Laura writes:

Hi Twiv team,

I was alarmed to see that Mark Lipsitch published his views on “potentially pandemic pathogens” in Scientific American. It is too bad that the readers are getting only one side of this argument. If you are already aware of this, please disregard my email.

I can’t thank you enough for your tremendous science outreach.

The air in Salt Lake City currently contains 33 micrograms/m^3 particulate <2.5 microns. With air quality this bad, who cares about temperature, dew point, etc.

With great admiration,

Jo Ellen writes:

Dearest Twivers,

Thank you for being a part of my life the past four years. I realized I was behind listening this winter, as I live in Minneapolis and am usually either weeding or shoveling enough to stay caught up with all three and NPR podcasts as well. I read the Scientific American article referenced in 321 and realized just how behind I was when I went immediately to TWIV for the rebuttal and had three more in between to listen to. It is currently 16 F and Starry.

I have been reading William James’ “Varieties of Religious Experience” and directly after listening to TWIV 321, came across the following quote and decided I must finally contact you. So here it is; “If any of you are enemies of what our ancestors used to brand as enthusiasm, and are, nevertheless, still listening to me now, you have probably felt my selection to have been sometimes almost perverse, and have wished I might have stuck to soberer examples. I reply that I took these extreme examples as yielding the profounder information. To learn the secrets of any science, we go to expert specialists, even though they may be eccentric persons, and not to commonplace pupils. We combine what they tell us with the rest of our wisdom, and form our final judgement independently.”

Thank you for being some of my favorite eccentric persons. While I would love to meet many of you personally, I will enjoy your company via TWIX.

Jo Ellen
Massage Therapist, MPLS, MN

Sandra writes:

Latest TWIV: Paul Duprex is an incredible diplomat! My indignation button is much more sensitive than his, and his cautions in the latest TWIV about how scientists speak of GOF, and about how people “hear” those scientific remarks, seemed very reasonable. I honestly felt a bit guilty about the intensity of my negative opinions about some of the scientists and “ethicists” who have commented on GOF.

Re Relman at the Dec GOF symposium:
Session 3 began with Yoshihiro Kawaoka’s presentation which “wowed” me when I first saw it in December, and wowed me again tonight watching the video of it on Youtube. (Tonight I don’t have pneumonia, so hopefully my brain absorbed more of it this time.)

Among other things, Kawaoka put up a slide showing Lipsitch and Galvani’s three recommended alternatives to GOF work and then a number of slides explaining why each “alternative” is inadequate. He concluded “We cannot rely solely on alternative approaches.” Incredible presentation – so much factual, relevant data presented so succinctly!

Relman comments start at 17:35 on the video. At 28 minutes Relman speaks about how benefits of GOF must be immediate.

At 47.25 minutes Harvey Fineberg very politely called out Relman’s stated concern about GOF resulting in the development of a virus that is simultaneously highly pathogenic, transmissable and resistant as “kind of an extreme straw man.”

As a non-scientist I would never engage in an argument with anyone about the GOF dispute; but as a science-curious and analytical human, I feel much more confident in what I hear from you and from Kawaoka than from what I hear from Relman and Lipsitch.


ps- high temp today hit low 70’s F and forecast high is for upper 70’s later this week. This would have been a great week for you to interview a scientist in Texas!

John writes:

In TWiV 319 Alan picked a book on making a toaster from ingredients.

The toaster tale feels like an update of a classic essay “I, Pencil.” No one person can make a pencil. The process requires a complete economy with hundreds or thousands of kinds of specialized labor.,_Pencil

For the younger listeners, pencils are an archaic weapon once carried by students to ward off attacks by standardized tests. They came in only one kind, inexplicably called a “number 2.”

Yegor writes:

Dear Vincent and friends,

I want to praise you for doing this immunology-heavy paper as part of a virology podcast. I’m a virologist by training myself, but at some point my work shifted to HIV vaccines, so I had to quickly learn some immunology and it gave me a whole new perspective on viruses. Studying viruses in cell culture is great fun and one can certainly learn a lot, but one always have to remember that these are artificial systems that minimally reflect the complexity of the environment in which the virus has to survive and propagate. Antiviral host responses are the major driving force behind viral evolution. If I may play on the famous quote: “Nothing in virology makes sense except in the light of immunology.”

Please do more papers like that.
Best regards,

Yegor Voronin, PhD
Senior Science Officer
Global HIV Vaccine Enterprise

Johan writes:

+3˚C, humidity 86%, wind 3 km/h and light rain here in Sollentuna, just north of Stockholm, Sweden at 23:30.

BBC Newshour is BBC World Service’s premier news show for the international audience, and today they are doing a single topic show on Ebola. This is the first time I have heard them do a single topic show, so I think they are quite rare, I certainly haven’t heard one before and I listen daily since a few years back.

BBC World Service – Newshour Extra, The Ebola Response (about 55 minutes)

Thank you so much for TWi{V,M,P} etc., etc.. Bla bla bla.


Don writes:

Do you know the number of infections compared to the clinical (symptomatic) infection rate? Thank you all for the wonderful TWI series.

Geoffrey writes:


I thought that I might pass along a small but potentially interesting article that I ran across:

Puumala Hantavirus Infection Alters the Odour Attractiveness of Its Reservoir Host. Oecologia (2014) 176:955-963. DOI 10.1007/s00442-014-3072-x

I suspect that this is behind a pay-wall but I’m not sure.

Anyway, the gist of it is that there seems to be a small but detectable (and temporary) aversion among healthy bank voles to the urine of bank voles infected with Puumala Hantavirus. It is erratic but measurable. It has interesting implications in both transmission modelling and viral manipulation of community (though not, necessarily, host) behavior. Beyond that, however, is the interesting idea that we might be able to run some relatively quick diagnostics by volatiles analyses of urine. I know that there are medical conditions where the color and odor of urine is a diagnostic but this points to the potential for using urine volatiles analysis as a more powerful diagnostics tool – unless this is already used for the detection of specific diseases and I didn’t know about it.

There was also mention of an interesting reservoir for polio (and noro-) virus that you might not have noticed in:

Localization of norovirus and poliovirus in Pacific oysters. Journal of Applied Microbiology (2009) 106: 1220–1230. DOI 10.1111/j.1365-2672.2008.04091.x
Any thoughts on if and how this might affect polio eradication campaigns? I assume that the virus flushes through oyster beds within a generation or so but I don’t know. Also, given how often polio was contracted at the beach, has this reservoir been noted before?

Thanks for the informative podcasts!


Christopher writes:

Greeting TWiVodes!

So, I have a question about a possible approach for an antiviral. Is there a way to produce a particle that at one end binds to a glycoprotein (or anything on the surface of the virus really) and on the other end simply has a piece of an antigen that we currently have a successful vaccine against?
Is this a viable option to make the virus visible to the immune system? Has this been tried?

It might provide a way around a couple of the existing challenges of passive immunity. For example Zmapp had to find a way to “humanize” the mouse antibodies, instead of having to do that you could utilize the existing antibodies.

The downside might be that antibodies get to the particle before it binds to the viral particle.
Any thoughts?
(I’m including a crude hand drawn diagram just for kicks!)

Jody writes:

Hi Twiv team,

Just for your interest a paper has been published on the link between one of the H1N1 vaccinations used and an outbreak of narcolepsy among Finnish children during the swine flu pandemic.

The findings were related to differences in viral proteins between the different vaccination preparations, Pandemrix used in Europe, and Arepanrix used elsewhere. It was previously thought that the narcolepsy cases may have been caused by one or more of the adjuvants.

In Finland right now it is dry, partly cloudy, and -1 deg Celsius.

Best regards,

Anthony writes:

avian influenza responsible for an outbreak at poultry farms in
southwestern British Columbia is H5N2

Varun writes:

Greetings Profz,

More recently I have noticed credibility of peer reviewed publication to have come under the attack of scams and lack of trust. I wish to know what the comments are by the TWiX team. Please find the links below

As always, long term TWiX fan. Whatever you are doing to educate the world, keep it coming.

Thank you

Erik writes:

Hello TWiV crew,
Lately I’ve been listening to the earlier TWiV episodes while I eagerly wait for the new ones each week and I just finished episode 57: Virology in High School. I was curious if there are plans on the agenda to do another episode like this one? At the time, the pandemic H1N1 strain of influenza was the major theme of the kids’ virology questions and, presumably, Ebola would be what’s floating around their heads now. But even so, I think it would be so rewarding, as it was in episode 57 to understand what high school students are thinking about viruses in the world today. The episode was actually very helpful to me. I was practically taking notes on how you answered questions in a way that a high school student could understand it.

Being the “scientist” in the family (the virologist, no less), I was inundated with Ebola questions this past Thanksgiving by my aunts, uncles, and grandparents. Though many of them do have a high school education, the field of virology is very foreign to them and, of course, media outlets capitalize on that misunderstanding (intentionally or not), and many of them were actually kind of on-edge about Ebolavirus. While I may not have done a perfect job of explaining the current situation in West Africa, I do think I answered a lot of their questions and might have allayed some of their concerns. I think your episode 57 was helpful in understanding how to approach discussing something a bit complicated to someone who doesn’t necessarily understand biology/virology/epidemiology.

I think it would be well worth-while for another episode like episode 57 to come out at some point in 2015.

Kindest regards,

Jon writes:

‘Bourbon Virus’ Is Deadly, Unlike Anything Seen In U.S. –

Paul writes:

To the TWIVome

A great year for TWIV. Thank you for all the good work. An unseasonably warm, drizzly and foggy 11 degrees in Philadelphia, PA.

Thanks for mentioning National Influenza Immunization Week in episode 315 and giving an outbreak update in 316.

I read that the flu vaccine for the coming season will be the same as last year. (MMWR August 15, 2014 / 63(32);691-697 , quote below).

In 315, one of you advised that even if the vaccine is unchanged, you should get it as a booster. Revaccination for new strains is one thing, but revaccination for the same strain is confusing to me. No other vaccine has an annual booster schedule. I thought the mechanism of protection from vaccine depended on the establishment of various types of memory cells that hasten and strengthen the adaptive immune response upon later infection.

The reuse of prior year strains seems to focus on the strength and persistence of the primary antibody response (making bullets) rather than the establishment of a population of memory cells (making bullet factories) that might be quiescent until activated upon a later infection.

Is immunization sometimes more like passive immunization than it is like the body’s experience of actually surviving a disease? I got my flu shot this year, but I am not sure why.

I reference below an interesting note from Plotkin (2008) on the difference between antibody levels as direct and indirect indications of protection and a couple of cites about antibody persistence.

Also, nomination for pick of the week:

From “The History of Vaccines, a project of the College of Physicians of Philadelphia” a game that goes through the development of society as it fights disease: Illsville:



Anthony writes:

Dear Twiv friends;

An iron-chelator pill called Deferiprone induces the apoptosis death of HIV-infected cells.

Another drug called Romidepsin activates hidden HIV, and drives it out of its reservoirs.

The links below say Deferiprone cannot be considered a cure for HIV, because these pills eradicate the virus in infected cells, it can’t reach all of them.

Meanwhile, Romidepsin isn’t considered a cure, because it can drive the viruses out of hiding, but it cannot eradicate them.

Could you explain what you theorize might happen if Deferiprone is ever COMBINED with Romidepsin in patients infected with HIV?

Happy holidays! I love listening to your netcast!


Drug-Induced Reactivation of Apoptosis Abrogates HIV-1 Infection

The HDAC inhibitor romidepsin is safe and effectively reverses HIV-1 latency in vivo as measured by standard clinical assays

Caroline writes:


I have two questions. One a virology question and one a bit more personal.
Are virus infections more likely to be species specific than bacterial infections? It seems to me they would be since viruses rely so much on the specialized relationship with cells for “survival”.

Second question.
I am a bachelor’s level clinical laboratory scientist (Medical Technologist) working in a large hospital laboratory in toxicology and chemistry for the past 15 years but my love is really infectious disease – virology in particular – and I’m hoping you can give me advice.

I’m considering pursuing graduate work on a part-time basis in virology. Since I am now “middle-aged” I have to consider the marketability of my choice. What are some areas of study that involve virology but are also marketable? I do want to pursue what I love but I have to be realistic as well.

Thanks so much for your advice. I LOVE your show and even if I never have a degree or work in virology I will still be listening to Twiv.


Ramon writes:

Recently you talk about sexual route of infection and HCV. I thought you would be interested in this article.

Ramón Canet, MD
Internal Medicine dept
Ibiza (Spain)
Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America 2014 Dec 15; 59 (12) : 1678-85.
Hepatitis C Virus (HCV) Antibody Dynamics Following Acute HCV Infection and Reinfection Among HIV-Infected Men Who Have Sex With Men.
Joost W Vanhommerig, Xiomara V Thomas, Jan T M van der Meer, Ronald B Geskus, Sylvia M Bruisten, Richard Molenkamp, Maria Prins, Janke Schinkel
PMID: 25186590

Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America 2014 Dec 15; 59 (12) : 1694-5.
Editorial Commentary: Acute Hepatitis C Virus Infection in HIV-Infected Men Who Have Sex With Men: Should We Change Our Screening Practice?
Thomas Reiberger
PMID: 25186589

Bill writes:

Vincent, this might interest you.

Nick writes:

Dear Twivologists,

Short time listener, first time writer.

As someone raised in New England, I am naturally a huge hockey fan (Go Bruins!). As someone who is an aspiring biologist, I am naturally very pro-vaccine.

If you have been keeping a close eye on the news you know where this is going (and I mean very close because not many people seem to be talking about this problem or the NHL in general). There is currently a Mumps outbreak in the NHL with teams all across the country having infected players and coaches. What is further alarming is that reportedly all of these players have not only had the MMR vaccine but some of them have recently received a booster as well. Can you help explain why the vaccines are failing? Is it just regular old vaccine failure? Or is it something more worrisome?

I also want to thank you guys. Your team has been a regular inspiration to keep on pushing on as I attempt the arduous process that is applying to graduate school (and yes at your behest I did apply to Icahn as well as Vincent’s current employer as well).

Weather report: Ditto to Vincent.


Efi writes:

My name is Efi, and I’m a Master’s student at the Weizmann’s Institute of Science in Israel, and a devoted listener to your wonderful podcast. Also, I am currently taking your course on coursera and enjoy it tremendously, I must add. Actually, I like the course so much that I decided to dive into the world of virology, though in my own work in a neurobiology lab. Recently, my current work incorporated a new tool to decipher an enigmatic question with regards to a neural circuitry which involves certain sexual behaviors. Funny enough, this tool is no other but the H129-∆TK-Herpes virus, which was developed by the talented people of the David Anderson team, at Caltech. Using the famous Cre-Lox system we can trace the circuit in the forward direction (anterograde) within the circuit.

I have a small question to which I could not find an answer in the literature. I would be grateful if you could suggest a possible explanation:

As a security measure, the authors of the paper (and developers of the virus) knocked out the Tyrsoine Kinase sequence from the original vector, stating that without it the virus won’t be able to replicate at the ganglion. However, I can tell you that the receiving animals show serious illness, and the virus still holds the capacity to infect and jump from synapse to synapse (it must. Otherwise I won’t be using it). Therefore, what exactly is the purpose of shutting down the TK component? Does it mean the virus can infect but not replicate? I am a little confused on the issue. What happens to the animal once it is infected? Does it carry the infectious particle in the saliva too? I am asking that because the animals often become rather aggressive few days after the injection (or jumpy) and I’m wondering if there is a chance that I’ll get infected from a bite? Is it possible? The correct use of this tool is quite important for my current work (and my life..) , and hence I bothered you with the email. Nevertheless, I truly hope you weren’t discussing this on the subsequent lectures in your course on coursera, (I still haven’t completed it yet); if yes, my sincere apologies for wasting your time with the email, as I’m sure I’ll get to this lecture soon.

Regardless, I have another question: in your coursera course, on the 2nd week, you showed a wonderful movie of a neuron infected with a herpes virus. I’m giving a talk in the two weeks on my project and was wondering if you can somehow refer me to this movie (website or a link)? I would really like to show the movie to the audience as the movie exemplify the unique capability of the herpes virus to move within the circuitry so well (in comparison to other viral methods we use). Needless to say that all references would be made accordingly and appropriately.

Again, I want to thank you for all these wonderful and enriching hours of podcasting.


Department of Neurobiology
Weizmann’s Institute of Science

Lynn Enquist writes:

I helped Anderson build this HSV-1 H129 recombinant. We send it out to neuroscientists as part of our NIH National Center for Neuroanatomy with
Neurotropic Viruses grant. I have considerable experience with this virus.

The thymidine kinase deletion (not tyrosine kinase) is the main selective feature of the Anderson virus. It is not a security measure!! An HSV strain defective in TK will not replicate in non-mitotic cells like neurons. It will replicate in transformed tissue culture cells since they are always dividing – this is how we grow the virus for distribution. When this recombinant infects a cre-expressing cell, a silent TK gene built into the virus is expressed and the virus replicates. Since Cre
recombination is not reversible, the virus that is produced after cre recombination continues to replicate and spread among synaptically connected neurons. Ideally,as I said before, in the absence of Cre, this recombinant virus will infect but will not replicate and make particles. It should be essentially avirulent, completely attenuated.

If the animals being injected are getting sick, then there are at least two possibilities:
1. The virus is being injected into a site where there are mitotic cells and the virus can replicate even if it is TK minus
2. The virus is not TK minus.

A TK minus virus is resistant to acyclovir (which blocks replication when TK phosphorylates the pro-drug). TK minus viruses are sensitive to acyclovir while TK+ viruses are resistant.

If you are injecting HSV into a mouse brain, there will not be any virus in the saliva.


Dennis writes:

Good news on vaccination rates and public opinion supporting vaccinations in Australia up from 53% in the ’90s to over 90% now. There’s a corresponding drop off of funds to anti-vaccination snake oil salespeople.

It will reach 22C here today and very sunny in Santa Cruz, CA.

Best to you and the team,


Judi writes:

Thought you and listeners might find this interesting…

As usual – thanks for all you do and keeping my brain wondering.

Judi (retired HS science teacher)

(San Diego – 18 degrees C , 64 F, 10% chance of rain, cloudy, winds 3MPH NE)

Grant McFadden writes:

Yes, it is essentially true. The live vaccine chain transmission on boats, using serial passage in young “volunteers”, was the key to getting live “cowpox-derived” vaccine to the new world.

Once the boats landed, the skin of inoculated cows then took over the job of propagating the “orphan-mediated” stock of new vaccine that had arrived in the arms of the orphan donors.

These passages were very poorly documented Now you can see why it has been so hard to trace the original lineage of vaccinia virus! There are still debates about what exactly the progenitor virus was (i.e. horse pox?) that then evolved through the skin of inoculated people and cows to become what we now call vaccinia virus.


Yue writes: (pronounced like Yoo-Ay)

I was just listening to the very latest episode of TWIV. Dickson and you raised up a “non-virology” question as to why there are currently only four serotypes for dengue virus or, more broadly, why many viruses have a given number of serotypes. However, as far as I know, the fifth serotype of dengue was reported in 2013, as shown here:

With regards to why we haven’t seen the six serotype of dengue, I think it is probably the matter of time in the context of evolution. I’d like to quote a sentence from Field Virology: “Based on comparative sequencing studies using the hemagglutinin molecules, it has been postulated that the influenza A viruses diverged about 2,000 years ago, and the influenza B and C viruses about 4,000 and 8,000 years ago, respectively”. If we went back to 2000 years ago when there wasn’t influenza A viruses, we might have asked a similar question of why there are only influenza B and C viruses existing.

Yue (pronounced like Yoo-Ay)

Anthony writes:

Thank you for covering two letters from me on TWiV 319

The quote from Dr, Linfa Wang is from the email that I’m forwarding

I don’t know what Web Site was being looked at that resulted in the “high maintenance” verdict for opossums, That’s certainly so compared to cavies, but the American marsupials require no more care than a domestic cat — and certainly much less than any non-human primate.

In TWiV 296 –the Linfa Wang episode — there’s talk of establishing a colony of fruit bats and the difficulty involved. That would be multiplied many times over for a researcher in the United States. Opossums seem to have a similar resistance to viruses. Someone here could lay the foundation by finding out what (or if) that is, Once a cause has been established, it could be checked to see if the same mechanism is in operation with bats in Asia and Africa. I mentioned road kills not as an optimum source of data, but as one very easily available and at basically no cost. In addition to the Virginia Opossum common throughout the eastern US, there is a much smaller — around rat-size — South American species that’s already domestically raised for the pet trade.

Opossums can be maintained quite easily in tall pens. All bats clearly should have lots of space to fly. (Linfa Wang mentioned that his colony would not have room to fly. I believe that you replied how this would make it difficult to discover if the high rate of metabolism during flight was what provided the resistance to viruses. Opossums don’t have any high power aerobic capacity, but do seem to have the same resistance. What they do have in common with flying mammals is
the opposite — low body temperature, always for opossums and when not flying for bats.)

Most small bats are for all practical purposes impossible to maintain in captivity because they consume huge numbers of flying insects. As they eat fruit, the flying foxes are easy to feed, but these large animals truly are “high maintenance.” If any researcher was establishing a colony of Opossums, I’d guess that few would take any notice. How would the public feel now about numbers of bats being brought from Africa to the US?

I think that the NJ State Rabies spread sheet that I sent you has question marks. The data comes from Animal Control officers responding to complaints. A question that I have is whether Opossums afflicted with Rabies simply crawl into a hole and die without causing a ruckus and so are not counted. Even the supposed “symbiosis” of fruit bats with viruses (Symbiosis is a misleading term, for most tend to think mutualism, not commensalism or parasitism.) seems to need a lot of work to establish. Fruit bats require a lot of food and their only defense is flight. Like birds, they won’t look sick for very long — if at all. When to any degree they lose their edge, they die or are killed. It seems that there haven’t been any longitudinal studies to find out how long any individual bat has a virus. Could an infected bat be like a person with HIV?

Bats in the US were thought to be “carriers” of Rabies — not killed by the virus themselves. That seems to be wrong. I was googling Charles E Rupprecht, for he is one of the lead authors here Bats, emerging infectious diseases, and the rabies paradigm revisited It is stated that:

“More recently, the asymptomatic excretion of RABV in the saliva of experimentally infected vampire bats, which survived the challenge during at least 2 years of observation, was documented again (18).”

But the cited research — despite what one might expect from the title Salivary excretion of Rabies virus by healthy vampire bats states that “Rabies virus was not detected in the saliva of any of the 11 animals that succumbed (somewhat early) to rabies challenge, nor in the control bats. In contrast, virus was detected early, and only once (days 6, 6 and 21) in each of the three animals that survived rabies challenge and remained healthy for at least 2 years after challenge. At that time even vigorous dexamethasone and cyclosporine administration failed to provoke further viral excretion.”

Which appears to show that bats once recovered are no longer carriers and not that apparently healthy ones are.

Many thanks to you and your colleagues for TWiV and the other great series of podcasts.


Natalie writes:

Hello TWIV Team,

I’m a former chemist in my late 20s that’s been waffling with the decision of leaving my cushy six-figure job to go back to school for a PhD because I believe research is extremely important for our society and want to contribute. However, I recently came across an article with some very sobering and compelling reasoning to not pursue grad school and a career in academia titled “A Career in Science Will Cost You Your Firstborn”.

Although the author has a bit of a cynical, one-sided take on the matter, (at least grad students aren’t going further into debt), and the title is a bit dramatic, I think the points raised and quantitative analysis are fairly accurate. And, to be fair, I know plenty of equally cynical grad students who would agree with the author.

To summarize, the article shows that wages lost by opting out of a non-academic job to instead pursue a career in academia could roughly equate to the amount it costs to raise a child, about $200,000. This financial analysis really struck a chord with me because I, myself, am weighing buying a house versus getting a PhD in the next five years.

A bit of background on myself: I earned my chemistry degree five years ago from a top research university and intended to continue my education with a PhD. After graduating, a bad viral infection, (mono caused by EBV), side-tracked me into a career in which working from home while recovering was possible: software engineering. (My two year battle with mono is also coincidentally how I found your wonderful podcast.) I’ve recently been accepted into a PhD program, and, though I remain wildly passionate about science, falling into the lucrative software industry has made the decision to return to academia all the more difficult because of the significant pay cut it would require. Money is not everything, of course, but grad student stipends seem drastically low given the average rent in areas like California and New York.

I’ll feel incredibly guilty if I ‘sell out’ and cite personal finances as a reason for not pursuing science, but the pragmatic side of my brain is struggling to justify a pay cut of at least 70k per year for the next five years. My friends think I’m crazy for even considering it. It’s a shame this is such a hard decision. I think I would make a great scientist, and I fear that other capable graduates shy away from academia for financial reasons too.

So, in your opinions, is academia still worth it? Is it too late to start an academic career in your late 20s? Please share any advice you might have for anyone wrestling with such a decision.

I’m happy to see that grad student and postdoc issues are being brought up for discussion more frequently and hope that such discussions ultimately lead to an improved quality of life for grad students and postdocs and make pursuing a career in academia a more feasible option for those with a passion and aptitude for it.

Thank you for all the podcasts!


P.S. My ears perk up every time EBV is mentioned in your episodes. Any chance of an EBV episode? 🙂

Apologies, forgot the weather!
San Francisco is 50 degrees F and, oddly, not foggy for once!

Jakob writes:

Dear Twivers
Thanks for the great episode covering the recent Dengue vaccine trial.
The antibody dependent enhancement theory that has been put forward to explain the increased risk of developing severe dengue during secondary infection is immunologically interesting. If this was a general mechanism it would be highly unlikely that it only affected infection with dengue virus. Many viruses are capable of replicating in cells bearing Fc receptors and the spectrum of antibody specificities in a given individual at the time of a specific infection likely offers lots of antibodies that can bind an infecting virus with “suboptimal” affinity and thus potentially give rise to antibody dependent enhancement. It has however not been obvious from the study of infectious diseases that this is occurring. On the contrary most “suboptimal” antiviral immunity, either from vaccination or infection with similar viruses tend to result in a milder disease course (i.e. some immunity is better than nothing). Even for dengue the data supporting a causative mechanism for antibody dependent enhancement in severe disease is not clear in my opinion.
If such a mechanism truly exists in vivo I would think that it should have been visible in this large vaccine trial. There are also a number of other publications that have failed to find a clear connection. As an example:

As an aside it is always striking to see how low the mortality rate really is in well conducted dengue trials.
Kind regards
Jakob Nilsson MD, PhD
Department of infectious diseases
Karolinska University Hospital
Stockholm, Sweden

Ramon writes:

Pick of the week?

Ramón Canet, MD
Internal Medicine. Hospital Can Misses
Ibiza, Spain

Sandra writes:
Moth Radio Hour Released Jan 13, 2015, go to the episode “ A special live edition…” at and start at 38:50

“The week of April Fool’s Day of 1981…began badly.”

I would recommend you listen to this 15 minute story without reading anything about it first – the ending will be that much more shocking.

I listened to it a few nights ago and was so impressed with it that I emailed Kathy about it, only to find out that she too had heard it and thought it was great.

It would be great if Kathy could present it since she has the same enthusiasm for it that I do.


As of 10:30 a.m. Central time, Thursday Jan 15, it is 43 degrees F with 5 mph winds out of the NNW. Humidity is 54%. First sunny day we have had in a while – which is unusual for Dallas.

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