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Monday Micro – Is the new Saudi coronavirus a pandemic in waiting? Siouxsie Wiles May 13

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Between November 2002 and July 2003, a novel respiratory virus appeared in South China, spreading first to Hong Kong and going on to infect people in 37 countries around the world. As the virus spread, thousands were quarantined, schools were shut, and many airports implemented thermal screening programmes to stop potentially infected people from getting on planes. By the end of the pandemic, the Severe Acute Respiratory Syndrome (SARS) coronavirus (SARS-CoV) had resulted in 8,273 cases and 775 deaths, a case fatality rate of 10%.

So it’s not surprising that many are now nervous after the World Health Organisation (WHO) reported that a novel coronavirus (nCoV), closely related to the SARS virus, has emerged in the Middle East. Since early 2012, there have been 34 confirmed cases of infection with nCoV, which causes severe acute pneumonia and renal failure. With 18 deaths so far, the case fatality rate currently sits at over 50%, a frightening statistic. But is this new coronavirus going to go pandemic, like the SARS virus did? With such a small number of cases to date, it is too early to say for sure.

In 2002/2003, the SARS virus spread rapidly, infecting otherwise healthy individuals. It arrived in Hong Kong via a mainland doctor who stayed at a hotel in Kowloon. He infected 16 of the hotel visitors, who themselves traveled on to Canada, Singapore, Taiwan, and Vietnam, taking SARS with them.

In contrast, the majority of nCoV cases have remained within Saudi Arabia and while there have been cases exported to Jordan, Qatar, the United Arab Emirates, the United Kingdom and France, the virus does not seem to have spread much beyond the index cases. There have been a small number of cases of family members becoming infected. This confirms that nCoV can transmit from person to person but suggests that prolonged exposure is needed to become infected, at least for healthy people.

One of the interesting features of this novel coronavirus, is that the majority of infections have occurred within health care facilities. The most recent cluster of cases within Saudi Arabia have occurred within a single facility and all patients had at least one other underlying disease. Furthermore, the Ministry of Social Affairs and Health in France has just informed the WHO of a confirmed case of nCoV in a patient who spent three days sharing a hospital room with France’s first nCoV patient. These cases suggest that underlying diseases may also make people more vulnerable to infection with nCoV.

So far, the evidence is suggesting that nCoV is unlikely to turn into a pandemic. But the thing about viruses is that you never know. What we do know is that nCoV is highly infectious to human airway epithelial cultures in the laboratory, and that the virus can hide itself from the human immune system (1). But somehow this isn’t currently translating into epidemic spread out in the real world. But we shouldn’t be complacent. It is certainly not inconceivable that nCoV could mutate in some way to become more infectious to healthy people, the first step towards a SARS-like scenario. And there is still so much we don’t know about nCoV. Where did it come from? What is nCoV’s natural reservoir? In the case of SARS, the virus was found in samples of wild animals sold as food in the local markets, many of which show no clinical signs of infection. So far, there is limited information on any potential links between nCoV cases and exposure to animals, although nCoV is closely related to coronaviruses from bats (2).

If nothing else, though, the emergence of nCoV is another warning of the threat we face from novel viruses. As many of these viruses cross over to humans from wild animals, these threats are going to increase as humans continue to encroach on the natural habitats of so many creatures. And our interconnected global world means any virus is less than 24 hours from anywhere else on earth. A sobering thought.

References:

1. Kindler E, Jónsdóttir HR, Muth D, Hamming OJ, Hartmann R, Rodriguez R, Geffers R, Fouchier RAM, Drosten C, Müller MA, Dijkman R, Thiel V. 2013. Efficient replication of the novel human betacoronavirus EMC on primary human epithelium highlights its zoonotic potential. mBio 4(1):e00611-12. doi:10.1128/mBio.00611-12.

2. van Boheemen S, et al. 2012. Genomic characterization of a newly discovered coronavirus associated with acute respiratory distress syndrome in humans. mBio 3(6):e00473-12. doi:10.1128/mBio.00473-12.

New Zealand’s National Science Challenges announced Siouxsie Wiles May 01

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NZ’s National Science Challenges announced alongside a massive funding boost

In the beautiful blue Ocean gallery at the Auckland War Memorial Museum, the Prime Minister John Key, the Honourable Minister for Science and Innovation Steven Joyce and the Prime Minister’s Chief Science Advisor Sir Peter Gluckman, today announced the 10 National Science Challenges.

The PEAK panel*, chaired by Sir Peter Gluckman, was charged with developing the Challenges using the following criteria:
1) Target high level goals, which if achievable would have a major public benefit to NZ
2) Be seen as being of public importance, hence the public engagement campaign
3) Have scientific research as essential to solving the Challenge
4) The scientific capability and capacity existing in NZ

The panel considered 223 submissions from the science and research sector, 138 from the public via the web, and 616 ideas and comments posted to the Great NZ Science Project website and Facebook page. The main 10 Challenges are listed on the Ministry for Business, Innovation and Employment’s website here, and the document explaining them in a little more detail is here.

The big surprise came with the announcement that the budget for the Challenges had been more than doubled with the allocation of an extra $73.5M, bringing the total budget over the next four years to $133.5M. It will be interesting to see where this money has come from. The second exciting announcement was of a special extra ‘Science and Society leadership Challenge’ brought about by what the panel identified as deficits in science education, science communication, science literacy and the application of evidence in all levels of decision making. This challenge therefore covers a huge array of themes, from promotion of science literacy in schools, to developing science communication as an academic discipline and encouraging members of the public to participate in science as ‘citizen scientists’.

But other than the Science and Society Challenge, is it ‘business as usual’? It does look awfully like it. Just looking at the biomedical related Challenges, I was really shocked to see that infectious diseases don’t get a mention. In fact, in the Challenge 3 Healthier Lives: Research to reduce the burden of major New Zealand health problems, they are specifically excluded as the focus is on non-communicable diseases (NCDs). I do hope the 792 people who ‘voted’ for my illustrative ‘Fighting Diseases‘ Challenge on the Great NZ Science Project didn’t think they were actually voting for me! I asked Sir Peter about this at the Science Media Centre’s media briefing afterwards and he explained that they had considered infectious diseases, but that more people die from NCD’s in NZ, and that in the panel’s opinion, infectious diseases research in NZ didn’t meet the criteria of having sufficient capability and capacity to address a Challenge. This is depressing as NZ is bucking international trends, with our rates of infectious diseases on the increase rather than decreasing, which is what would be expected of a developed country like ours.

At the media briefing I also specifically (and rather cheekily) asked Steven Joyce and Sir Peter how much of the funds would be used to support post-doctoral fellows and PhD students to actually do the science, and how much would be spent on the salaries of Principal Investigators. It is an important question, especially given that the Challenges have multi-disciplinarity and collaboration at their heart. If the Challenges are funded like normal contestable granting bodies like the Marsden and Health Research Council, we could find most of the money going to pay the time contribution of the ‘silverbacks’ and not on salaries for younger researchers. Both the minister and Sir Peter answered that ‘workforce development’ would be a key measure of success so we’ll see how that works out.

*PEAK panel members: Peter Gluckman, Jacqueline Rowarth, Ian Ferguson, William Denny, Elf Eldridge, Peter Hunter, Mary O’Kane, David Penman, Te Ahu Karamu Charles Royal, Richie Poulton and Rachel Wiltshire.

UPDATE: I live-tweeted the announcement so have storified the tweets here.

Monday Micro: living night lights Siouxsie Wiles Apr 29

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One of the latest Kickstarter projects to create a buzz is promising its backers a living nightlight that shines without electricity. Enter the Glowing Plant project, developed by a group of biohackers from BioCurious* in California. Launched just a few days ago, Antony Evans, Omri Amirav-Drory and Kyle Taylor have already exceeded their $65,000 target needed to create a genetically engineered plant that glows in the dark. In fact, they have already passed the $115,000 mark with over a month left to go. Their new goal is $400,000 to create a glowing rose. Check out their short video by clicking the link below:

Glowing plant vid

So how are they going to do it? Back in 2010, Alexander Krichevsky and colleagues published a paper in PLOS One showing that tobacco plants could be engineered to glow in the dark by incorporating the genes (known as the lux operon) which make the marine bacterium Photobacterium leiognathi** glow (1). The light generated by one of the plant lines they created could be detected by eye in a dark room after about 5-10 minutes suggesting they could make quite neat night lights. This was exciting stuff as previous attempts to make glowing plants had revolved around getting the plants to express the luciferase gene from the firefly, which required plants to be sprayed with luciferin, the substrate for the reaction, in order for light to be produced. In contrast, cells that express the whole bacterial lux operon glow without needing any additional cofactors.

Glowing tobacco plants

Glowing tobacco plants

Interestingly, Krichevsky declares in his PLOS One paper that he is founder of BioGlow Inc, a company which aims to develop commercially available glowing ornamental plants. BioGlow Inc is listed as a tenant of the Bio-Research & Development Growth (BRDG) Park at the Danforth Plant Science Centre in Missouri, but otherwise doesn’t have much of a web presence.

But back to the Glowing Plant project. Antony and his team say they are planning on building on the work of Krichevsky and colleagues, making a synthetic version of the bioluminescence genes so that they will be better expressed by the plant cells. Fingers crossed!

Reference:
1. Krichevsky A, Meyers B, Vainstein A, Maliga P, Citovsky V (2010) Autoluminescent Plants. PLoS ONE 5(11): e15461. doi:10.1371/journal.pone.0015461

*The BioCurious ethos is that innovations in biology should be accessible, affordable, and open to everyone. They have built up a complete working laboratory and training centre for citizen scientists and hobbyists to get together to do science.

**I’ve blogged about P. leiognathi before. They use their light to trick zooplankton into eating them. In a nutshell, the zooplankton ingest the glowing bacteria but are unable to digest them. The glowing bacteria mean the hapless zooplankton are then more visible to their own predators, nocturnal fish, who devour them. P. leiognathi are unfazed by all this, ending up in the fish’s digestive system which is where they wanted to be in the first place. Genius.

Why stereotyping scientists matters Siouxsie Wiles Apr 27

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I’m always interested to find out what people think I do for a living. No one has ever said scientist. It’s usually something in the arts or fashion*. You know, creative industries. I’m guessing it’s because of my hair. What is interesting about this though is that somehow people don’t think of science as being creative. Such misperceptions are largely due to the way scientists are portrayed in the media. It’s really interesting looking at stock photos to see how different professions are portrayed; some of the best of scientists have been collected together by various bloggers. Male scientists are usually older with crazy hair, while women scientists are scantily clad or have completely forgotten to wear any clothes. White coats abound, as do glass vials of coloured liquids. But how representative are these images of scientists? Not very, I’d say. But should we care? Yes!

This 'scientist' remembered her gloves and safety glasses but forgot her clothes!

This ‘scientist’ remembered her gloves and safety glasses but forgot her clothes!

A few days ago I gave a talk to primary school teachers about why stereotyping scientists matters. It was partly inspired by data looking at pictures of scientists drawn by school children before and after a visit to the Fermi National Accelerator Laboratory, near Chicago, which specialises in high-energy particle physics. Lots of the before images are of crazy haired old men in white coats, with many children describing careers in science as unobtainable. But after the visit, the scientists start to look just like normal people, and the children even start to suggest they could see themselves as scientists one day.

After my talk, the lovely Dr Sally Birdsall sent me a paper published in 1999 that looked at children’s portrayals of scientists [1]. The authors collected 562 drawings done by 281 children aged 5-13 living in different socioeconomic areas of London. I’ve plotted some of the data showing the percentage of drawings that represented male and female scientists, as well as those where scientists are portrayed wearing a lab coat or doing chemistry-type experiments. As you can see, more males are portrayed than females, a trend which increases as the children get older, at least until the age of 10. What is really interesting is that the numbers of drawings of scientists in white coats/doing chemistry increases with age, presumably as children are exposed to media portrayals of stereotypes.

How kids portray scientists

How kids portray scientists

It seems clear to me that being exposed to more realistic portrayals of scientists makes a difference, at least to children. Meeting real scientists is even better. If you are a scientist reading this, consider getting in touch with your local school and volunteering to go in and meet some of the kids. The younger the better! In the absence of having any scientists volunteer, in my talk I pointed to some online resources that teachers could use to show scientists in all their real glory. There is the fantastic ‘This Is What a Scientist Looks Like‘ which has pictures and profiles for over 600 scientists of all colours, shapes and sizes. There is also the ‘100 Women, 100 Visions‘ project, a series of 100 pictures taken by photographer Jackie King in 2009 to celebrate the variety of women scientists and engineers at Imperial College London**. And finally, there was the Great NZ Science Project, the public engagement campaign for the National Science Challenges***, which used 8 scientists to illustrate the diversity of science going on in New Zealand. What I love about this campaign is that it showed that science happens everywhere, not just in labs. And only three of the 8 scientists are wearing lab coats****. The TV advert below got a lot of airplay on NZ TV so I hope that will go someway to busting some of the stereotypes.

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Slides from my talk:


Reference:
1. Changing children’s images of scientists: can teachers make a difference? Brian Matthews and Daniel Davies (1999). School Science Review. 80 (293): 79-85.

*Fashion always cracks me up. I got the award for being the worst dressed two years running in high school. True, the award was coveted by the ‘alternative’ crowd – it meant your efforts to be different had been recognised :)

**See if you can spot a familiar face.

***Which are being announced on Wed 1st May…

****Make no mistake though, the campaign wasn’t perfect. One of it’s main features seemed to have been to perpetuate the myth that all scientists are bad communicators. One stereotype at a time I guess.

Monday Micro – Influ-Venn-Za! Siouxsie Wiles Apr 15

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A new strain of bird flu (H7N9*) has appeared in China. Since the first report two weeks ago, 51 people are known to have been infected of which 11 have died. Transmission seems to be from close contact with poultry and many birds are being culled as a precaution. Cases started in Shanghai and the eastern provinces of Jiangsu and Zhejiang but have now been reported in Beijing.

For those struggling to tell their H7N9 from their H5N1, the lovely peeps who run Information is Beautiful have come up with a handy guide to flu in the form of a beautiful Venn diagram:

Influenza types

Influ-Venn-Za!

*Flu viruses are classified into subtypes based on antibody responses to the two large glycoproteins on the outside of the viral particles, hemagglutinin and neuraminidase.

Astrosquid! Siouxsie Wiles Mar 27

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What is the value of blue-skies research?

This is a question often asked by politicians and the public. Why should public money be spent funding science that seems to have no obvious benefit beyond generating scientific knowledge? The simple answer is that it can be almost impossible to predict what new avenues that scientific knowledge will open up. Take the Hawaiian bobtail squid, for example. What could studying this little nocturnal hunter possibly lead to? Take a guess. No ideas? Let me help you out.

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It lead to the discovery that bacteria are able to communicate with each other, including how they sense when the time is right to turn on genes needed to cause disease. I’m not sure anyone could have seen that coming! Importantly, this research has provided scientists with another potential weapon with which to fight antibiotic resistant superbugs. In a world rapidly running out of antibiotics, we need all the weapons we can get.

This animation was produced with the support of a public engagement grant from the UK Society for Applied Microbiology, to engage the services of graphic artist Luke Harris and his team. Dr Siouxsie Wiles (@SiouxsieW) is a microbiologist and bioluminescence enthusiast who heads up the Bioluminescent Superbugs Group at the University of Auckland in New Zealand. She and her team make nasty bacteria glow in the dark to help understand and combat infectious diseases.

What we couldn’t fit into 3 minutes…

The Hawaiian bobtail squid, Euprymna scolopes, is just 3 cm in length and lives in the shallow moonlit waters off Hawaii. It spends its days sleeping buried in the sand, emerging at night in search of food. It has a very cunning trick to hide its shadow from fish looking for a meal, or from creatures like shrimp that it feeds on. It houses a colony of glowing bacteria (Vibrio fischeri) in a special organ on its underside. These bioluminescent bacteria shine their light down so that to any creatures looking up, the squid just looks like the moon. What is even more clever is that the squid uses its ink sac to match the intensity of moonlight hitting its back, dimming the light from the glowing bacteria as needed. This is important not just for cloudy nights but as the squid moves through different depths of water.

Baby squid are born without V. fischeri or a light organ. Instead they just have a small opening in their mantle (the bulbous bit of their body) that is bathed by sea water. What is incredible is that only V. fischeri can colonise this opening – once they do, the squid cells start to change and the light organ forms. The ability to glow is crucial though – scientists have made versions of V. fischeri which can’t glow and they aren’t able to colonise either.

Adult squid have an ingenious way of ensuring that there is plenty of V. fischeri floating around in the water to colonise baby squid. Each morning, before they settle down in the sand to sleep for the day, they expel 99.9% of the bacteria from their light organ into the sea. This serves another purpose too, ensuring the bacteria left behind in their light organ are constantly growing and have plenty of nutrients. Bacteria that run out of nutrients start to shut down to save energy. Producing light takes quite a bit of energy and the last thing the squid wants is a mantle full of lazy dim bacteria!

When scientists first identified V. fischeri and grew it in the lab they noticed something quite interesting. The bacteria only switch on their light when they have reached a critical population size. This makes perfect sense. There is no point going to all the trouble of making light if it isn’t bright enough to be seen. Each bacterium produces a chemical, called the autoinducer, that diffuses out of the bacterial cell. The more bacteria there are, the more autoinducer is produced. If those bacteria are growing in a confined space like a flask, or the light organ of the squid, the autoinducer will accumulate. Once it reaches a critical concentration, the autoinducer triggers the bacteria to switch on the genes for producing light*. This phenomenon is called quorum sensing.

Scientists then used the bioluminescence reaction to see if other species of bacteria produce autoinducers. Surprise, surprise, it turns out that lots of different bacteria use quorum sensing to signal to each other that they are in the right numbers or environment to do something, which is not worth doing otherwise. From the bacterial form of sex, to swimming, to switching on the genes needed to cause disease in plants, animals and humans. Now we just have to find a way of exploiting this to our advantage!

You can hear me chatting about the squid and quorum sensing on Radio New Zealand’s Nine to Noon programme with Kathryn Ryan here (13’12”):

*For those who really want to know, the autoinducer is the product of the luxI gene. When it reaches a critical concentration, it interacts with the product of the luxR gene, and together this complex binds to a region of DNA upstream of the genes under their control called the lux box which then triggers their transcription.

Monday Micro – World TB Day Siouxsie Wiles Mar 25

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Yesterday, the 24th of March, was World TB Day which aims to build awareness for tuberculosis, a lung disease which kills about 2 million people around the world each year. That’s 3 people a minute. Why the 24th March? This was the day, in 1882, that Dr Robert Koch* announced he had discovered the bacterium that causes TB, Mycobacterium tuberculosis.

TB, or consumption as it was known, had long been thought to be a hereditary disease. In 1869, French physician Jean-Antoine Villemin showed the disease was infectious. He injected rabbits with material taken from people who had died of TB. Not surprisingly, the rabbits became ill. Thirteen years later, Robert Koch, purified the microorganism responsible, for which he won the Nobel Prize in Physiology or Medicine in 1905.

But despite it being over 100 years since M. tuberculosis was discovered, we are a long way from eradicating TB, hence World TB Day. The Global Fund, supported by the Gates Foundation and others, have put together this nice infographic highlighting some facts and figures.

GatesTB20130321FINALJPG

M. tuberculosis is one of the organisms my lab at the University of Auckland are busy working on. If you want to know what we are doing, here’s the little animation I made with graphic artist Luke Harris and his team to show how we are using fireflies to make TB research faster and more humane.

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*Koch is best known to microbiologists for what we now refer to as Koch’s Postulates, four criteria he stated needed to be proven to establish a causal relationship between an microorganism and a particular disease. These are:

1. That the microorganism is found in all cases of the disease examined, while absent in healthy organisms
2. That the microorganism be isolated from a diseased host and grown in a pure culture
3. That the microorganism should be capable of producing the original infection when introduced into a healthy host, even after several generations in culture
4. That the microorganism is retrievable from an inoculated/experimental host and cultured again.

As with everything though, it turns out that there are exceptions to every rule, and we now know many microorganisms that fail one or more of Koch’s Postulates but are still clearly the cause of a particular disease. For example, many nasty microorganisms can be carried asymptomatically by healthy people (including Vibrio cholerae, the agent responsible for cholera), while there are a number of microorganisms which we are unable to culture in the laboratory (including Mycobacterium leprae, the agent responsible for leprosy, which can only be grown in the footpad of a mouse, or a nine-banded armadillo).

Monday Micro – roller derby micro! Siouxsie Wiles Mar 18

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There were a smorgasbord of micro stories to choose from this week, but how could I pass up a story which combines microbes, open access and gorgeous women on roller skates?!

James Meadow and colleagues, from the Institute of Ecology and Evolution at the University of Oregon, have just published a paper looking at the effect of contact sports on the microbial communities living on the skin of the participants. This is where the roller skates come into the story, as the contact sport James and his colleagues studied was roller derby*.

This great picture by Emily Thomas AKA Mummy'sLittleMonster sums up roller derby perfectly!

This great picture by Emily Thomas AKA Mummy’sLittleMonster sums up roller derby perfectly!

James’ paper is one of the first to be published in new online open access journal PeerJ which launched recently. More on this new journal below, but one feature I do want to point out is that authors can elect to make the review history of the article public, which James and his colleagues did. It makes for fascinating reading!

But back to the paper. James and colleagues hypothesised that close contact between people would create shifts in the microbial communities living on the skin. And that’s pretty much what they found. Here is a nice plot showing the microbial composition of the skin of each team member before and after playing. Each symbol represents a player, each colour represents a different team (they looked at three teams: the Emerald City Roller Girls, the DC Roller Girls and the Silicon Valley Roller Girls) and the coloured ellipses show the standard deviations around the community variances from each team. Before they started, the skin microbiomes of members of each team clustered nicely together – presumably because they train together and therefore often come into contact with each other. After playing you can see that the skin microbiomes have changed and become much more similar between the teams – they’ve shared their microbes!

Variation in skin microbial community composition is significantly explained by team identity.

Variation in skin microbial community composition is significantly explained by team identity.

The authors concluded that:

“contact sports provide an ideal setting in which to evaluate dispersal of microorganisms between people.”

Certainly looks that way!

Reference:
Meadow et al. (2013) Significant changes in the skin microbiome mediated by the sport of roller derby. PeerJ 1:e53 http://dx.doi.org/10.7717/peerj.53

Conflict of interest statement: I am a PeerJ academic editor but did not handle or review this manuscript.

* For details see the official Women’s Flat Track Derby Association (WFTDA) rules. Two competing teams, each composed of up to 4 ‘blockers’ and 1 ‘jammer’, simultaneously circle the track while the jammers, who start behind the pack, try to score points by lapping players of the opposing side. The catch is that the blockers can use their bodies (arms from shoulder to elbow, torso, hips, booty** and legs from mid to mid to upper thigh) to try to stop the jammers from lapping the pack. There is some great footage of some teams in action on You Tube:

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**Official WFTDA nomenclature..

***PeerJ was founded by Peter Binfield (formerly at PLOS ONE) and Jason Hoyt (formerly at Mendeley) and is backed by O’Reilly Media. PeerJ aims to be a biological and biomedical version of PLOS ONE, with papers judged solely on their scientific and methodological soundness, rather than potential ‘impact’,. Like PLOS ONE, PeerJ papers are freely available to read and published under a Creative Commons licence which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Like PLOS ONE the costs are covered by the researcher but in the form of membership fees per author, rather than article processing charges. a one off payment of $99 allows an author to publish one paper per year for life, while $299 allows an author unlimited publications per year.

Monday Micro – extremophiles & 50 shades of … immunity! Siouxsie Wiles Mar 11

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In last week’s Monday Micro I mentioned horizontal gene transfer (HGT), the process by which bacteria acquire new genes from other microbes in their environment. HGT is one of the primary ways that genes for antibiotic resistance are able to spread between different bacteria. It is also how plenty of bacteria pick up genes for things like toxins which help them cause disease. But it’s not all bad. A few years ago, a team of scientists reported in the journal Nature that the gut microbes of Japanese people had picked up the ability to digest the unique carbohydrates present in seaweed through HGT from a seaweed chomping microbe called Zobellia galactanivorans (1).

This week, in a paper just out in the journal Science, Gerald Schönknecht, Wei-Hua Chen and colleagues report that HGT is the secret to the success of the extremophile Galdieria sulphuraria, an algae that is able to thrive in hot, acidic springs, like those found in Iceland or the Yellowstone National Park. When the researchers sequenced the genome of G. sulphuraria, they found it had acquired at least 5% of it’s protein-coding genes through HGT (2). These genes give G. sulphuraria the ability to detoxify heavy metals, deal with high concentrations of salt, and to consume a variety of unusual food sources.

Galdieria sulphuraria growing on a rock in an  Icelandic hot spring near Reykjavik.  CREDIT: Christine Oesterhelt

Galdieria sulphuraria growing on a rock in an Icelandic hot spring near Reykjavik.
CREDIT: Christine Oesterhelt

And finally, also leading on from last weeks description of the CRISPR system, Michael Criscitiello and Paul de Figueiredo have written a piece in the open access journal PLOS Pathogens challenging the dogma that is the black and white existence of the innate and adaptive immune systems*. Playfully nodding to the Fifty Shades phenomenon, their piece is entitled Fifty Shades of Immune Defense, and lays out the immune system as a continuum (3).

Different immune mechanisms with adaptive properties are being discovered in species originally considered to only possess innate immunity. Taken from (3)

Different immune mechanisms with adaptive properties are being discovered in species originally considered to only possess innate immunity. Taken from (3)

*We are generally taught that the immune system has two parts to it: the innate immune response, in which cells recognise and respond to pathogens in a generic way, but can’t confer long-lasting protection to the host, and the adaptive immune response, in which cells respond in a specific way, and confer long lasting protection to the host.

References:
1. Hehemann, J., Correc, G., Barbeyron, T., Helbert, W., Czjzek, M., & Michel, G. (2010). Transfer of carbohydrate-active enzymes from marine bacteria to Japanese gut microbiota. Nature, 464 (7290), 908-912 DOI: 10.1038/nature08937
2. G. Schonknecht, W.-H. Chen, C. M. Ternes, G. G. Barbier, R. P. Shrestha, M. Stanke, A. Brautigam, B. J. Baker, J. F. Banfield, R. M. Garavito, K. Carr, C. Wilkerson, S. A. Rensing, D. Gagneul, N. E. Dickenson, C. Oesterhelt, M. J. Lercher, A. P. M. Weber. Gene Transfer from Bacteria and Archaea Facilitated Evolution of an Extremophilic Eukaryote. Science, 2013; 339 (6124): 1207 DOI: 10.1126/science.1231707
3. Criscitiello MF, de Figueiredo P (2013) Fifty Shades of Immune Defense. PLoS Pathog 9(2): e1003110. doi:10.1371/journal.ppat.1003110

Monday Micro – smart viruses Siouxsie Wiles Mar 04

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I’ve always loved bacteriophage, the spaceship-like viruses which prey on bacteria*. They really do look like something from another planet.

Phage are abundant in nature, found everywhere, from soil and water, to the guts of animals. They have two different life cycles; in the lytic cycle they infect bacteria, replicate themselves and then lyse and kill the bacteria as they spill out looking for more victims to infect. This turns out to be a rather useful form of bacterial ‘biocontrol’ – there are currently a few products based on lytic viruses approved to control the bacterium Listeria monocytogenes in packaged food products.

The second life cycle is known as the lysogenic cycle. In this phase, the phage integrates into the genome of the bacterium and bides it’s time (referred to as a temperate phage). Think of it as a form of genetic modification of bacteria – when integrated, the genetic information of the phage is replicated along with the genetic info of the host bacterium and so is passed on to the next generation when the bacterium divides. This is one of the mechanisms of horizontal gene transfer, by which bacteria can pick up new genes, for example, encoding new toxins or antibiotic resistance genes. When conditions are right, the phage can become active again, switching back to a lytic lifestyle.

As phage are so abundant, bacteria have developed numerous forms of ‘immunity’ to protect themselves. One of these is called the CRISPR system, which stands for Clustered Regularly Interspaced Short Palindromic Repeats. In this quite elegant system, short segments of foreign DNA, called spacers, are incorporated into the bacterial genome between CRISPR repeats. These spacers serve as a sort of immune ‘memory’ of past exposure. CRISPR spacers are then used to recognise and silence foreign genetic material in a similar manner to RNA interference (RNAi) in eukaryotic organisms.

In a paper just out in Nature (alas, its not open access so here is the write up of it on Science Daily), Tufts University’s Prof Andrew Camilli and his postdoc Dr Kimberley Seed have found that a phage which infects the bacterium Vibrio cholerae, the agent of cholera, has turned the tables on it’s prey, by having its own CRISPR system. It uses its spacers to encode the genetic information for a chromosomal island normally used by V. cholerae to counteract phage. Kimberley showed that phage that were missing the spacer sequences were no longer able to lyse V. cholerae carrying the chromosomal island. This is pretty neat. By possessing its very own CRISPR system, the phage can rapidly adapt to any new weapons in its adversary’s arsenal.

Reference:
Kimberley D. Seed, David W. Lazinski, Stephen B. Calderwood, Andrew Camilli. A bacteriophage encodes its own CRISPR/Cas adaptive response to evade host innate immunity. Nature, 2013; 494 (7438): 489 DOI: 10.1038/nature11927

*According to Wikipedia, the term phage comes from the Greek for ‘to devour’.

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