Genes in DNA or RNA can be expressed to make gene products, but proteins cannot be expressed because nothing “reads” the protein to produce another product. DNA makes RNA makes Protein (or RNA makes DNA, makes RNA, makes protein). Now one should be able to “express a protein” because that means it is being made by translation. BUT one cannot say proteins are “expressed”.
Genes are expressed (they carry info), and I mRNAs could be (but why not say what really happens, mRNAs are translated), but proteins are NOT – they are made, produced etc. – they are information, if you like.
This jargon, like so much other, has gained widespread use, as people
1. use phrases they have encountered in papers they have read,
2. do NOT think about what they are actually saying,
I just wanted to let you know that I managed to catch the live hangout on YouTube for about 40 minutes. I was really surprised when I got home from the lab to see a live TWiV. The time when it was live was also perfect for me as an European listener (about 6 p.m. in Sweden at the time). Do make it into a habit!
I would also like to add that I wrote in, and got my letter read, on TWiV 183. There I was asking for help deciding if I should continue with a Master in Biomedicin or Master in Infectionbiology. To this Alan answered that “I think you’re underestimating microbiology”, which I then realized I was! I’ve now got accepted and will be starting my Master in Infectionbiology at Uppsala University in a few weeks. Thanks Alan!
Membrane proteins are deployed to membranes. Deployment implies a purpose. While the purpose may not be obvious or easily discernable, it is not an unreasonable assumption that every protein has – or once had – a purpose. Serving in the Army adds to one’s vocabulary, both printable and unprintable.
The hullabaloo about publication of HeLa genome is a reflection of an unstable phase in societal transition.
The hierarchical structure that constitutes society makes every component including the organisms that constitute that society increasingly dependent on every other part of that society. This dependence includes ceding control to the societal structures. Domesticated animals and humans are no longer capable of faring as well in the wild as their feral forebears. The dependence is reflected in the shrinking of brain size in all domesticated species: even human brain size has shrunk by about the volume of a tennis ball (for the average adult male) from that of our ancestors of 20,000 years ago. Even mitochondria ceded part of their genome to the nucleus.
Concerns about the ability to buy insurance with one’s genome laid bare arise because there are not yet in place the alternate societal structures that can provide the needed support and care. Such mechanisms will carry concomitant constraints on human behaviour.
Already, anyone who has recently served in the Armed Forces has their DNA in the military databank, to permit identification of otherwise unknown remains. It is also perfectly legal to acquire a sample of someone’s DNA from saliva on a soda straw (as in the Stephanie Lazarus case) or from clothing (even someone else’s blue dress) and sequence it. A day can perhaps be imagined when cord blood will be routinely sequenced and deep frozen, both to guide future medical care and provide a reservoir of autologous stem cells. The information could also be used in employment medical examinations to identify persons at undue risk from certain occupational exposures. If such a day arrives, the issues raised with the publication of the HeLa cell genome could seem quixotic.
A fourth domain may explain why the viruses with large genomes have such large genomes: if organisms from those domains parasitised more familiar cells, they could have ceded only the limited number of functions that they held in common. If the parasitism started very early on, their preference for protozoans may reflect an difficulty in shedding their different ancient baggage. Could it shed some light on the radiations from our last common ancestor?
Kia Ora folks,
In TWiV 246 you talk about the agreement that was come to with the Lacks family and publishing the genomes of the HeLa cells. Firstly and quickly Rich mentions the German group then how “we’re” in an age of HIPPAA. No, the US has HIPPAA, other countries have different systems that can vary a lot. Coupled with universal public funded healthcare and the thought processes around the handling of genome data can be very different to what you would think.
Now onto the more thorny issue of the family. Yes the HeLa cells contain the same basic genome that is present in parts of the children and grand children. However how similar are they? The cells used were diseased and have spent decades mutating and being mutated in different ways whilst the descendants have ever shrinking parts of this genome and have the much more stable parts.
All the way back around TWiV 105 you mention the Personal Genome Project that will put in the public domain the genomes of people. Not the genome of some cancerous cell but the genome of healthy tissue. How can this person consent in the place of their descendants to have parts of their genome publicly available with detailed history of the person it came from? When do we say that a descendant has no further say in the release of data? For example the great great great grandchildren of Henrietta Lacks will only have 1/32 of her genome.
I do think the HeLa agreement is a useful stepping stone but it is far from the endgame as more and more of these genomes are released or leak out. As Alan said, it’s a flimsy barrier when there are so many ways around it even without access to the cell line to sequence yourself. And I seriously doubt that the final setup will look anything like what was agreed on with the HeLa genome.
Please don’t avoid these thorny topics as the discussion is important. 🙂
Aotearoa (New Zealand)
In week 2 of the Coursera class I’m currently taking, we learned that a cell is either Susceptible, Permissive or both. We learned that a susceptible cell is a cell that has a receptor for a virus while a permissive cell has the components to support viral replication.
…Enter this plant virus you speak about in this episode which doesn’t require a surface receptor. Does this now mean that all plant cells are susceptible? Are there any examples of human/animal viruses which don’t require a surface receptor?
To me, this seems like a fundamental distinction…a “principal” of virology 🙂
Hello — in order of first TWiV appearance — Vincent, Dickson, Alan, Rich, and Kathy,
I plan on going through each TWiV podcast starting from the beginning with TWiV 1: West Nile Virus. In addition to learning, I’ll be listening for a type of statement. If there is anything you’d like me to capture from the podcasts while doing this review, just let me know.
I’ll begin next week, June 10th. I am guessing this review may take six months to a year to complete.
Hello TWiV doctors,
I’ve just recently graduated from UConn with a degree in Pathobiology and a minor in Molecular & Cell Biology. I am passionately interested in viruses and how they interact with the immune system. I have a fair amount of research experience from a viral immunology lab that I worked in last summer at UMass Medical School, as well as some experience in a lab at UConn. I applied to about six PhD programs in Microbiology/Immunology departments at universities across the country but, unfortunately, wasn’t accepted into any of them. Now I am looking for a research job that I can work at for a couple years, then I’d like to re-apply to PhD programs. So far I’ve looked into biotech companies, research hospitals, and even university research jobs in the Boston area. I must have sent out at least 20 or 25 applications and, so far, all I’m met with is crickets chirping. I’m running out of ideas for places to apply to.
I’m wondering if the TwiV crew, or even any of the listeners, have advice on, A ) different kinds of institutions that I might be able to look into for research jobs besides hospitals and biotech companies, B ) What I might be able to do to make myself a more attractive candidate for these jobs, or C ) Know of any virology/immunology researchers in or near Massachusetts that might be looking for research assistants.
I understand that this soon after my graduation I can’t be picky about jobs. Also I know that the job market isn’t exactly the greatest right now. I’d take any research position at this point. Any advice that you might have would be greatly appreciated.
Keep up the great work with TWiV, TWiP, and TWiM. I’m a huge fan of all three podcasts!
Dear Twiv team,
I’ve been a happy listener of your podcast since I discovered a link to Twiv on Viralzone, which is run by my former colleague Philip Lemercier (I worked 7 years at Swiss-Prot). I am currently with the Seattle Structural Genomics Center for Infectious Diseases (ssgcid.org). I heard that you are visiting Seattle in June and wondered whether you would have time to meet and allow one of our PIs to advertise our services to the virology community.
Our primary mission is to determine the structure of 75-100 protein targets from NIAID Category A-C agents, as well as emerging and re-emerging infectious disease organisms, each year for a period of five years. In order to do this, we seek the active engagement of the Scientific Community in nominating targets of interest for entry into our pipeline. This can be easily done from our website and involves no expense on the part of the requestor.
We also provide materials (clones and proteins) to the scientific community free of charge.
About half of our current targets have been either submitted directly by the community (classified as Community Request targets by NIAID) or ‘adopted’ by collaborators (Community Interest). NIAID is keen to have the community lead publications that describe or use our structures. This is an example of a publication with a community collaborator:
Yamada S et al. Biological and structural characterization of a host-adapting amino acid in influenza virus. PLoS Pathog. 2010 Aug 5;6(8):e1001034. http://www.ncbi.nlm.nih.gov/pubmed/20700447
Hello from sunny Florida. Every week I enjoy the content, presentation and repartee on TWiV.
Today in my RSS feeds, Next Big Future points to an article ‘Synthetic Biology Could Speed Flu Vaccine Production’ on MIT’s Technology Review site. The Next Big Future post is at
and the link to the MIT publication is
Would it be accurate to say that the steps involved in the process are: gathering sequences from a virus strain causing an outbreak and using those sequences as a basis for chemically re-creating (synthesizing) the virus? If this description is inaccurate or grossly oversimplified, feel free to have a laugh at my ignorance. That no longer bothers me, so long as I hear an accurate (but still simplified) explanation.
While it seems from the links that the time needed to create a vaccine might be greatly reduced using this technique, how long does it take generally to isolate the flu virus when an outbreak occurs? Looking at the other end of the steps in creating a vaccine, once the proposed vaccine is created or available, how long generally does testing take?
Apologies if these questions have been answered in a previous episode.
Written near Daytona Beach, where it’s currently 66F, 19C with partly cloudy skies.
Just finished listening the new episode of TWiV. No much comment on the H7N9, but you mentioned that you need a line of HeLa cell which is sticky to the culture dish and makes flat monolayer, we have some HeLa cells in culture and they attach to the dish tightly. The cells grow really fast, once reach confluence, the cells kind of become plump and round, but still attach well. Attached please find the pictures of our HeLa cells, if it is the type of cells you are looking for, I will be more than happy to send it to you.
Ps. In this episode, Rich called TWiV “The Weather in Virology”. In my last email (actually the only one) to TWiV, I called it “Today’s Weather in Virology”. So, you may consider to use that as a subtitle of TWiV J .
Haitao Guo, Ph.D
Dept. Microbiology & Immunology
Drexel University College of Medicine
& Hepatitis B Foundation
I am a licensed research applicator and i enjoy listening to your podcasts.
My current job is bed bug identification, prevention and control.
I have witnessed an population explosion over the last four years in Los Angeles.
Due to the population density of our urban environment, modern construction (hollow walls and carpet) and global travel, these creatures have been able to spread and establish themselves rapidly.
I have been doing some reading on the potential of C. lectularius as a disease vector and come up with mixed information.
According to what I read, bedbugs could potentially transmit flavivirus, and possibly lentivirus, but this has not been proven in studies as of yet.
In addition, I know that that kissing bug Reduviidae can transmit chagas.
I would like to know what you guys think the potential disease threats are with bedbugs. I often see, in heavy infestations, blood spots from smash adult bugs, as well as droppings.
I would like to know what the possible threats are from bedbugs feeding, as well as the diseases or parasites that could be picked up from smashed Cimex and lastly if the fecal droppings could carry chagas or some other infectious agents.
I know this is a touchy subject because bedbugs are common and people may panic – I have to calm people all the time who think rats have hantavirus – but I would like to know the truth about this. Is there a possibility that virus can pass to a human from bedbugs ?
I have another request that is important to me. I had a friend Tom and myself Jerry would debate the validity of the existence of HIV. He had it but believed since the virus was never isolated by the standard set out by the Pasteur Ins. using a sucrose gradient and such, that HIV was not really proven and he claimed that much of the illness was iatrogenic.
I disagreed based on demonstrative evidence, although I must admit some of his sophistical arguments appeared to have merit.
Some of the virologists whose works he embraced we Papadopolis of the Perth Australia group.
He would state that the genetic sequences were from endogenous retrovirus.
GP 120 and 41 were not specific to HIV.
The leukemic cell line used for HIV diagnosis was in and of itself somehow flawed.
That protease inhibitors were nonspecific to HIV and they somehow help people by preventing bacteria and parasites from proliferating and that explained the efficacy of this class of drug.
I know this is ancient history. My friend embraced his belief and bet his life on it. He did not treat for HIV believing it unproven and he was not a complete fool in doing so. He had what seemed to be strong support of his idea. He is no longer with us now, I believe he held on to his belief until the end.
Tom and I spent many days in 1997-98 in a lively debate and learned a great deal about virology (thanks to a wonderful comprehensive virology book courtesy of Glaxo) and a myriad of other related subjects.
Do you have any opinions on these matters
It was this experience that drew me to TWIV et. al. It often reminds me of our debates. I know it would be a great podcast and it is. Kudos
Pardon the unpolished nature of the email. Its 200am
Take care guys
I love TWIM and will be using it in my course on Microbiology for High School Teachers. BUT as regards humans, empirical observation and Jenner/smallpox, please check the article at the Welcome Trust Who got credit for the first vaccination Jesty or Jenner?
The Jesty story of vaccination ties in with the current citizen scientist movement and illustrates how social class affected scientific standing.
or documented here
or in Wikipedia