Seconding the vote on dumping politics as a continuous subject on TWIV. How about if you bring it up again when you have a genuinely new idea on it and not the same old tired complaints. Act as if I’m as bright as you, I get it the first time.
Should scientists be involved in politics?
Today, it is no longer the cholera or plague bacillus that threatens us, but the traditional, cynical reasoning of politicians, the indifference of the masses, and the physicists’ and other scientists’ evasion of responsibility.
Max Born, 1964
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Scientists don’t have the right; they have the obligation.
Greetings Leaders of the TWiVites,
I am writing in strong disagreement to Hanna from Boulder’s email on TWIV 431 regarding the discussion of politics on TWiV. I enjoy the great balance that TWiV provides between both cool virology and the surrounding nontechnical aspects that affect virology. Many great benefits come from hearing you talk about subjects falling in the latter category: for example, “TWiV 385: Failure” is among my favorite episodes.
I am a senior undergraduate student who has tailored my undergraduate experience primarily to pursuing a career in research. However, years of aggressive funding cuts and other deleterious policies affecting scientific research in my home state of Kansas drove me to become involved in writing and influencing public policy on the state level while still a student. I believe that we as young scientists cannot remain disengaged with this reality, and this especially includes those of us pursuing research careers.
There was an excellent interview in ASM’s career newsletter written by Adriana Bankston (see link below) about Dr. Kate Stoll, who is the Senior Policy Advisor for the MIT Washington Office. Fellow students, many of whom likely share my discouragement yet strong call to action in light of current political events, may find it interesting and helpful if you had another science policy expert on the show who can talk about opportunities for engagement specifically in the context of the current situation.
It is currently 46°F and clear skies after a day scattered with heavy winds, golf ball-sized hail, a confirmed tornado, and what would have been in previous decades considered to be an uncharacteristic high of 79°F in Manhattan, KS (fondly known as “The Little Apple”).
I apologize in advance, as I am going to be ranting a little in this email. However, I am sick and tired of people complaining about the politics on TWiV, at work, in social circles, and on social media. The truth is that we live in a political world. Everything we do is affected by politics! Every privilege that you enjoy today in this free country you live in, has been brought about by some political movement or other. The moment you force scientists to ask the government for funding in order to do their work, you have politicized science. Accordingly, if something happens in the political world, which threatens or diminishes that financial supply, scientists will (AND SHOULD!) complain. Why? Because we live in a free country where we are allowed to practice freedom of speech! You DO not want to know what it’s like to not have that right! I grew up in such a country, and it really made me appreciate true freedom. We must fight to protect that freedom! So if you don’t like what you see or hear, then don’t look and don’t listen! I’ve certainly had to drive past many anti-abortion rallies by people holding up grotesque photographs and had to remind myself of the same thing! No progress of real value in the history of this planet has been effected by people who were quiet, or even “politically correct”. All progress in every facet of life has occurred due to the acts of people who were courageous enough to insist on change in spite of the consequences. In some cases these consequences were imprisonment, or even death. Here are a few people who said or did things that at the time were considered extremely controversial, but in retrospect literally changed the world: Rosa Parks, Martin Luther King Jr., Sojourner Truth, Charles Darwin, Galileo, Abraham Lincoln, and Harvey Milk, just to name a few. My point is that if you believe passionately in a cause, you SHOULD talk about it, no matter how controversial it is or how many people you might offend.
That being said, to all the people who are expressing their disgust, fears, and disappointment about our new administration, you have my support! And if you are marching in Atlanta on April 22, please come find me! I’ll be the one in the TWiV T-shirt.
Since we’re all happy in our pedantry, I’ll point out that orzo (as discussed in relation to a Blue Apron ad in episode 431) is NOT rice! It is a rice-shaped PASTA. I’m really sort of shocked that none of the five of you knew this.
Here are two other podcasts that I listen to, showing my nerdiness in other arenas besides science:
Pod Save America (politics, current events, lots of snark and a good bit of swearing from several of President Obama’s speechwriters)
The SweetGeorgia Show (fiber arts, especially knitting, and color)
To bring two of my loves together, here’s my self-serving pick of the week: my knitting patterns for socks and fingerless gloves featuring a DNA cable that I designed. The cable is pretty accurate in both major/minor groove ratio and in number of bases per full twist of the helix. In addition, the sock pattern features a visual pun on a historic style of knitted socks, where a band of pattern runs down the side of the sock and splits so that half runs down the side of the heel flap and half runs down the foot. In my socks, the double-stranded DNA denatures so that one strand that runs down the heel and one down the foot (giving the pattern its name, Denature). The fingerless glove pattern features the DNA denaturing around the thumb and annealing to keep running up the hand. These pieces aren’t really bold enough to be perfect for the Science March, but if you are knitters or know knitters (e.g., Dickson’s wife, when she finishes Dickson’s brain hat) I hope you’ll enjoy combining your love of science with fiber!
Thanks for your great podcasts (and I’m bummed that the ant one has fallen through). They make my 2 hour commute (each way) between Tacoma and Seattle much more tolerable, and keep my brain engaged while I knit on the bus. Currently it’s 4oC and raining, somewhere along that route.
Ted Diehl writes:
I just listened to your most recent TWIV episode featuring the paper from Jim Cunningham’s lab (TWIV 431). I wanted to clarify a couple of points that were discussed during the show.
1) You refer to the assays done in figures 2A, 2C, 3A, and 3C as binding assays. But truly those assays measure GP “triggering” eg. exposure of the fusion loop and insertion of this into membranes. True binding assays (in the form of ELISAs) were performed by the Cunningham group and included as Figure 4A. That assay showed absolutely no difference between the ancestral GP and A82V.
2) In regard to our paper (and/or the associated TWIV episode), you said that we found evidence for the A82V mutation resulting in an enhanced binding to NPC1. In our paper we presented no data either way as to GP-NPC1 interactions and in fact we had heard of the data presented by the Cunningham group as Figure 4A. Rather, in the discussion of our paper we explored both the possibility that the mutation enhances NPC1 binding as well as the possibility that it increases “triggering”. Additionally, toward the end of our TWIV conversation Rich Condit asked us about performing such a binding assay. After my circumspect response, Jeremy chimed in and shared that our current belief was that the A82V mutation resulted in a GP that was more predisposed to conformational changes resulting in exposure of the fusion peptide. Indeed, this is exactly what the Cunningham report found!
Program in Molecular Medicine
UMass Medical School
James Cunningham writes:
Thank very much for choosing our paper for your podcast and for providing such a thorough and positive discussion.
All of us, but particularly the graduate students May Wang and Soo Mi Li who carried out the studies, were very flattered. They have been bombarded with congratulatory texts, emails from their peers in the Virology Program, which is the ultimate form of validation for young scientists.
So thanks again—it means a lot. And I hope we can discuss some of the details in the future.
This is in response to Rich’s comment that the differing divergence patterns of cifA or cifB compared to core wolbachia genes implies that the selective pressures driving the evolution of this system were likely acting specifically on the prophage. I took a look at the paper, and while the analysis did show this, it also showed that the divergence pattern for a phage structural protein was different from those of cifA/cifB. Thus, it seems the differing divergence patterns are gene- and not organism-specific (although I’d expect correlation to some extent within a genome), and so I don’t think you can say which organism the selective pressure is acting on based on such a difference. Please let me know if I’m missing a key point in yours or the authors’ argument.
My two cents is that the selective pressures driving the evolution of this particular system act on the holobiont. The function of this system appears to be to ensure the propagation of wolbachia, so it seems there must necessarily be a selective pressure acting on the host, which of course is a selective pressure acting on the prophage as well (it needs a place to live). I’m not sure you can really subdivide which component of the holobiont feels the selective pressure in this case.
On a somewhat related note, I keep running into an issue when trying imagine how this system could have evolved, namely that it only works when all/most of the males are already implementing it (i.e. females only require a wolbachia infection for reproduction when males are providing cifA/cifB in the sperm). In that case, it is a self-sustaining system in that cifA/cifB-expressing wolbachia drive selection of their own retention by killing progeny of uninfected mothers. However, if only a small number of cifA/cifB variants were present, it would be highly unlikely that one of them would infect a male arthropod that would go on to breed with a female arthropod variant that preferred to keep the wolbachia, and extremely unlikely that there would be enough to kill all the progeny of females that lacked this tendency. Thus, it seems you would require the result of the selection to perform the selection. Does anyone have any idea for a possible scenario that could explain the initial propagation of this system? Is it likely that this system arose out of genetic drift, and could then sustain itself?
Also, would any of you care to speculate about the wolbachia/WO factor that suppresses the embryonic lethality? I’m wondering whether it could be any old wolbachia gene, or if it must be one specific to the strains that use the embryonic lethality strategy. The latter case seems unlikely given that the authors’ search for genes specific to such strains returned only cifA and cifB. I wouldn’t expect that oocyte-derived cifA/cifB could suppress the effect of those same proteins derived from sperm, but it’s technically possible that they could interact differently with the chemical environment of the sperm vs. the egg. An experiment where cifA/cifB transgenic males were crossed to cifA/cifB transgenic cifA/cifB females would have been nice.
I think it’s more likely that the suppressor is a common wolbachia protein rather than cifA/cifB, but this also raises questions about how this system could have evolved. If there was a subpopulation of rare variants that had acquired cifA/cifB, why weren’t they simply diluted out through matings with non-cifA/cifB wolbachia-containing arthropods? If the suppressor is a common wolbachia protein, there would have been no selective pressure to force reproduction specifically from cifA/cifB females, which would be required to propagate these alleles since the female arthropod transmits the parasite.
By contrast, if cifA/cifB were indeed the suppressors, initial rare variants would have formed an instant bottleneck as they would only be able to mate with each other. Could that explain the evolution of this system? This also seems like an easier path to speciation, but it is quite biochemically dubious.
I’d love to hear your thoughts on all this.
Thanks again for the great podcast,
Montreal, QC (it’s cold here)
This is my second attempt at a book giveaway and I hope I’m more successful this time around! TWIV and TWIM are still two of my favorite podcasts, and I’m still hoping to be able to add more to my ever-expanding playlist. I’m looking to keep one step ahead of some very bright undergraduate students in my Microbiology course here at Louisburg and your discussions definitely help me with that! The last time I wrote we were expecting wintry weather; that has come and gone and we are anticipating a return to the balmy 60s in the next few days. Keep up the great and lively discussions!
Hello TWIV team,
Long time listener first time writer. I began listening when writing a paper about Autism, I’m an elementary school teacher for Chicago Public Schools. I was looking for active discussion debunking the myths around vaccines and you folk fit the bill.
I enjoy your discussions of virology. The way your podcasts intertwines the papers, politics, and real world discussion is both user friendly, informative and fun. I frequently find myself citing information from your podcast when talking with parents and coworkers.
Keep up the great work and the weather in Chicago is a balmy 29F with some flurries.
I hope I win!
Hey TWIV friends,
You said to write in immediately to get the contest done quickly so I’m doing so. It’s a pleasant -9C early morning listening to you folks and feeding my dairy cattle.
Hello again from Philadelphia! I was unsuccessful in winning a previous book, but I am determined to be the 27th email! I would love to learn as much as I can about new topics in science since I am currently deciding whether to go for my Master’s and what to study. Maybe one of your books will give me the inspiration I need to pursue my next degree.
The weather today in Philadelphia is pleasant for February! We have mostly cloudy skies with a high of 48F and a low of 32F, though it feels much colder with the wind blowing in between all the buildings!
Thank you for all you do!
I happened across this article today:
> Border Collie Collapse, or BCC, is recognized as a form of exercise intolerance in Border collies, Kelpies, and related breeds in the United States, Canada, and Australia. Dogs with BCC are normal at rest, but after 5–15 minutes of strenuous exercise can develop incoordination and altered mentation. Recently, JAAHA posted an exercise study on dogs with BCC in issue 52.5 and a survey on observations of dogs with BCC in issue 52.6.
It struck me that the exercise intolerance here seems to resemble the description of exercise intolerance associated with ME/CFS. Animal model?
While I’m sure I’m not writer number 27, I can at least bump you one closer to getting Emerging Infections sent on its way to the lucky listener who wins it. I appreciate your podcasts and try to make sure I can squeeze in TWIV, TWIM, and TWIP into my listening schedule.
Be nice to Dickson!
Good day TWiV hosts!
I’d love to be the winner of your latest book contest on Emerging infections. This semester I am one of the instructors of an undergraduate virology course and the topic I selected was Emerging Viral infections thus this book may come in handy! As always I put in a plug for the TWiX podcasts in my lectures.
I would also like to put in a positive review for the writing of Mary Roach, who you also mentioned you had on your shelf. I’ve read most of her books and she takes a very fresh and funny look at the science around some pretty interesting topics such as the use of human cadavers in research (Stiff), sex research (Bonk), food science (Gulp), and space exploration (Packing for Mars). I have yet to read Grunt, but it’s on my list!
Have a great day!
Ursula LeGuin on alternative facts
A recent letter in The Oregonian compares a politician’s claim to tell “alternative facts” to the inventions of science fiction. The comparison won’t work. We fiction writers make up stuff. Some of it clearly impossible, some of it realistic, but none of it real – all invented, imagined — and we call it fiction because it isn’t fact. We may call some of it “alternative history” or “an alternate universe,” but make absolutely no pretense that our fictions are “alternative facts.”
Facts aren’t all that easy to come by. Honest scientists and journalists, among others, spend a lot of time trying to make sure of them. The test of a fact is that it simply is so – it has no “alternative.” The sun rises in the east. To pretend the sun can rise in the west is a fiction, to claim that it does so as fact (or “alternative fact”) is a lie.
A lie is a non-fact deliberately told as fact. Lies are told in order to reassure oneself, or to fool, or scare, or manipulate others. Santa Claus is a fiction. He’s harmless. Lies are seldom completely harmless, and often very dangerous. In most times, most places, by most people, liars are considered contemptible.