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TWiV 167 Letters

Joe writes:


I did the homework Professor Vince assigned and went to see the movie Contagion. I really liked the movie and was very pleased with the way the science was portrayed.

I am an Environmental Health and Safety Manager for a Bio-Tech company and started listening to TWIV about 2 1/2 years ago when I was researching Avian flu and pandemic response planning about 6 months before it hit the headlines. As someone who had to consider all the social impacts and mitigation measures so I could write a response plan, I thought the movie hit just the right tone with the various stages of panic, denial, fear mongering, and good public health science going on in the background. They touched on the emotional impacts of losing loved ones, quarantine zones, panic buying, looting, and becoming self reliant very well. I liked that the science was done by a number of people within their own specialties and not by a single hero protagonist. I appreciated that they created a slimy huckster fear mongering the uninformed to fill the bill of a Wakefield charlatan (who gets his in the end, yea!).

I can't speak to accuracy of the details of virus isolation and vaccine development. The only part that seemed weak to me scientifically was at the end when they showed the case zero details. It seemed to me that the woman got exposed to a cook with virus on his hands. Then somehow she contaminated all these other people by touch even though she was not yet producing virus herself. This seems like a fairly small nit to pick when it was just an issue of time compression. If they had shown her 2 days after getting it from the chef when she was just about to have symptoms then it would be more credible.

Very good movie, I may use this a training tool once I can get it on DVD.

Thanks for everything that Y'all do!


EH&S Manager

Alex writes:

Finally, I'm glad to see that the movie Contagion didn't fall under TWIV's radar, as it was selected as a weekly pick in TWIV#148. Thought I might help simulate some conversion on things that I picked up on during the course of the movie. The following contains spoilers so I suggest you view the movie before reading further...

About half way through the movie, we become aware that Matt Damon's character was probably exposed to the virus but did not exhibit symptoms- by most accounts immune to the virus. They hold him in a containment cell for several days- but eventually he is released. If this was a real world epidemic would they hold him for longer? Really with a novel virus like that-the health officials have no idea how long he could have sequestered the virus within him. Do you have any idea what the CDC protocol is for a situation like this?

In regards the epidemic shelter set up after the virus was in full swing- it seemed like a terrible way to manage an air borne virus. Placing patients in close approximation to one another with little to no barrier between them. If you look at real life pictures of stadium shelters set up in the past, like those of the Astrodome during Hurricane Katrina, it would take a matter of hours for a virus with an airborne virus with R0 factor (Basic Reproduction Rate - vr: not a rate) of 2 or greater to completely overwhelm the entire stadium. I attempted to brainstorm ideas for managing containment of a virus when there is suddenly an influx of 100,000 people infected but came up empty. It does seem like stadiums are a poor choice however. It's clear that it's best to catch these types of outbreaks early.

As the investigation of where the virus started progressed, a WHO official reviews the videos from the casino and determines that Gwyneth Paltrow's character is the originating case. She is viewed blowing on the other executive's casino chip for good luck- which the WHO official views as transmission. If you take a look at Paltrow's dress at this time it's red and sparkling. We know from the camera pictures which Matt Damon views that Paltrow received the virus from the chef via a handshake (who was actively preparing a pig moments before) on the same night (because she is wearing the same dress). How could she could transmitted the virus through her breath? Seems to me that the virus would first have to become established within her respiratory tract before she could transmitted to the other executive. I find the other two examples of transmission- handling a phone and a used glass much more likely.

At the very end of the movie we get a glance of how the actual virus mutation occurred. A bulldozer plows through a forested area disturbing a bat, who then goes to bite a pig. The virus then progresses into humans. Do you think global deforestation and habitat encroachment is leading to an increase in these unfavorable interactions? And thus is putting us at an increased risk for an epidemic of a mutated strain? On a smaller scale, I think there is evidence to support this theory. Take for example the Ebola Outbreak in Mayibout Gabon in 1996 where two men butchered a dead monkey they had found, leading to the spread of the virus.



Bachelor of Science

Lance writes:

I saw contagion recently and was disappointed. They figure out the incubation period within a week, too fast I think. They seemed to have a crystal structure (which was a protein not a virus) before the virus was grown in cell culture (impossible). It's odd to have a genome that varies between 14 and 19 kilo bases - variation of over 20% in size! if I could calculate R0 from sequence alone I would be rich.

Thomas writes:

Hey gang,

So I have yet to see Contagion but with my birthday coming up I figured I would dig deep into my graduate school empty pockets and scratch for the cash to treat myself this weekend. However, with its release, I was very interested in how reliable and how true this movie remained to science. Well I did what any student would do to find such information and I "Googl-ed it" and came across this website http://www.scriptphd.com/ (Script PhD).

I was interested in what your thoughts are on this site and I especially hope you will consider a Contagion review podcast because, by the sounds of the reviews, this movie is a great representation of a possible threat. Also, the editor of this website, Jovana J. Grbić, PhD, seems to be well-trained and I love the timing of this websites beginning (very shortly after your TWIV podcasts began). Any friendly or collegial connection there?

Nonetheless, thank you and all your guests and co-hosts for your excellent work in bringing the best of virology (and microbiology and parasitology) to your faithful listeners. I look forward to your comments and future podcasts.



MD Candidate, Class of 2014

The George Washington University

Nina writes:

First off, love the show! It makes a great alternative to listening to the radio at my desk :)

Do you think you could combine my two favorite topics, microbiology and the movies, by discussing the movie Contagion? That's if you haven't already...

Keep up the great work!!



Roberto Cattaneo writes:

Thanks for enthusiastically discussing the measles virus host exit receptor in the “breaking and entering” TWiV 166.

When SSPE was considered, the impression was that measles virus is gone when symptoms occur. However, there is a lot of virus in brain autopsies: 1000-4000 copies of nucleocapsid per average cell were documented by quantitative Northern blots (the paper is from 1987):


By the way, biased hypermutation of viral genomes (up to 50% of the U residues in one gene mutated to C) was discovered (in 1988) in autopsy material of SSPE patients:


On a personal note, after graduating in 1984 I joined to laboratory of Martin Billeter in Zurich, Switzerland. Martin was a bacteriophage Qbeta virologist who just started working on an eukaryotic RNA virus - measles.

The project was of great interest to me because of SSPE - the ultimate example of long-term persistence of a RNA virus. Martin had access to SSPE autopsy material though the group of Volker ter Meulen in Wurzburg, Germany. I was hoping to be able to clone and analyze measles virus genomes that had replicated for 5-10 years in the same person.

In retrospect, ignorance was my luck. More insightful colleagues were scared by the perspective of working with minimal amounts of viral materials (if any!). However, there was a lot of viral mRNA in these autopsy material – piece-of-cake project.

Thanks again for discussing my favorite virus!



Kartik writes:

I very much enjoyed listening to the latest TWiV podcast that includes a discussion of our paper about Ebola virus entry and NPC1. I just wanted to clarify that the proteins Ebola and HCV need -- NPC1 and NPC1-like1, respectively, are in fact different (but related) proteins. They are paralogs that are ~50% similar. They are both cholesterol transporters, but are expressed in different cells and are regulated differently (NPC1 is present in all cells; NPC1-like1 is present only in gut epithelial cells and liver hepatocytes). We know that Ebola doesn't need NPC1-like1 at all. Also, Zetia (ezetimibe) blocks NPC1-like1 but has no effect on NPC1, which is why we didn't use it in our experiments.

Thanks and best,


Kartik Chandran, PhD

Assistant Professor of Microbiology and Immunology

Albert Einstein College of Medicine


Judi writes:

Hello professor TWIVers:

First, let me say thanks for all the work you do and the great discussions. I am a high school science teacher and you are my professional development since (for the most part) K12 education is spending their money on kids not teachers - probably a good thing for the short run.

Second, I want to say thanks for the heads up on Emperor of All Maladies - I am almost finished with this book and want more - Vincent, please write one about polio (in your spare time, but you're not allowed to stop the TWIVs)

Third, I have a question about TWIV 166 and the making of haploid cells. Someone, and I don't remember who, said you could make haploid cells by disrupting the spindle formation. I was wondering is this is true since DNA is replicated during the S phase of interphase, it seems you'd end up with single chromosomes, yes, but they'd have multiple strands of DNA and therefore multiple copies of genes. I tried to look this up and found that there are polytene chromosomes in Drosophilia salivary glands with 1024 copies of DNA. Am I misunderstanding the life cycle of cells? or do different cells replicate differently? Sorry to ask such a basic biology question, but I don't want to be giving my students inaccurate information.

Lastly, a reading suggestion from project Guttenberg: a short children's book; Makers of Many Things by Eva March Tappan, who lived from 1854 to 1930 [ad:she lived backward in time?]http://en.wikipedia.org/wiki/Eva_March_Tappan. She wrote a book that explains how things are made - The little friction match -- About india rubber -- "Kid" gloves -- How rags and trees become paper -- How books are made -- From goose quill to fountain pens and lead pencils -- The dishes on our tables -- How the wheels of a watch go around -- The making of shoes -- In the cotton mill -- Silkworms and their work. A fascinating old-style kids book -http://www.gutenberg.org/ebooks/28569

Thanks again for all you do...


Lori writes:

Part of my graduate work addresses the sweating sickness. Less what it actually might have been, but rather whether people thought it was contagious or not (comparing medical writings with chroncles, letters, and other such materials).

That said, there has been several articles written about the potential identity of the disease, most of which come to different conclusions. Until the latter part of twentieth century, medical historians largely believed that the sweating sickness was a form of typhus, a virulent relapsing or miliary fever, or influenza. Since the 1990s, historians have examined contemporary accounts of the disease’s symptoms in minute detail. Analysing those symptoms in correlation with virulence, spatial and temporal distribution patterns, potential transmission models, concurrent environmental conditions, and the clinical features of modern diseases, they have variously speculated that the disease was a viral hemorrhagic fever, an arbovirus, a hantavirus pulmonary syndrome, an enterovirus, inhalational anthrax, or dengue fever.

Here is a list of some of the better articles written about the disease:

Bridson, Eric. “The English 'Sweate' (Sudor Anglicus) and Hantavirus Pulmonary Syndrome.” British Journal of Biomedical Science 58, no. 1 (2001): 1-6

Carlson, J.R. and P.W. Hammond. “The English Sweating Sickness (1485-c.1551): A New Perspective on Disease Etiology.” Journal of the History of Medicine and Allied Sciences 54 (January 1999): 23-54.

Dyer, A. “The English Sweating Sickness of 1551: An Epidemic Anatomized.” Medical History 41, no. 3 (July 1997): 362–384.

Flood, John L. “‘Safer on the Battlefield than in the City’: England, the ‘Sweating Sickness’, and the Continent.” Renaissance Studies 17, no. 2 (June 2003): 147-176.

Hunter, Paul R. “The English Sweating Sickness, with Particular Reference to the 1551 Outbreak in Chester.” Reviews of Infectious Diseases 13, no. 2 (March - April 1991): 303-306.

McSweegan, Edward. “Anthrax and the Etiology of the English Sweating Sickness.” Medical Hypotheses 62, no. 1 (2004): 155–157.

Taviner, Mark, Guy Thwaites, and Vanya Gant. “The English Sweating Sickness, 1485-1551: A Viral Pulmonary Disease?” Medical History 42 (1998): 96-98.

Thwaites, Guy, Mark Taviner, and Vanya Gant. “The English Sweating Sickness, 1485 to 1551.” New England Journal of Medicine 336, no. 8 (February 1997): 580-582.

Wylie, John A. H. and Leslie H. Collier. “The English Sweating Sickness (Sudor Anglicus): A Reappraisal.” Journal of the History of Medicine and Allied Sciences 36, no. 4 (October 1981): 425-445.

Hope this helps.

best wishes


University of Ottawa

Jon writes:

I must confess, first of all, that I am very critical about retrospective diagnosis as a properly historical exercise as well as rather sceptical about the alleged results provide by new methods from molecular biology and genetics to identify past diseases.

Some years ago I used the case of the mysterious English sweating sickness to rise a historiographical question, namely to what extent the exercise of retrospective diagnosis of epidemic diseases may depend upon the variable, fashionable medical concerns of each time about this group of diseases.

If you were interested on this work, here you have its bibliographical reference: J. Arrizabalaga (2002), “Problematizing retrospective diagnosis in the history of disease”, Asclepio, 54(1): 51-70, pp. 62-67 (specifically on the ESS). It is downloadable from http://asclepio.revistas.csic.es/index.php/asclepio/article/view/135/132

This article is a sort of companion of another more general one I published three years before, namely, J. Arrizabalaga (1999), “Medical causes of death in pre-industrial Europe: some historiographical considerations”, Journal of the History of Medicine and Allied Sciences, 54(2), 241-260. It is downloadable from http://digital.csic.es/bitstream/10261/33163/1/Arrizabalaga%201999%20%28Medical%20causes%20of%20death%29.pdf

Hope that this stuff could be of any help to you. Best wishes,



Barcelona, Spain


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