as important nutrients that are precursors of neurotransmitters like serotonin.

Several studies done on different populations of children affected by autism spectrum disorders (ASD) have reported some form of gastro-intestinal (GI) dysfunction (such as food intolerances, abdominal pain, diarrhea and flatulence), with proportions ranging from 20-60% of the study population [4]. It's true that ASD children are often very picky eaters with drastic dietary habits, which would of course cause the GI issues. However, given the previously mentioned evidence that the gut microbiota shapes brain development since early infancy, the question of which is the cause and which is the effect at this point is legitimate. In other words, what came first, the chicken or the egg?

Studies have pointed at alterations of the gut microbiota in ASD children who experience gastro-intestinal issues, and some have reported that ASD children receiving antibiotics seemed to experience behavioral improvements. Drastic changes in diet (for example adopting a gluten-free and/or casein free diet) have shown behavioral improvements in some ASD studies, but not in all (meaning that some studies still didn't observe any improvement). Some papers report a higher risk of ASD in children who have not been breast-fed or who have been weaned after the first month of life. All of these instances would cause the gut microbiota to change, including breast feeding, which plays a fundamental role in establishing a healthy bacterial flora in infants. But why aren't any of these studies conclusive? And why are some conclusions the opposite of others? Such differences in results can be explained by differences in sample sizes (too few patients, for example, would cause a false negative), and also by the fact that many of these children have impaired communication skills, and therefore the symptoms, rather than being self-reported, are gathered from the observations of the parents, which can potentially introduce a bias.

Studies that have compared the microbial composition of stools in children affected by ASD with healthy children have had mixed results: the majority report some differences in the composition of the microbial populations, while a few found no significant differences. And despite many studies have looked into it, no ASD-specific gut disturbance has been found, meaning that whatever gut issues ASD children may experience, they are no different than the ones healthy children may experience as well. At the same time, there is some evidence that probiotics help relieve some of the gastro-intestinal issues ASD children experience and at the same time, improve some of their behavioral issues.

What conclusion can we draw from this? Well, first of all that there's no black and white but a lot of gray and anyone who will tell you it's either black or white does not understand how science works. Look at Lamarck's theory of the evolution of traits, first dismissed by Darwin and now (sort of) coming back in the form of epigenetics. Science is not a means to get a definitive and absolute truth, rather, it is our drive to keep asking questions in the search for working answers. [On a side note, this is exactly why I do not like certain showmen out there who proclaim themselves scientists just because they promote science "truths"; real science educators should be promoting scientific thinking, instead.] More than once in the history of science we've corrected and generalized theories. That doesn't mean that we were wrong, rather, it means that we've expanded our knowledge and acquired better investigative tools.

Unfortunately we don't have historic data on autism, since the term was first used in the early 1900s and the definition of the disorder has changed over time. This questions whether or not case prevalence has been truly rising over time, or, instead, the rise we're seeing is simply the effect of a more comprehensive diagnosis. Regardless of whether this is true or not, the fact that most cases are reported in industrialized countries raises an important speculation: these are countries that have seen the most drastic dietary changes over the past 100 years and also lifestyle changes in terms of hygiene and use of antibacterial products, both in household items, as well as in livestock farming (and the use of antibiotics in livestock farming has indeed been increasing over the past few decades). There is no denying that dietary changes and increased use in antimicrobial products will affect the bacteria coexisting in our environment. Are these changes significant? Can they be play a role in the rise in autism prevalence? Can they play a role in the etiology of other disease whose prevalence appears to be on the rise, such as asthma, food allergies, and autoimmune disorders?

I do believe that these are legitimate questions that call for a deeper understanding of how our body interacts with the environment, both outside and inside. Throughout time, evolution has provided us with ways to adapt, but such adaptations are slow. Instead, over the past 100 years we've introduced drastic changes both in the environment as well as in our lifestyle in ways that are too fast for our genetic make-up to adapt. Anything concerning humans is complex, layered by multiple interactions between genetics, environment, and behavior. That’s why we need to keep looking and, most importantly, that’s why we need to always keep an open mind on things. Anyone who claims to know the absolute truth has misunderstood what science is about. Fighting bogus facts like the ones brought forth by the anti-vaxxers with analogous “absolute truths” will only reinforce the globally spread misunderstanding of what science is and what function it covers in our path toward understanding the world. The day we stop asking questions because we’ve found all the answers is the day we’ve stopped growing.

[1] Kushak RI, Buie TM, Murray KF, Newburg DS, Chen C, Nestoridi E, & Winter HS (2016). Evaluation of Intestinal Function in Children with Autism and Gastrointestinal Symptoms. Journal of pediatric gastroenterology and nutrition PMID: 26913756

[2] Li, Q., & Zhou, J. (2016). The microbiota–gut–brain axis and its potential therapeutic role in autism spectrum disorder Neuroscience DOI: 10.1016/j.neuroscience.2016.03.013

[3] Heijtz, R., Wang, S., Anuar, F., Qian, Y., Bjorkholm, B., Samuelsson, A., Hibberd, M., Forssberg, H., & Pettersson, S. (2011). Normal gut microbiota modulates brain development and behavior Proceedings of the National Academy of Sciences, 108 (7), 3047-3052 DOI: 10.1073/pnas.1010529108

[4] Mulle, J., Sharp, W., & Cubells, J. (2013). The Gut Microbiome: A New Frontier in Autism Research Current Psychiatry Reports, 15 (2) DOI: 10.1007/s11920-012-0337-0

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Wednesday, March 2, 2016

March IWSG


This is a monthly event started by the awesome Alex J. Cavanaugh and organized by the Insecure Writer's Support Group. Click here to find out more about the group and sign up for the next event.

OMG, I almost forgot about this month's IWSG! That alone tells you what a stressful month February has been. But, but, but, I do have some awesome news to share with the group.

1) My science blog is now on the Huffington Post! Please come say hi, subscribe to the RSS, and give me a cheer because as exciting as this is, it is also extremely unnerving to have my name on such a huge platform.

2) My WIP is moving along, and the characters are finally taking shape (and personality!). As I mentioned in my previous IWSG post, us writers have to face this dichotomy of delivering new stories fast in a highly competitive and fast-changing market, yet it takes time to produce well thought-out characters. So this year my goal has been to let the characters "simmer" in my head so I can get to know them better before I deliver them to the page. So far so good. :-)

3) Three of my favorite images will be part of a collective show in Albuquerque next month, dedicated to Women's Photography. More details to come.

What about you? What awesome news do you have to share?

Thursday, February 18, 2016

Ice caps melt, prehistoric virus escapes. No, it's not a movie.



Last week I talked about the connection between global warming and the Zika virus. This week I'll discuss another interesting side effect we might observe in the next decade thanks to global warming. The ice caps will melt. Big deal, we already knew that. But have you ever thought of the stuff trapped in that ice that's going to thaw? What if some of that stuff isn't really dead, just dormant, waiting to come back? Sounds like fiction, but it's not.

Up until a few years ago the general notion was that viruses were small. How small? Let's think in terms of genome units: viruses usually carry a handful of genes, either coded into DNA or RNA, and you can think of these as longs strings of four letters: A,C,T (or U if it's RNA), or G. The letters are called nucleotides, and the genome of most common viruses is typically in the order of tens of thousands of nucleotides long. By comparison, the human genome, with its 3 billion nucleotides, is enormous.

The notion of viruses being "small" compared to living cells was turned upside down with the discovery of megaviruses in 2010 (over one million bases) and, in 2013, of the pandoraviruses, a family of viruses that can reach a staggering 2.5 million bases in genome size.

Before you freak out: so far these gigantic viruses have only been found in unicellular organisms called amoebas, not in humans or any other animals. Amoebas acquire their nutrients through phagocytosis and that's also how the gigantic viruses infect them: the cell membrane forms a vesicle around the particle and engulfs it.

The two specimens of pandoraviruses were found in shallow water sediments, one in Chile and the other one in Australia. They were both so big that they could be visible by optical microscopy, reaching 1 μm in length and 0.5 μm in diameter. Now to the interesting bit: the researchers found over 2,000 genes in these pandoraviruses, of which over 90% looked nothing like any other previously known gene. In fact, they appear to be unrelated to the previously discovered megaviruses. So what are they? A fourth domain of life? A completely isolated niche in the tree of life? Or could they be -- as the sci-fi writer in me wants to think -- the remnants of a completely different form of life, one that existed so long ago that these gigantic particles are all there is left of it?

Ok, I thought I was original when I posed that question, but I wasn't. The researchers who'd first discovered the pandoraviruses wondered about the exact same thing and, in order to find an answer, they went digging through fossils. They found a giant virus (which they named pithovirus) in a sample of Siberian permafrost radiocarbon dated to be over 30,000 years old. And I have to say, they beat me in sci-fi imagination because they go as far as to claim that there may be more gigantic viruses frozen out there that could be released from the ice as global warming takes over. *Insert apocalyptic soundtrack here*

The researchers took a sample of Siberian permafrost layer (corresponding to late Pleistocene sediments older than 30,000 years) and used it to inoculate a particular culture of amoebas (called Acanthamoeba castellanii). Lo and behold, they indeed observed particles of a prehistoric giant virus called pithovirus multiplying in the amoeba culture, making it the most ancient eukaryote-infecting DNA virus revived to date! The observed viral particles were amplified and examined through transmission electron microscopy and were found to have many similarities with the pandoraviruses, only they were even bigger. Contrary to pandoraviruses, though, these pithoviruses showed many more similarities to present-day viruses that normally infect humans and animals. This prompted the researchers to raise the alarm:
"Our results further substantiate the possibility that infectious viral pathogens might be released from ancient permafrost layers exposed by thawing, mining, or drilling. Climate change in the Russian Arctic is more evident than in many other regions of the world. Whereas the average global temperature has increased by 0.7 °C during the last 100 y, the average temperatures of the surface layer of Arctic permafrost have increased by 3 °C during the same period."
As the authors themselves put it,
"This work is a reminder that our census of the microbial diversity is far from comprehensive and that some important clues about the fundamental nature of the relationship between the viral and the cellular world might still lie within unexplored environments."
Now, if you'll excuse me, I think I just got an idea for the next bestselling post-apocalyptic thriller.

Philippe, N., Legendre, M., Doutre, G., Coute, Y., Poirot, O., Lescot, M., Arslan, D., Seltzer, V., Bertaux, L., Bruley, C., Garin, J., Claverie, J., & Abergel, C. (2013). Pandoraviruses: Amoeba Viruses with Genomes Up to 2.5 Mb Reaching That of Parasitic Eukaryotes Science, 341 (6143), 281-286 DOI: 10.1126/science.1239181

Legendre, M., Bartoli, J., Shmakova, L., Jeudy, S., Labadie, K., Adrait, A., Lescot, M., Poirot, O., Bertaux, L., Bruley, C., Coute, Y., Rivkina, E., Abergel, C., & Claverie, J. (2014). Thirty-thousand-year-old distant relative of giant icosahedral DNA viruses with a pandoravirus morphology Proceedings of the National Academy of Sciences, 111 (11), 4274-4279 DOI: 10.1073/pnas.1320670111

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