Joe writes:

Dear TwiEvo,

I am a physiologist with an evolutionary bent who has been listening to your TWiV episodes since keyed in by a past student of mine who is a molecular biologist … and now your TwiEvo episodes.  

I have a deep interest in evolutionary mechanisms and have been trying to see how far the phenomena we have described in higher organisms, some of which communicate with one another apply to lower levels of communication.  When higher organisms like birds, whales and primates communicate with one another they broaden their interface with the environment, which is the driving force in evolution.  We called that phenomenon ‘behavioral drive’ (Wyles et al. 1983).

In my education in cell biology from 1960 on we learned that some bacteriophage cooperate through their limited gene products to prevent confection with other bacteriophage. 

I am interested in whether vertebrate viruses also communicate during their infections, which could be described as behavioral drive, involving cooperation during an infection to their mutual benefit.  I am particularly interested in why for instance clusters of bacteria or a particular load of virus is necessary for a successful infection.  Is it possible that they are cooperating in the infection and that ‘cultural communication’ is needed for a successful microbe infection and that there are aspects of cultural inheritance in viruses.

Wyles J, JG Kunkel and AC Wilson (1983). Birds, behavior, and anatomical evolution. PNAS 80: 4394-4397.

I am glad I found your podcast and encourage your efforts.

Joe Kunkel ’60 Columbia College

-·.  .· ·.  .><((((º>·.  .· ·.  .><((((º>·.  .· ·.  .><((((º> .··.· >=-       =º}}}}}><

Joseph G. Kunkel, Emeritus Professor
Biology Department
UMass Amherst 
Amherst MA

Brian writes:

Dear Vince and Nels,

Another take on the claim that SARS CoV-2 is lab made, or why it’s not.

It’s like saying a lab built a weaver-bird nest or termite mound. Humans can pretend to imitate neural networks, but not evolution. Consider GMOs. A gene, a promoter, and a terminator get inserted. No chromatin shaping, alternative splicing, RNA feedback, protein networks, the myriad things that evolution causes. It may work, because the gene is well-known. But it’s like inserting a twig in a spider web. To anyone who knows spider webs, it stands out like a sore thumb. To anyone who knows viral genomes, a human inserted gene will be as peculiar. It also won’t do something predictable, because there aren’t viral genes like the Bt genes used in crops. 

Darwin may have been inspired by dog breeding, but no one who studies canines mistakes a wolf or coyote for a dog. SARS CoV-2 is like a new fox species, while conspiracy theorists claim its a Labrador Retriever. Nice dogs, but don’t blame labs for spreading this virus.

Brian Michael Coyle

Chulites LLC, Founder 

Volker writes:

Dear Nels,

in TWIEVO 59 you argued that viruses tend to become less virulent over time. I think that the Calicivirus used against rabbits is very weak evidence for this claim. A virus with 100% mortality will obviously burn out immediately. The Calicivirus started with some 99,9% and is now by 90% mortality if I remember David Quammens’s Spillover correctly. Would you maybe consider the formula of Roy Anderson and Robert May Quammen cites (R_0 = beta * N / (alpha + b + v)) consider for a future TWIEVO episode?

Thanks and best regards,


Ken writes:

While I agree that there doesn’t seem to be good evidence that variants of SAR-CoV2 are more transmissible I’m uncomfortable with the claim that there is no selective pressure since it is already reproducing so well.

Consider a variant that is doubling the number of hosts every week competing with one that increases by 2.1 instead. After 20 weeks

2^20 = 1,048,576

2.1^20 =2,782,184

The 2.1 variant will have 2782184 / (2782184  +  1,048,576) or over 72% of the hosts. And the percentage will just keep increasing.

Great show, keep it up.



Scott writes:

Dear TWiEVO people,

TWiEVO 58 discussing bat coronaviruses was great. Heather and Simon did an awesome job explaining their latest work.

I was a graduate student in the Rollins-Smith  lab at Vanderbilt when Heather was an undergraduate in the lab. It was great to hear about her scientific progress since graduating from Vanderbilt. Heather did an amazing job explaining her findings and putting it into the appropriate evolutionary and virology contexts. 

Among the MicrobeTV podcasts, TWiEVO has the least number of regular hosts. TWiEVO would benefit from another voice on each episode. I don’t know if Heather would be able or willing, but if the latest episode is any judge, Heather would be a great addition to your team. 

Looking forward to future episodes,


Pete writes:

Man, men, people,

What an amazing episode. It brought it all together in a way I hadn’t considered before. Not that you all don’t try to explicitly state the implications of a paper. But this was another level.

I loved the contributors who acknowledged their appreciation of twivo, but I am sure they all felt the same.

PS I have been listening to twiv since Vincent was on SGU

Thanks, all you people are amazing, and adding to the rationality of the world.

Pete, Sydney Australia

Ben writes:

Hi TWiEVOlutionaries,

Congratulations on 5 fantastic years!

 Listening to the future of the field of evolution, something I thought that had never previously crossed my mind is the impact of evolution among somatic cells that is not heritable to the next generation.

I suppose this is best understood in the context of cancer, where cells obtain a replicative advantage but I was more curious about otherwise healthy humans. If you take a sample of somatic cells, do you find an accumulation of deleterious de novo mutations in genes that would not have contributed to the fitness of that cell or its parent cells since embryogenesis? On the contrary do we observe de novo mutations in somatic cells that give them growth or survival advantages without contributing to the onset of cancers? Might these contribute to other diseases, particularly those of the elderly? I suppose the number of replications of the average somatic cell before apoptosis occurs would complicate this, but I can’t see why these mutations couldn’t occur in tissue stem cells too.

Curious to Hear what you have to say about this, hear what’s already known, or learn why this might not occur!

Keep on TWiEVOlving,


Anthony writes:

Concerning the CRISPR technology Nobel Prize

“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

Yury writes:

Dear Drs. Elde and Racaniello,

I have been an avid listener of TWIEVO for about a year now. You are doing a great job! I currently work in vertebrate genome evolution myself. I am new to the field and I find your podcasts both enlightening and entertaining. I would like to suggest two potential guests for your future programs, perhaps when you once again have time to talk about things other than viruses.

  1. Dr. Erich Jarvis is a professor at Rockefeller University: Erich leads the Vertebrate Genomes Project, an ambitious international effort to produce reference quality genomes of all vertebrate species. He is also doing some interesting work in genetic underpinnings of vocal learning in birds. I know Erich as a current collaborator and can make an introduction by email if you think that would be helpful.
  2. Dr. Scott Edwards is a professor at Harvard: He has done some very interesting work on discovering non-coding genetic elements that are connected to loss of flight in paleognathous birds, such as ostriches and emus. 




Yury V Bukhman, Ph.D.
Computational Biologist
Regenerative Biology
Morgridge Institute for Research
Madison, WI