Philip Minor writes:

Happy New Year!

Andy sent me the TWIV thing which I thought was pretty good. I am less used to reasonable discussions than I used to be or would like to be, to tell you the truth. However, this business about licensing needing a protective efficacy trial so no change is possible is all very well but Japan has licensed Sabin IPV and so has China and the issues are the same i.e. no protective efficacy trial. WHO have guidelines on what you need in a clinical trial although one does not have to pay attention of course. WHO are also pushing Sabin IPV pretty hard with a view to getting its manufacture out into developing countries or at least new ones to reduce the cost of IPV. I accept that FDA will cut up rough and that it is a bit of a fiddle but I think new vaccines like sIPV will appear and if them why not S19 I ask you?



I think the UK might. They did meningitis C vaccine with only immunogenicity data, although to be fair that was backed up  a year after introduction by data that showed it worked like magic in preventing disease. HPV was put on the market on the basis of its effect on CIN rather than cervical cancer which it is intended to deal with; I suppose you can argue that cervical cancer is always preceded by CIN but that all cases of CIN do not lead onto cervical cancer so if you prevent CIN you prevent cancer, but it is still indirect. Given that humoral immunity protects against polio…… I am sure that these arguments will only convince certain regulators, but there are political reasons for them to be convinced i.e. the need for lots of cheap IPV. Do you think a new manufacturer using the current strains could get a licence without efficacy data? This gets a bit tricky.

Fernando writes:

Hi TWiVers,

I was just listening to 371, where you kindly discussed my letter. Later in the show, Kathy seemed to be having trouble with the Google Ngram searches I had suggested, I wonder if she was including the quotes. I put the quotes to separate the queries from the body of the letter text, they should not be entered in the Ngram viewer search box.


Catheryn writes:

Dear TWIV,

Thanks for the great podcast. I always enjoy listening to it.

Just a few points about the Tasmanian Devil segment:

1) Devils are not the only carnivore native to Tasmania. Quolls are also found there.

2) I believe that the tumorous cell that is the cause of DFT is thought to have originally been a Schwann Cell.



Basel writes:

Dear TWiV team,

I hope this email makes it in time as I wanted to follow up on the cell type of Devil Facial Tumor Disease.

The same group from the paper you discussed (G.M.Woods) had previously characterized these tumors as of Schwann cell origin, primarily based on the expression of periaxin.

Here is the link:

You’ve heard it many times, but thank you a ton for this wonderful podcast.

Kind regards,


P.S. I like that the authors are from Tasmania. It can’t be any more authentic than this (University of Tasmania, Tasmania, Australia).

P.S. A shout-out to all veterinary scientists and pathologists out there who contribute to such great science.

Josephine writes:

Dear Twivologists,

What a lovely surprise this morning when I checked out TWIV for today’s download.  You used George’s “Take Aim at West Nile” painting for this week’s podcast illustration. Thank you for your positive comments.  I have asked my husband what the little upside down umbrella thingy is in the cartouche. His best guess, this many years later,  is that it is a stylized bulrush in a marsh – another mosquito breeding area (the marsh,  not the bulrush).

The weather here has improved considerably over the last 24 hours.  Yesterday morning was a chilly -26C, a beautiful winter wonderland with everything covered in hoar frost.  This morning the temperature reached 0C – so much more pleasant for outtdoor activities.

Best regards,


Anthony writes:

In the recent TWiV you remark that human gene modification is part of evolution.  That brought to mind this by Chardin.


# # #

“With the discovery of genes it appears that we shall soon be able to control the mechanism of organic heredity. . . . The dream upon which human research obscurely feeds is fundamentally that of mastering, beyond all atomic or molecular affinities, the ultimate energy of which all other energies are merely servants ; and thus, by grasping the very mainspring of evolution, seizing the tiller of the world.”


Pierre Teilhard de Chardin

I would be proud to have written “Access is not just a convenience or courtesy, it is essential. Without access, it’s not science, it’s authority.” but I did not.   It actually was a tweet by the anthropologist John Hawks that I retweeted.

Chris writes:

Dear TWiV team,

First of all, a very Happy New Year to you all !

Thanks for your discussion of the paper on reactivation of HSV from latency. It’s great that we are getting a better understanding of the mechanism behind this. The discussion reminded me of lysogeny where temperate bacteriophage is latent in its host bacterial cell. In this case latency is maintained by a repressor protein. When under stress of DNA damage, the host bacterial DNA-repair mechanism kicks in. This also has the effect of degrading the phage repressor protein allowing the phage to switch into lytic mode, with the production of progeny phages.  It is always tempting to view viruses as clever little beasties, being able to respond to changes in their host cells, and enabling them to ‘escape’ from a potentially damaged cell, but this isn’t the case. Vincent said that…”if the neuron is going to die the virus needs to replicate and get out”. But why ? Why do viruses in neurons need ‘to replicate and get out’ ? Viruses have no desire to survive. They survive because they possess features enabling them to continue infecting and persisting in their hosts. Viruses, like all other infectious agents are populations, not just individuals. Individual viruses do not adapt or evolve an ability to respond to changes in their host cells, enabling them to escape and survive….but populations of viruses certainly do evolve. It is interesting to ask why HSV or phages, can respond to stresses in their host cells by switching into lytic mode, but all we can say is that, somehow, the ability bestows a survival advantage on the virus. After all, if my understanding is correct, latency and reactivation from latency, is a feature of all herpes viruses, and therefore the ability to reactivate is unlikely to be accidental.

Regarding the discussion on inhibiting reactivation, an ability to prevent symptoms resulting from reactivation would be great, but how would we know when to administer an inhibitor, even if we had one that lacked significant side effects ? But at least we do have a number of effective antivirals against herpes viruses and a vaccine to prevent reactivation of varicella zoster virus in neurons of the elderly.

Thanks again for your great podcasts…all the best for 2016 and beyond !


Christopher Ring MSc PhD FIBMS FHEA

Senior Lecturer in Microbiology.

First Year Tutor for BSc Biomedical Science.

Programme Leader for MSc Biomedical Science (Medical Microbiology) and the BSc Applied Biomedical Science programmes. Module Leader for specialist postgraduate Medical Microbiology and postgraduate Biomedical Science Research Project modules.

Department of Natural Sciences,

School of Science & Technology,

Middlesex University,

The Burroughs,



Jim writes:

Vincent ran “viruses” through Engram and noted the percentage of references fell off in recent years.  I’d heard that published titles in 2014 were 400,000, but in 2015 they jumped to 700,000. Those numbers aren’t defined, but do indicate published material has greatly increased.  It makes me wonder if the percentage of references to virus fell off because of the huge number of increased publications, but the actual number could have increased.  It would be helpful if Engram could provide raw numbers, too because references to viruses may be steadily increasing, but are overshadowed by the increasing amount of material that’s available.

Interesting site to play with, though.  Thanks.


Smithfield, VA

Mark writes:

Hello Vincent and the TWiV-osphere,

Happy New Year 2016. Congratulations on launching

In episode 369 Vincent mentioned sampling a physics-related podcast, and that he didn’t want to regularly listen because of its poor audio quality. As I recall, only Alan Dove agreed commenting that poor audio quality is inexcusable.

Since 2008 I’ve sponsored over 50 different podcast shows for several high tech companies. The first thing I looked for is consistent high quality audio. The second factor was the level of engagement between the show’s host/hosts and listeners. Podcasts, like old fashioned radio shows, are an intimate medium where listeners voluntarily give their time and attention to the show, its hosts, and guests. Listeners will consider, and dare I say trust, recommendations for products that hosts genuinely use.

Due to the intimacy of the podcast medium, content quality does not compensate for bad audio quality. Bad audio quality is an insult to listener’s ears and an affront to their intelligence. Sadly some podcast shows never improved their audio to a level where I would sponsor them. TWiV listeners who aspire to create podcasts take note! Borrow and adopt how TWiV engages listeners, and copy or improve on tools and techniques for producing consistent high quality audio.

Here is a Shakespearean analogy from Hamlet In Act 1, Scene 3 Polonius shares worldly wisdom with his children Laertes and Ophelia. One line applies here:  “clothes don’t make the man, they announce him.” So it is with podcast audio quality.

Enough of this gushing appreciation.

Here are some show ideas – repeat visits by Gabriel “Concerto in B” Victora, Lynn Enquist, Karla Kierkegaard, or Eugene Koonin. A stretch goal is to book and interview Nobel Laureate James D. Watson as a special TWiV guest while time permits. My father had a mild acquaintance with JDW whom I met briefly when he came to express condolences at my Dad’s wake.

Now, for some fun.

About 18 months ago I sent you a bingo card based on common phrases used in your podcasts. In the interim there has been phylogenetic drift in the phrases used in the TWiV-osphere. Attached are updated bingo cards reflecting my observations of changed phrasing. Bingo squares containing “gain of function” or the name “Dickson” are the most obvious changes since the last TWiV bingo card was drafted.

Today’s weather in San Jose CA, after 4 days of rain. The El Nino weather pattern is opening up and we are finally getting good rainfall in this drought stricken region. Let’s hope things continue for the next few months. With luck a precipitation heavy weather front will passage from California eastward and deposits on MI, MA,and NY.



Bob writes:

Good morning and happy new year. I just heard your picks on the New Years Eve show and wondered if you’ve come across Make magazine and the whole maker movement. This is apropos the Edmund Scientific catalog and Heathkit. If you haven’t seen it check out; there is a whole ecosystem growing up around home technology development.

I also came across this today on a veterinary newsletter I happen to subscribe to:

Travel-Related Zika Virus Infection Has Been Identified in the Harris County Area

Harris County, Texas – Harris County Public Health & Environmental Services (HCPHES) has received confirmation from the Centers for Disease Control and Prevention (CDC) that the Zika virus has been confirmed in a traveler who recently returned from Latin America. The individual developed symptoms that are often associated with the Zika virus which include: fever, rash, and joint pain.

It’s a clear and cold 10 degrees F today in Chicagoland after snow last night.


Jarrett writes:

Hello Virologists,

This morning I read a report that a confirmed case of Zika virus has turned up in Harris county Texas, rather near to me in Austin. Having listened to TWIV 368 my ears perked up at the mention of said Flavivirus. Often such illnesses are acquired by tourists traveling abroad who become symptomatic after returning to the United States, whereupon the discovery is made that we have a new viral neighbor. My question is this: what is the time frame wherein an individual infected with a mosquito-borne Flavivirus could transmit the virus to another mosquito of the appropriate species (the Aedes genus), who may then go on to possibly spread the infection? Is it possible for a latent Flavivirus to reactivate once it is in the body of an Aedes mosquito? In other words, once a person has recovered from their infection, could they spread the virus in future exposures to mosquitoes? And, more generally, is it so that all viruses have periods of latency? These questions came to me as I wondered if the infected person in Harris county was asked to avoid the outdoors in order to prevent further spread of Zika virus, or if such a measure would even be necessary. As always, thanks for the excellent podcast. Right now it is a very comfortable 16 degrees C, in cloudless, Zika-free Austin, Texas.

-Jarrett H.

Bob writes:

Dear Twiviola,

Regarding your discussion on temperature conversion – when I was a kid my dad taught me an approximate conversion you can easily do in your head. Take the temperature in C, add 17, double it, and subtract 10%. This gets the right scaling but the result is offset by a degree or so.

Partly sunny and 33 outside Chicago today, humidity 61% with 16mph wind.


Paul writes:

Dear TWiV,

Thanks for your interesting discussion of our manuscript on biofilms and filamentous phage in your recent podcast, TWiV 368.   

To answer your question, we haven’t looked at Phi X. However, since its structure isn’t filamentous, I don’t think that it will assemble polymers into a liquid crystal.  It’s a good question though and I’m constantly surprised by what phages can do. We’ll check and let you know.

As for the question of what’s in it for the phage, perhaps by making themselves useful to their bacterial hosts, Pf phages have managed to increase their abundance and prevalence.   Certainly they seem to be ubiquitous among Pseudomonas clinical isolates and are present at very high concentrations (averaging 10e7/ml) in Pseudomonas biofilms.  Pat and I like the idea that Pf phages may be symbiotic with their Pseudomonas hosts.  In support of that argument, Pf phage production is under host regulatory control, and these phages are, for the most part, non-lytic.

All the best,


Paul L. Bollyky, MD, D.Phil

Assistant Professor

Division of Infectious Diseases

Department of Medicine

Stanford University Medical Center

Christiane writes:

Hi Kathy,

This is a nice article that summarizes how to give good powerpoint presentations. Nothing new in there but it highlights the main points, so might be good to spread the word widely…


Christiane Wobus, PhD

Associate Professor

University of Michigan

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