Musings is an informal newsletter mainly highlighting recent science. It is intended as both fun and instructive. Items are posted a few times each week. See the Introduction, listed below, for more information.
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Introduction (separate page).
Current posts -- 2018 (May - ??)
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Posted since most recent e-mail; they will be announced in next e-mail, but feel free...
May 22, 2018
The following figure shows a sample from a Solar System planet that was destroyed over four billion years ago.
This is the top figure in the Phys.org news story.
The numbers on the ruler are presumably centimeters, but I don't see anything that says that.
That is the claim made in a recent article. It's a fascinating argument. Let's walk through some of the key steps.
The sample shown above is from a meteorite that landed on Earth in 2008.
The sample contains diamonds, interspersed with graphite. That was shown in 2015.
The current work builds on that. In particular, the authors study the nature of the inclusions in the diamonds.
All the points so far are pretty much "facts" -- things that can be observed or measured. The question now is, how did these diamonds form? Of course, we don't know. We now go to hypotheses, even speculations.
Using their understanding of the various ways diamond can form as well as the particular properties of these diamonds, the authors argue that these diamonds could have formed only with sustained high pressure. (A shock wave, such as from an impact, can lead to diamonds. But these diamonds are too big to have come from such a brief process.) That means inside a planet-sized body -- one at least as big as Mercury, probably considerably larger.
The meteorite that landed was considered an asteroid, and likely from the common asteroid belt between Mars and Jupiter. However, an ordinary asteroid would not be big enough to produce such diamonds; it would not have had the high pressure needed to make these diamonds. We need a planet.
Which planet? The overall chemistry of the samples, including the inclusions in the diamonds, is not consistent with any known planetary source.
Those points lead to the suggestion that the sample was originally part of a larger body -- a planet. The diamonds formed while in the larger body. That body may have been part of the large mess during the early stages of the Solar System. Crashes were common back then, and most large bodies were broken up. The planets and asteroids we now see remained. But this body, which spent four billion years in the asteroid belt, was once part of a planet-sized body large enough to make diamonds. It then delivered those diamonds to Earth upon another collision just a decade ago.
Are we really supposed to believe all this? It's a scientific hypothesis. It's based on evidence, and then logic. The arguments are of interest. We can't find a planet that no longer exists. But scientists can critique the logic, examine other materials, and explore alternative hypotheses.
* Study: Diamond from the sky may have come from 'lost planet'. (F Jordans, Phys.org, April 17, 2018.)
* This Meteorite Contains Diamonds From a Lost Planet. (Science Page, April 21, 2018.) Be patient with the English here, but overall this is a useful presentation of the story.
The article, which is freely available: A large planetary body inferred from diamond inclusions in a ureilite meteorite. (F Nabiei et al, Nature Communications 9:1327, April 17, 2018.)
A previous post about this meteorite: Asteroid hits earth (April 3, 2009).
More about the early mess in the Solar System: Birth of the Moon: Is it possible that Theia was similar to Earth? (June 20, 2015).
Another unseen planet in the Solar System: A ninth planet for the Solar System? (February 2, 2016).
A recent post about diamonds: Ice in your diamond? (April 23, 2018).
May 20, 2018
Zika virus is causing serious problems, including brain defects in newborns. Zika can be transmitted by blood -- usually with the aid of a mosquito. A blood test for the virus is now available. Screening blood donations for Zika virus should reduce the problems.
The logic seems clear. How is it working out?
A new article provides results from the early experiences with testing blood donations in the US for Zika. The overall result is that the cost has been about 5 million dollars (USD) per detection of a blood donation that was Zika-infected.
Is that "good"? What does "good" mean here? Is the value of a medical intervention (in this case, a screening) to be measured in monetary units?
The article is (mainly) from the American Red Cross. They are a major player in the US blood supply; they carry out the tests that are mandated -- and thus incur the costs. In the article, they present their data. They also present their analysis. They make clear that they think the screening is not a good use of their funds.
The article is accompanied by a Commentary, which turns out to be a quite extensive discussion of the matter. It explores numerous issues involved in choosing a screening strategy; it does this without getting bogged down in the nuances of the tests per se.. I particularly encourage people to read that Commentary.
There is no intent here to reach a conclusion. The point is to think about the issues -- and to recognize the overall complexity. Balancing the considerations is not simple. The conclusion may change over time; Zika is still a developing story. And although I posed a yes/no question as the title here, a better question might well be: how should we do screening?
The focus is on the US. The issues to consider are general, but how they get weighed may not be. The US has been at the edge of the Zika zone, with a relatively minor impact. The number of US Zika cases reported in 2017 due to local transmission was two. (Cases in travelers are a different problem.)
As to "how"... One alternative is to screen the blood in small pools, for example, 16 blood samples mixed together for a single test. (If the pool test is positive, then the members of the pool are tested individually.) This leads to a substantial cost reduction, with a reduction in sensitivity (due to dilution). Is this ok? It's actually done for some other tests, and the data available so far suggests it might be sufficient for Zika -- but the data is limited.
News stories. Caution... As you read about the article, you may see numbers that seem inconsistent for how many positives were found. They are probably referring to different specific findings. It doesn't matter much; the point is that the number of positives is very small.
* Are Zika Blood Tests Worth the Cost? (D W Hackett, Precision Vaccinations, May 10, 2018.)
* Study: Zika blood donation screening costly, finds few cases. (L Schnirring, CIDRAP News, May 9, 2018.) Good overview of both the article and the accompanying Commentary.
Both of the following may be freely available...
* Commentary accompanying the article: Revisiting Blood Safety Practices Given Emerging Data about Zika Virus. (E M Bloch et al, New England Journal of Medicine 378:1837, May 10, 2018.) Highly recommended.
* The article: Investigational Testing for Zika Virus among U.S. Blood Donors. (P Saá et al, New England Journal of Medicine 378:1778, May 10, 2018.) In addition to the summary numbers, noted above, there is considerable discussion of the types of Zika tests, such as nucleic acid and antibody tests. There is also discussion of classes of Zika cases and donors, such as cases due to local transmission vs travel. Those interested in these other issues may find the article worth a read, regardless of the specific numbers here.
Previous Zika post... A recent genetic change that enhanced the neurotoxicity of the Zika virus (December 1, 2017).
A recent post about testing blood: A blood test that detects multiple types of cancer (March 30, 2018).
There is a section on my page Biotechnology in the News (BITN) -- Other topics on Zika. It includes a list of Musings post on Zika.
May 18, 2018
Toluene is a major industrial chemical. It's made from petroleum. A new article explores the possibility of bio-toluene.
A lake near the University of California Berkeley campus.
This is reduced from the figure in the Phys.org news story.
The following figure gives an example of the biological production of toluene. It also shows the key chemicals.
This was done with a sample of lake sediment serving as the catalyst. That is, the action here is due to a mixed culture of microbes from the lake. Anaerobic, as one might expect for the lake bottom.
Phenylacetate was added to the culture. The amounts of both it (blue) and the product toluene (red) were measured over time. You can see that the phenylacetate declines and the toluene increases.
The data is consistent with a simple conversion of one to the other. Casual reading of the graph suggests that about 90% of the input was converted to toluene.
The structures of the two chemicals are shown at the top.
The conversion occurs by loss of the CO2 from the carboxylate ion of the phenylacetate. (An H+ ion from the medium -- or, more likely, from the cell cytoplasm -- is used to complete the reaction.)
This is Supplementary Figure 1 from the article. (That is, it is from the Supplementary Information file accompanying the article.)
The basic phenomenon had been seen before, but work to understand what is going on was not successful. Now, with new tools, the scientists were able to isolate both the enzyme and its gene, and to characterize the enzymatic reaction. One major tool was metagenomics, the sequencing of bulk DNA in the community. But to sort that out and find the gene of interest, it helped to have a sense of what they were looking for.
Biochemical work using crude extracts of bacteria suggested that the toluene-producing enzyme had properties of a class of enzymes known as glycyl radical enzymes (GRE). Only a few examples of GREs are known, but they provided some clues as to what the gene sequence might look like.
The scientists had two microbial communities that produced toluene. One was from the lake sediment; another was from sewage sludge. DNA sequencing revealed that each contained about 300,000 genes. Restricting the search to genes that plausibly might code for GREs was the key in narrowing the number of targets. Importantly, when they were done, they had an appropriate gene (actually, two genes), and could demonstrate that the resulting enzymes carried out the process.
Is it possible that this work could lead to a process for making toluene biologically, rather than from petroleum? The authors are certainly interested in that possibility. But it is a long way from showing a reaction in the lab to making a process that is practical at a large scale. The current article is interesting biology. Whether it leads to anything useful, short term or long term, is open.
And that lake at the top of the post? The figure legend says it is one source that the scientists used for the bacteria studied here.
Why do bacteria make toluene? At this point, the scientists have no idea. They offer some speculations, including that it might serve as a toxin. The breakthrough in this work is "how". "Why" will have to wait.
Where does the phenylacetate come from? It is a known degradation product of the standard amino acid phenylalanine.
News story: Enzyme discovery enables first-time microbial production of an aromatic biofuel. (Phys.org, March 26, 2018.)
The article: Discovery of enzymes for toluene synthesis from anoxic microbial communities. (H R Beller et al, Nature Chemical Biology 14:451, May 2018.)
This post is listed on my page Introduction to Organic and Biochemistry -- Internet resources in the section on Aromatic compounds.
May 16, 2018
Some molds, of the group Mucor, can grow straight up. How do they know where "up" is?
The top part of the following figure shows an example of such growth. The bottom part shows their gravity sensor.
The top part shows the fungus (mold), Phycomyces blakesleeanus, during fruiting body formation. Successive images show that the stalk elongates by several millimeters over the hours. That stalk is a single cell, with a packet of spores at the top. Of particular importance, the stalk grows "up".
The lower part shows how the stalk knows where "up" is. You can see crystals -- of a protein that weights the stalk vacuole down. The crystals are about 5 micrometers (µm) across.
This is trimmed from Figure 1A of the article.
A role for those crystals in gravity sensing by the mold has seemed likely for several years. Mutants defective in the gravity response fail to make those crystals.
A new article explores this gravity-sensing protein further.
One part of the work is looking for similar proteins -- and their genes -- in diverse microbes. Analysis of many forms of the protein suggests that the current gene in these fungi came from bacteria by horizontal gene transfer (HGF). That follows because there is no clear pattern for the gene within the fungi; the distribution is best explained by suggesting that it has been transferred multiple times, to various fungi.
What did the original protein do in the bacteria? It is quite unlikely that it was a gravity sensor. The crystals shown above are considerably larger than the bacteria. Further, no gravity response is known in bacteria.
Both the bacterial and fungal forms of the protein aggregate in lab experiments. However, the fungal protein forms larger aggregates. From these results, it seems that the fungi acquired a gene for a protein that had a tendency to aggregate. Then, selection within the fungal context led to more aggregation -- and an effective gravity sensor.
The authors suggest, then, that this is an example of HGT followed by re-purposing the protein for another use. Most HGT uncovered so far has resulted in the direct acquisition of a function from the donor. Transfer of antibiotic resistance by HGT is a commonly discussed example.
It's an interesting story. I would emphasize that parts of it are quite speculative at this point. In particular we really don't know what the original protein did, and perhaps we don't know all of its functions in the fungi. Nevertheless, the story is worth noting; perhaps further evidence will be developed to test the ideas presented here.
* Fungus Repurposed a Bacterial Gene to Sense Gravity with Crystals. (V Callier, The Scientist, April 24, 2018.)
* This fungus senses gravity using a gene it borrowed from bacteria. (M Andrei, ZME Science, April 24, 2018.)
The article, which is freely available: Evolutionary novelty in gravity sensing through horizontal gene transfer and high-order protein assembly. (T A Nguyen et al, PLoS Biology 16:e2004920, April 24, 2018.)
More about HGT in fungi: Cheese-making and horizontal gene transfer in domesticated fungi (January 19, 2016).
I don't see any previous posts about gravity in a biology context. The closest, perhaps... The potato we call home: a study of the earth's gravity (May 3, 2011). Links to more about gravity.
May 15, 2018
Counting wildlife is an important task in biology. The traditional way is that a person finds a place with a good view, without disturbing the animals, and counts what they see; they may use binoculars or such for magnification.
Modern technology allows us to fly a drone (remotely-piloted airplane) over the field and take a photograph, which can be analyzed later. In fact, people have been doing this, but without much effort at optimizing the procedure.
A new article explores the use of drones to count birds on the ground. Here is the scene...
Three views of a field of wildlife.
Frames a and b (main parts) are from a drone, at two different altitudes (30 meters in a; 60 m in b). Frame e (bottom) is what a human observer would see, from a position commonly used to count the animals.
The insets for frames a and b show an enlarged view of one animal. You can see that it becomes more blurred but still distinct at the higher altitude.
What are these wildlife? Fake birds, in this case. Plastic ducks.
This is part of Figure 1 from the article. The full figure also has views for two additional elevations of the drone. (Part e is trimmed here.)
Here are some results, comparing the counts obtained by observers on the ground and from analysis of photographs from the drone...
The figure summarizes the results over ten trials. In each trial, there was an artificial colony of fake birds -- several hundred of them. It was counted by the usual experts on the ground, and also from photographs from the drone at four different altitudes. The graph above is a summary of the results for the ground counts and the lower two elevations (just as in the top figure).
The data are presented here as absolute count errors: how far the count was from the known value. That's the x-axis. The various conditions are plotted in regions above, and labeled along the left side.
To start, just consider the graph as having two parts; ground (at the bottom) and drone. The main observation is that the errors from the drone-based measurements are much smaller than from the ground-based measurements. Given the views, as shown in the first figure, that shouldn't be a surprise.
This is part of Figure 3a from the article. Again, the full figure also has results for two additional elevations of the drone.
Further analysis of what the scientists did may be interesting, but does not lead to any clear conclusions.
Some of the drone-based images were very good and some were not. (The reason is not entirely clear. The poorer ones may have been due to wind, but they aren't sure.) To take this into account, the scientists separately analyzed the data for the six trials that gave high quality images. In the figure, the shaded results are for the total set of ten trials; the unshaded results are for the six trials with high quality images. The results are better with high quality images. Not a surprise, perhaps, but it is part a complete report of what happened here. It also makes clear that the problems that led to some imaging being poorer need to be addressed.
Another issue is how to count the animals in the photographs from the drone. One way is to manually count the spots in a photo. Another is to develop image-analysis software to count the spots. Each set of drone data in the figure has two parts, labeled AUTO and MAN. The latter is the manual (human) count of the spots on the photo. The AUTO data was acquired using a semi-automated procedure... Software is trained with human assistance, and then turned loose to do the counts.
There is perhaps no clear picture for how to count the drone-based photos -- except that photo quality matters. Software training is still a work in progress, and will presumably improve. Importantly, automated counting is simpler, and that is particularly important for large data sets.
Overall, the article supports use of aerial drones and trained software for counting wildlife. Getting consistently good image quality is an issue that still needs work. Image analysis software is important. It undoubtedly has to be customized to each job, so learning how to train it will be important.
* Duck! It's a drone! (J John, Wildlife Society, February 27, 2018.)
* 'Epic Duck Challenge' shows drones can outdo people at surveying wildlife. (J Hodgson et al, The Conversation, February 14, 2018.) From the authors of the article.
The article, which is freely available: Drones count wildlife more accurately and precisely than humans. (J C Hodgson et al, Methods in Ecology and Evolution 9:1160, May 2018.)
* A better way to collect a sample of whale blow (November 28, 2017).
* Crashworthy drones, wasp-inspired (October 16, 2017).
* What if there weren't enough bees to pollinate the crops? (March 27, 2017).
More fake wildlife: Studying predation around the world: What can you do with 2,879 fake caterpillars? (July 28, 2017). Links to more.
More about watching the animals:
* Monitoring the wildlife: How do you tell black leopards apart? (August 10, 2015).
* Ants: nurses, foragers, and cleaners (May 24, 2013).
May 13, 2018
The World Health Organization (WHO) has recently released their updated list of major concerns: diseases that should be top priority "for research and development in public health emergency context". These are "diseases that pose a public health risk because of their epidemic potential and for which there are no, or insufficient, countermeasures". (Quotes are from the WHO page noted below.) Eight such diseases -- including such familiar ones as Ebola, MERS and Zika -- are on the list.
On the list this time is Disease X.
The WHO project to define disease priorities began a few years ago in the wake of the West African Ebola outbreak. It's interesting that they now explicitly include Disease X.
An announcement from WHO: List of Blueprint priority diseases. (WHO, March 14, 2018.) This is based on a WHO meeting on February 6-7. This page links to a fuller meeting report.
News stories about the WHO announcement:
* 'Disease X' Added to the R&D Blueprint List -- R & D Blueprint committee reviews viruses, bacteria, and infectious disease to consider potential epidemics and pandemics. (D W Hackett, Precision Vaccinations, March 11, 2018.)
* Mysterious 'Disease X' Could Be The Next Deadly Global Epidemic, WHO Warns. (P Dockrill, Science Alert, March 12, 2018.)
How many diseases are on the list of eight? The WHO announcement includes eight items, some of which combine related diseases. Others present the list differently. You will see various numbers; it's the same basic list.
* * * * *
* The role of WHO: the view of its director (December 1, 2015). The person interviewed here is Margaret Chan, who was WHO director-general at that time.
* After Ebola, what next? and how will we react? (September 5, 2015).
There is a section on my page Biotechnology in the News (BITN) -- Other topics for Emerging diseases (general). That page also contains sections for some of the specific diseases; see the Table of Contents of the top of that page.
May 11, 2018
The Arctic has been warming. The winters on the east coast of the United States have become more severe. Is this all really true? Is there some connection? Are those in the East going to be buried under more and more snow as Earth warms?
A recent article explores these questions. The findings are rather chilling -- especially for those in the East.
The following graph summarizes the observations for three sites. Caution... the graph is somewhat odd.
Quick glance... The green lines tend to be below the blue lines, especially toward the right side.
That shows that bigger snowstorms have become more common. But to see that, we need to make sense of what is plotted.
The x-axis scale is the snowstorm size, in inches of snow.
The y-axis scale is the time between snowstorms. (Both axes are the same for all frames.) That is, the smaller the number, the more frequent the storms.
The two lines are for two time periods, as labeled at the right. The green line is for recent years -- for years since the clear trend of Arctic warming began. The blue line is for the earlier reference period, with a colder Arctic.
As an example... Look at the middle frame, for New York. For 18-inch snowstorms, the interval was about 14 years (blue), but is now about 6 years. That is, such storms are now more frequent.
Overall... For recent years, the green line is below the blue line. That is especially true towards the right, which is for larger snowstorms. The lower green line means that the storms are more common in recent years (fewer years between them).
What does it mean if a graph line stops before the right side? For example, look again at the New York frame. The blue line stops at 18 inches of snow; the green line continues. This means that in the blue period there were no such storms. The interval between such storms is big. If something were to be shown, it would be off the scale at the top. That is, missing points are high values -- given the nature of this y-axis scale.
Where are these three sites? Loosely, the cities of Boston, New York and Washington. All right along the Atlantic coast. The first is at a state park near Boston; the other two are at airports.
This is slightly modified from part of Figure 9 from the article. The full figure contains four such columns of graphs, for a total of 12 sites across the country. The figure above shows the right-most column of those graphs, for the sites on the east coast. I have added all the labeling at the right side.
The graph, then, shows a correlation: since Arctic warming began, winters along the US east coast have had more severe snowstorms.
Climate change is complex. The overall effect is warming of Earth, but there is local variation. Some of it has been predicted. The current work helps to document an example.
How can something like this happen? Global warming -- the overall effect -- reflects that there is more energy around. But local weather depends on local atmospheric conditions. Circulation patterns couple weather in one place to weather in another. In this case, the coupling is negative, with one region getting warmer and another getting colder. There is nothing wrong with that -- as a possibility. It's getting the evidence that such coupling actually occurs that is the challenge. Weather data is messy, as we all know. The current article makes a claim of finding such a coupling, a negative coupling.
If you compare the results shown for the three cities above, the effect seems smallest for Boston. That is the most northern -- and snowiest -- of those cities, and there is only a small effect, at the highest snowfalls. For the more southerly cities, the weather is less severe, but there seems to be a larger effect. Is this significant? It's hard to say, based on these data. We can only note the observation, and hope that further data, for more sites and longer times, will test the idea.
The authors analyze data for other cities across the US. The general pattern is that the effect becomes less at one moves west; it may even reverse near the west coast. The full Figure 9 of the article shows that full data set.
The negative effect of the Arctic may also occur in Eurasia. That's briefly noted in the current article, but the focus is on the eastern US.
Caution... As with much climate research, there is controversy. The authors here have long promoted the idea of a coupling between Arctic warming and northern-US cooling; this work supports their consistent position. But not everyone agrees. As so often, this is a story still in progress. The work here is an interesting contribution, but it may or may not turn out to be the full story.
* Arctic Warm Spells Linked to Nasty Winter Weather on East Coast -- Evidence builds for controversial idea linking Arctic temperature spikes to changing weather patterns. (C Harvey, Scientific American, March 14, 2018.)
* Warm Arctic means colder, snowier winters in northeastern US, study says. (Phys.org, March 13, 2018.) Interesting photo. Read the caption; "first author" there refers to the article itself.
The article, which is freely available: Warm Arctic episodes linked with increased frequency of extreme winter weather in the United States. (J Cohen et al, Nature Communications 9:869, March 13, 2018.)
Among other posts on arctic warming...
* Should we geoengineer glaciers to reduce their melting? (April 4, 2018).
* Methane hydrate: a model for pingo eruption (August 4, 2017).
A previous post about Boston: Boston is leaking (February 13, 2015). That leak should be warming the place.
For perspective... Global warming (August 3, 2008).
May 8, 2018
Chronic wasting disease (CWD) is a prion disease of deer and related animals. The incidence and range of CWD have expanded rapidly in the last two decades. In captive populations, it is transmitted both by direct contact and indirectly through the environment. Little is known about transmission in the wild.
A new article looks at one possible factor affecting CWD transmission in the wild. Is it transmitted -- via the environment -- in areas where the animals congregate? More specifically, the scientists ask whether mineral licks (sometimes called salt licks) contain prions.
What they did was to look for prions at or near 11 mineral licks in areas where there is a high incidence of CWD in the deer. It seems simple enough, but making any measurements of prions in the environment is technically demanding.
The results? Nine of the 11 mineral lick sites had detectable CWD prions.
The significance of the results is not clear, as the authors go to great length to make clear. Given the difficulty of making these measurements at all, much remains open.
Taken at face value, the results suggest that prions are present in the environment where animals congregate. Further, providing places for them to congregate, such as mineral licks, may promote direct transmission (e.g., by saliva).
If prions accumulate at sites where animals congregate, there is also the potential for transmission to other species, including local livestock. So far, there is no evidence for transmission of CWD beyond the deer and related animals (cervids). but it remains a concern.
There is no evidence that CWD is transmitted to humans, by any route, including eating infected meat. However, it is impossible to exclude the possibility of such transmission, and people are discouraged from eating meat from infected animals. (You may recall... variant Creutzfeldt-Jakob disease (vCJD) is the human form of bovine spongiform encephalopathy (BSE), resulting from eating prion-infected beef.)
News story: CWD prions discovered in soil near Wisconsin mineral licks for the first time. (E Hamilton, University of Wisconsin, May 3, 2018.) From the university where the work was done. Good overview, including the uncertainties.
The article, which is freely available: Mineral licks as environmental reservoirs of chronic wasting disease prions. (I H Plummer et al, PLoS ONE 13:e0196745, May 2, 2018.)
Previous prion post: Can prions, which cause brain disease, be transmitted by skin? (January 26, 2018).
A previous post that included CWD: Prion diseases -- a new concern? (March 19, 2012).
For more about prions, see my page Biotechnology in the News (BITN) - Prions (BSE, CJD, etc). It includes a list of related Musings posts.
May 6, 2018
This post is related to the preceding one, immediately below. Both involve effects of antibiotics on virus infections.
Some data from the current article...
This is about a model lab infection, with West Nile Virus (WNV). The experimental animal is shown at the upper right. (There are 23 of those things in the graphical abstract, alone.)
The graph shows survival curves for two conditions. In one case, the animals were treated with a mixture of antibiotics -- labeled as VNAM, for the four antibiotics (vancomycin, neomycin, ampicillin, metronidizole). The other was a control, with only the "vehicle", the buffer.
The results are clear: survival was much worse with the antibiotic treatment.
In this experiment, antibiotic treatment started 14 days before virus infection, and continued throughout.
This is Figure 1B from the article.
Further work showed that the effect is general for flaviviruses: not only WNV as shown above, but also dengue and Zika. The effect appears to be mediated via the host microbiome. That is, the antibiotics are acting directly on bacteria, and leading to secondary effects -- in this case, an enhancement of the virus. (How does changing the microbiome affect the virus? Probably via the immune system.)
The result here is the opposite of that from the previous post. In that case, the antibiotics were effective against the viruses, thus reducing disease. In this case, the antibiotics promoted the viral infection, thus harming the animals. Of course, the big point for the pair of posts is that neither result agrees with the simple prediction that antibiotics should be irrelevant for viral infections.
Overall, the two posts show that antibiotics may have various effects on viruses, using various mechanisms. That's not to overthrow the conventional wisdom. There is a reason for it: antibacterial agents typically act with some specificity on bacteria. However, as so often, biology is more complicated than we thought. Antibiotics act against bacteria, but that action may itself have secondary effects, and the antibiotics may in some cases do other things in addition to their simple role against bacteria.
In particular, it should be clear that nothing here is intended to promote use of antibiotics if you think you have "a virus". The other post showed a benefit, but the scope is not yet clear; this post showed harm.
If you are a little confused, that may mean you got the point. The big lesson from the pair of posts is that the relationship between antibiotics (anti-bacterials) and viruses is more complicated than we usually say. For now, it is unclear what the general messages may be.
Of particular interest to the authors was the possibility that one reason people respond differently to a viral infection is their microbiome status, which can be influenced by antibiotic usage. The work supports that connection. How big a factor it is in the real world remains open.
* Antibiotics Increase Mouse Susceptibility to Dengue, West Nile, and Zika -- The drugs' disruption of the microbiome makes a subsequent flavivirus infection more severe. (S Williams, The Scientist, March 27, 2018.)
* Antibiotic use increases risk of severe viral disease in mice. (T Bhandari, Washington University School of Medicine, March 28, 2018.)
The article, which is freely available: Oral Antibiotic Treatment of Mice Exacerbates the Disease Severity of Multiple Flavivirus Infections. (L B Thackray et al, Cell Reports 22:3440, March 27, 2018.)
Accompanying post: Antibiotics and viruses: An example of effectiveness (May 5, 2018). Immediately below; includes more links to other posts.
More on antibiotics is on my page Biotechnology in the News (BITN) -- Other topics under Antibiotics. It includes an extensive list of related Musings posts.
That page also has a section on West Nile virus. There is also a new section on Dengue virus (and miscellaneous flaviviruses). It's incomplete, but will be a good place for posts such as this one that include multiple flaviviruses.
May 5, 2018
You probably know the basic story... Antibiotics act against bacteria. If you have a virus infection, don't take antibiotics. They are not relevant -- and their overuse can lead to the development of antibiotic resistance, which makes things worse for those with real bacterial infections.
Terminology confusion... The word antibiotic can be confusing. We use terms such as anti-virals or anti-fungals for agents against viruses or fungi, respectively. But the seemingly broad term antibiotic refers to agents against bacteria. There is no logic to that; it's a historical accident. (The term anti-bacterial is also used.)
Of course, in biology, things are not always as simple as we might think. We now have two recent articles that illustrate the complexity of the antibiotic-virus connection. The effects are very different, and the mechanisms are very different. We'll present one here, and the other in the next post.
The graph shows results from a lab model system. It uses a herpes virus, HSV-2, infecting mice.
The y-axis shows a measure of the disease, called disease score.
Results are shown for two conditions. In one, the antibiotic neomycin was applied (red symbols; lower curve). The other condition is a control, called PBS (for the buffer used).
You can see that the neomycin reduced the disease score. It's a clear result.
This is Figure 1g from the article.
Let's repeat that... the antibiotic (anti-bacterial agent) neomycin substantially reduced the severity of an infection with a herpes virus in mice. That's contrary to the common wisdom.
There is considerable work in the article characterizing the scope and mechanism of how this works. Among the findings...
- The effect occurs for some other antibiotics of the same family as neomycin (aminoglycosides).
- The effect occurs for Zika and flu infections. That is, it occurs for a range of viruses.
How does it work? The gut microbiome is not relevant; the effect is similar with germ-free mice. However, the host's own anti-viral agent interferon is relevant. For some reason, neomycin, best known as an antibiotic, has a second effect: inducing the anti-viral agent interferon. The effects of neomycin as an anti-bacterial agent and as an anti-viral agent, acting via interferon, appear to be independent.
Preliminary experiments showed that neomycin also reduces viral replication in lab culture of human cells. That effect, too, seems to be mediated by interferon.
* Topical antibiotic triggers unexpected antiviral response. (Phys.org, April 9, 2018.) (Don't worry about the initial figure.)
* Some Antibiotics Rev Up Host Immune Response to Viruses. (S Williams, The Scientist, April 9, 2018.)
* News story accompanying the article: Antivirals: New activities for old antibiotics. (J I Cohen, Nature Microbiology 3:531, May 2018.)
* The article: Topical application of aminoglycoside antibiotics enhances host resistance to viral infections in a microbiota-independent manner. (S Gopinath et al, Nature Microbiology 3:611, May 2018.)
Added May 6, 2018. Antibiotics and viruses: An example of harm (May 6, 2018). This accompanying post, immediately above, shows a different effect of antibiotics on virus infections.
Posts that might hint at some of the complexity shown in this and the accompanying post...
* How our immune system may enhance bacterial infection (September 19, 2014).
* Antibiotics and obesity: Is there a causal connection? (October 15, 2012).
More about aminoglycoside antibiotics: Designing a less toxic form of an antibiotic (April 19, 2015).
More on antibiotics is on my page Biotechnology in the News (BITN) -- Other topics under Antibiotics. It includes an extensive list of related Musings posts.
May 3, 2018
The following figure gives an overview of the P world...
The major source of phosphorus (P) is rocks. Rocks containing insoluble phosphates.
P is used in two general ways. Most of it is used as fertilizer. For that purpose, the phosphate form is fine; most of the P in biology is phosphate-P. It's just a matter of dissolving the insoluble phosphate; some acid does the trick, making phosphoric acid.
Some P is used to make specialty chemicals, such as drugs. It's about 1% of the total. In phosphate, P is bonded only to oxygen. In these other chemicals, the P is bonded to other atoms, such as C or F. It's not easy to get those bonds. The right side of the figure shows that it is normally done by first making white phosphorus, a form of the pure element. That works, but white phosphorus is nasty stuff. Further, the whole process in environmentally unfriendly.
Is there a better way? A recent article reports a way to get to the specialty chemicals from phosphoric acid, avoiding the need to go through elemental P. That's what the box in the middle is about, a better way of getting from phosphoric acid to "phosphorus chemicals".
This is Figure 1 from the article.
What's the secret? It's that bis(trichlorosilyl)phosphide anion.
The following figure summarizes the chemistry...
Start with the box in the middle. That's the guest of honor, also noted there as compound 1.
Look to the left, and you will see how it is made. Trimetaphosphate is a readily available form of phosphoric acid (or phosphate), It's reacted with trichlorosilane, HSiCl3 -- a chemical well known to those who work with silicon. That gives the anion that is shown; it can be thought of as a derivative of the simple phosphide ion, P3-, but this one is nice and stable -- and useful.
The rest of the figure shows some things they made from the bis(trichlorosilyl)phosphide anion. All are of interest, and they are diverse. And the reaction conditions are relatively mild. (The "thermal process" referred to in the top figure for making elemental P is done at temperatures above 1400 °C.)
This is Figure 2 from the article.
A novel reaction. The authors suggest they have a general approach to making P chemicals, an approach that is safer and simpler than what is done now. As so often, this is step 1; time will tell how it works in practice.
Some chemistry notes...
You may recognize the reducing agent here, HSCl3, as the silicon analog of chloroform. It is sometimes called silicochloroform.
The anion I was isolated as a salt. The cation was tetrabutylammonium, chosen for other reasons. Interestingly, for some work, it was not necessary to purify the anion -- further simplifying the process of making P-chemicals.
The anion is stabilized by the six Cl carrying some of the charge. Nevertheless, the P is negative, and an effective nucleophile. That property is important for the further work.
* A less hazardous means to create phosphorus compounds -- Phosphoric acid as a precursor to chemicals traditionally synthesized from white phosphorus. (EurekAlert!, February 8, 2018.)
* Perfecting the phosphorous process -- The Cummins Group investigates the efficiency and environmental impact of industrial phosphorus processing. (T-L Vu-Han, Lab of the Week, The Tech (MIT), March 8, 2018.)
* News story accompanying the article: Inorganic chemistry: From rock-stable to reactive phosphorus -- A low-temperature route converts phosphate into an anion useful in chemical synthesis. (J D Protasiewicz, Science 359:1333, March 23, 2018.)
* The article: Phosphoric acid as a precursor to chemicals traditionally synthesized from white phosphorus. (M B Geeson & C C Cummins, Science 359:1383, March 23, 2018.)
Other posts on phosphorus include...
* The origin of reactive phosphorus on Earth? (July 5, 2013).
* A phosphorus shortage? (September 29, 2010).
* How do you make phospholipid membranes if you are short of phosphorus? (November 1, 2009).
Among posts about silicon... Carbon-silicon bonds: the first from biology (January 27, 2017).
Older items are on the archive pages, starting with 2018 (January-April).
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Last update: May 22, 2018