Nathan writes:

Dear TWIV,

My 4yo son often plays while TWIV is on in the background. Someone on the show mentioned fecal/oral transmission of SARS-CoV-2 a while back. He asked what that means and I told him. Since then he has been begging and badgering me to send a specific question in to you. I have resisted so far, but now I relent.

Is there any chance that SARS-CoV-2 can be spread through farts?

That is all, thank you.

Nathan in Goshen, IN

Bill writes:

Hello Everyone,

How risky do you think air travel is right now, assuming that social distancing is taken into account and masks are required? Would any of you fly on a plane? Why? Why not?

I’ve read a couple of articles claiming that it’s relatively safe because the cabin air is frequently replaced. However, in both cases, this information came from airline industry talking heads, so I’m skeptical.

Thank you,


Carolina writes:


Greeting from eastern CT where we currently have 33C/92F, and approximately 167% humidity. In relation to the C vs F debate, I feel compelled to weigh in that the clear advantage promoting the comprehensibility of the Celsius scale is that it is freaking linear! One degree is worth the same regardless of where it falls on the scale, which is clearly not the case for Farenheits. Also, from a scientific point of view, Celsius and Kelvins are highly compatible as each step on the scale is worth the same, and for conversion from C to K you simply add 273.15!  (rather than multiplying with 9/5 and adding 32 for F…)

I am a Scandinavian explant in the US -and the widespread use of the Fahrenheit scale is likely the most prominent obstacle to my integration in this country (perhaps along with the US customs and immigrations system…).

However, that is not my main reason for writing. I could not avoid reacting to the question in TWIV 628, regarding the potential viability of SARS-CoV-2 beyond death of the infected individual. 

I work with foot-and-mouth disease virus (FMDV), which is clearly a very different virus, perhaps specifically as it is non-enveloped. However, although non-enveloped, FMDV is not at all durable outside of the infected host, specifically as the capsid is highly unstable outside of a pH range of 7-7.5 and therefore quickly disintegrates in most environments. 

Due to food safety concerns, several studies have confirmed that FMDV quickly becomes inactivated in muscle tissue (i.e. meat) of infected animals due to post-mortem acidification (rigor mortis). However, the highest viral loads in infected animals are found in vesicular lesions in peripheral epithelial tissues (e.g. the feet and the mouth…). Due to the apparent lack of information regarding FMDV viability at these peripheral lesion sites, we recently conducted a largely opportunistic study to investigate this. 

We initially utilized carcasses from pigs that had been part of an experimental study during which they were humanely euthanized at the peak of clinical FMD. Carcases were stored at 4 degrees C (FMDV is a select agent, and our options for prolonged carcass storage were therefore limited to a designated cooler room). To cut a long story short, we were very surprised by our findings, and had to repeat the experimental set-up with another 3 batches of unrelated FMDV-infected pig carcasses before we had to call it quits. Although we did confirm that the virus was quickly inactivated in muscle, it was clearly perfectly happy and well for at least 11 weeks post mortem in the vesicular epithelium while still attached to decaying carcasses. I can confirm that the pigs were definitely dead as I had to visit them once weekly for sampling through 11 weeks, sparing only Christmas Eve. I apologize if these experimental details are maybe a bit morbid for the average listener. But, knowledge concerning potential viability of this highly infectious agent in decaying carcasses is critical in relation to practical handling of deceased animals during outbreaks of FMD.

So, I guess the take home message might be that some RNA viruses can apparently remain viable through prolonged periods, despite the death of their host, as long as the environmental conditions are favorable. In this case, this implied relatively cold and humid storage, and distant from the putrefaction that was inevitably happening within various body cavities.

Thanks for all that you do!

Carolina (DVM PhD -and a picornavirologist)

Barbara writes:


Dear Vincent and TWIV Team,

I am a writer specializing in communicating environmental (and wildlife) conservation in Canada, Mexico and the United States. I have been listening to your show since mid-January, well before we thought SARS-CoV-2 was going to turn into a pandemic that would forever transform the world as we knew it. When I first started listening, I thought it was Alan Alda’s podcast (he has a medical podcast apparently) and because Vincent sounds more like Alan Alda than Alan Alda, I was left gobsmacked by how much the American television and film actor knew about viruses. It wasn’t until the end of the first show that I realized Vincent is not Alan Alda but it was too late, I was hooked. To me you are Alan Alda, Vincent.

I am writing with a question for each of the TWIV hosts and also Daniel Griffin, if possible. 

Based on what you have learned about SARS Co-V2 over the last several months are you more or less afraid of catching the virus?

In closing, I “self identify” as a hypochondriac and have been acutely aware of SARS-CoV-2 since mid-January when the WHO was stressing that countries needed to pay attention. Yes, the WHO was telling this to the world way back then. Canada, my country, did not step up to the plate until the second week of March…long overdue, but formidable coordination and cooperation by the national government and the provinces nonetheless. As a hypochondriac, my advice to the pandemic planning teams around the world for the next time…is that you may want to consider having one of us (a hypochondriac) on your response committee…we would have had people mobilized for physical distancing, wearing masks and hand sanitizing months prior, and we would have saved a lot of lives.

If you’re ever in Guelph, Ontario, Canada (my town) drop by for supper. The yard is big and there is always room for one more!

University of Guelph is famed for its Veterinary School. In fact, there is quite a bit of current SARS-CoV-2 research underway. For example:

Thank you TWIV Team.


Jerry writes:

Maximum respect to Vincent, Rich, et al.,  this retired physicist [who studied microbiology & biochem., too] is addicted to TWiV.   Thank you!

It’s the GREAT WEATHER season here in Seattle mid 75ºF and DRY – here’s a photo I took yesterday from a block North of my apartment.

As you know, there’s now a massive outbreak in Germany [my other home] at the Tönnies factory & community in Gütersloh.

Of course the people work close to each other, and engage in vigorous physical activity.    But there are other jobs under such conditions.

There MUST be an environmental component – cold, damp fog in the refrigerated environment, providing a long-lasting suspension of virus-bearing droplets?

Thanks again for your thoughtfulness, even the prissy grammar & punctilious comments about what can mutate and what cannot!

Dr. Glomph

Doug writes:

Hi There;

    If an asymptomatic person is in a small gym on atreadmill, and presumably breathing hard, he/she will correct?  And these droplets can stay in the air for X number of minutes/hrs?  Air circulation in the gym would move those droplets around, increasing the area effected.

   Those who could not find an N95 mask, but instead wear a homemade or mass produced “economy” mask, will be at considerable risk?  Correct?  Assuming these lesser masks are lucky to be 60% effective.

    The same logic, but to a lesser degree, would be true in a restaurant, right?

           Your insight would be greatly appreciated,


Barbi writes:

Dear Twiv,

Love the show and listened in the car while driving to Northern Minnesota for a very socially distant trip to Voyaguers National Park, where the weather was nice, but we had 1 leech, 9 ticks, and a billion mosquitos.

You discussed the two Nature Medicine papers in this episode; the epidemiology study suggesting kids are infected less often, and the study showing asymptomatic carriers may not generate an antibody response. I was waiting for you to loop back and discuss this in the context of what might be happening in kids. 

My question- If kids are infected less often and it’s because of some form of cross-protection from another coronavirus, would you expect them to retain any form of immunity as they get older? Also, might this affect their ability to respond to vaccines? This is concerning because we likely won’t know the answer to this until much later since the trials won’t likely include children.

thank you,



Barbi A. Judd, Ph.D.

Managing Editor

Immunology Science Editors

Marcos writes:

Dear TWiV,

I write from Spain where we’ve recently opened our borders with the rest of Europe (or most of, anyway) and will open to third countries soon. Right now travelers are checked for fever, asked if they’ve been sick with Covid-19 and visually examined (I don’t know the extent of this visual exam). 

The government said that no PCR will be done to these visitors unless fever or other symptoms are detected because that kind of massive testing at arrival won’t be effective to control imported cases. Even if you don’t detect every infected person at entry point because of the limitations of this kind of testing (sensitivity, detection of ARN instead of active virus, etc.), wouldn’t it be useful?

Both my scientific and english background lies far away in time, sorry for any blatant mistake I made in these short paragraphs and thank you for your great work. I started listening recently and will continue to do so in the future.

Marcos Pérez.

Madrid, Spain. 

Mona writes:

FYI: The data on Nextstrain includes 113 SARS-CoV-2 RNA sequences (GISAID).  Abou 2/3 are G and about 1/3 are D at codon 614.  I think I got that right(?)

Dr. Mona Baumgartel 

Deron writes:

(pronounced Dare-in)

Dear Twivers,

I’m a computer programmer but I’ve been interested in microbiology for some time.

I’ve listened to one of Vincent’s virology classes and I’ve been listening to and enjoying TWIV, TWIM and Immune for years.

In TWIV 629, Alan expressed a concern that political forces in the U.S. might cause a SARS-Cov-2 vaccine come to market that has less than ideal effectiveness.

If a person gets a dose of such a vaccine and a more effective vaccine comes out would it be a good idea for that person to also get the second vaccine?

Would it be safe? Do vaccines based on different platforms have a booster effect

on each other?

Thank you so much for your tireless dedication to science education!


David writes:

Hi TWiV,

While listening to TWiV 621’s discussions of the different vaccines in the pipeline, I was wondering whether you could see a situation where people are told to get two (or three?  or more?) different COVID vaccines as part of their regular prophylactic care, especially if their modalities differ?  I don’t mean to get them years apart (like how I got the old shingles vaccine a few years ago and then my doc recommended getting then new one recently), I mean where people get Vaccine A this week and Vaccine B a week later – or even in the same injection?  Is anything like this done with another vaccine?

Thanks in advance,

David in Teaneck, where the temperature is way too hot

Ron writes:

Love TWiV, and have been following for several months now, although I should have caught on much earlier.  I am surprised that Rich did not pick up on the understanding that in much of east Africa, Zimbabwe included, many of the adult reproductive age population have succumbed to AIDS, lowering the average age of the population.

Have you reviewed the work of Frank Plummer and Alan Ronald, two of my mentors in Winnipeg, University of Manitoba from 4 decades ago on HIV in Nairobi?   Sadly, Frank, the previous director of the Manitoba viral labs, recently died, I believe while back in Kenya.

They were instrumental in describing HIV in Nairobi, where they had gone to research haemophilus ducreyi, and effective at bringing the viral labs to Winnipeg, where your much discussed Ebola Vaccine was developed.

I am a simple family physician/anaesthetist in Sechelt, a small peninsula up the coast from Vancouver, where we have had few Covid-19 cases, thanks to  the work of our public health department in British Columbia.  Our provincial government have been very supportive of the science behind the management of epidemics, although some provinces a little late to the game.

Several TWiV back, coronavirus researcher noted that a phosphodiesterase  inhibitor coded by this coronavirus inactivates interferon to some degree.  This will of course be structurally quite different than the multitude found in humans, however, there are a number of medically useful phosphodieterase (PDE) inhibitors, including caffeine and theophylline.  The most lucrative of these developed by David Brown in the UK, sildenafil, marketed as Viagra (PDE5 inhibitor).  Has he been involved at all in that he must have some significant background in PDE inhibitor research, which might be of value in SARS CoV2 inhibition.

Keep up the great work, this has brought me back to my microbiology roots from 4 decades back.  Boy things have changed!!!

Looking forward to more great coverage of the research.

Ron Mundy MD, 

Sechelt, British Columbia, Canada

(a constitutional monarchy- but also is a democracy)

David writes:

Hello – 

 I am a high school science teacher from Knoxville, TN that has been following your show for two years. Thank you for making the time to communicate science to the public. 

I am wondering if you could clarify something for me. I understand that an antibody test/ELISA test is used to determine if you have had an immune response to a virus. What is not clear is how we are able to identify if an individual’s antibody response is specifically due to SARS-CoV-2 (and, not some other virus)?

I find this confusing because I am under the impression that scientists are still not certain which antibody inhibits the SARS spike protein responsible for entering cells. In addition to this, from what I have read, scientists are experimenting with multiple monoclonal antibody treatments that could act in unison on the virus.  Do the monoclonal antibody treatments being explored mimic the amplification of antibodies seen in our serological assays?

More simply, are we able to assess whether an individual has had SARS-CoV-2 based on the distinct types of antibody proteins we see amplified after an infection? 

Thank you for your time. 

Your number 1 fan in south knoxville.


Dean writes:

I am a non science trained lay listener who loves your show (for sure  there is lots I don’t understand but it still seems very informative)

I am a very avid road rider but since the Pandemic I have not gone on any group rides.  My riding club is starting up again.  Normally we ride wheel to wheel but the new guidelines require increasing the distance to 6 feet with a max number of riders of 10.  I am worried that even at 6 feet we are riding in each others slip stream and we just don’t know where droplets will be by the time we hit them

Am I being too cautious



John writes:

Hi Ladies and Gents,

I work in IT. In IT we have reverse engineering. Can COVID-19 be reverse engineered?