Lindsay writes:
Dear TWiV Microbes,
This is a question for Dr Daniel Griffin, if he’ll entertain the musings of a lab researcher. Since we’ve been hearing that ventilators may not be ideal for treating COVID-19 patients due to the potential for further complications caused by positive pressure ventilation, would a negative pressure machine such as the now retired iron lung suffer the same problems? I remember at least one company in recent memory was trying to resurrect negative pressure ventilation because it would allow patients to remain conscious and speak easily during treatment. In this situation, it may also not carry the hazard of aerosol generation, which is a problem for even non-invasive positive pressure breathing machines like CPAP.
Thanks again for all of your hard work during this time and I look forward to the day when things calm down and TWiV can discuss some non-coronavirus content.
Vic writes:
Dear All,
Yesterday the Norwegian CDC (Folkehelseinstituttet) released an app to track Sars Cov 2 infections. It’s called “Smittestopp” or Infection Stop in English. It’s available on iOS and Android, and use is strictly voluntary.
The app uses GPS and Bluetooth to track your location and proximity to self-reported infected persons. The collected data is anonymized and will be destroyed after 30 days. The data will be used to inform communities about when and where people are gathering. Then, after analysis of the initial data, they will begin to inform users when they have been in contact with an infected person. The hope is they can begin to pinpoint where to focus their testing efforts and put in place regulations to limit the spread of the virus.
Of course, the very populist Progress Party immediately warned of the grave dangers to personal liberty inherent in the use of the app. Moral panic ensued. However, I think the vast majority of Norwegians will gladly use it. My family and I are all signed up.
Keep up the good work!
Best,
Vic
Joel writes:
Neat SARS-CoV-2 visualizations
“An in progress cutaway visualization of the #SARS_COV_2 virus, with spikes in yellow, M-protein in mauve, N-protein in blue, and RNA in red (E is in there, but not very visible in this slice)”
Amy writes:
I have been listening for many years and very happy to be getting such great information on the current pandemic.
My question is about some of the significant disease progressions in healthcare workers. It seems it is not necessarily due to infective dose. Could disease transmission route be a significant contributor? Would it be possible that a healthcare worker is getting both respiratory and an oral transmission, causing a significantly worse disease?
Thanks for all you are doing,
Amy
Frank writes:
Hello All,
I came across an article that towns in Westchester County, NY were banning leaf blowers because the politicians stated it spread COVID-19, see attached article. If that’s the case, these politicians need to contact Mother Nature and ask her to stop the wind! I don’t think it is possible but I wanted to get the opinion of the TWIV experts.
Thank you for all you do! Keep up the good work!
Frank
Kavinda writes:
Hello to whomever reads this email,
I have a question for the podcast and if it could be answered I would be most grateful.
With the decision to defund the WHO by the US, which is predominantly a power play from a diplomatic American standpoint. What i really want to know is taking to account the disastrous interview on Taiwan. Is it fair to say that since Dr Chan led the WHO, has it been more willing to take the Chinese accounts at face value? Calling into question its impartiality? I always thought the WHO was supposed to act like a judiciary sufficiently disconnected with daily political ramblings. But the way its top brass has spoken to the media I see it more in the light of a legislature. Am I wrong?
I was always under the impression that the WHO was the one intergovernmental organization above politics but clearly that is not the case. With all the double speak going on I’m having trouble understanding the truth of the matter.
In what way is the WHO ACTUALLY, culpable and in what is it just just a political shtick from the Americans and those who sympathize with Taiwan ?
If this question could be answered from purely a factual point if view I’d appreciate it.
Also love the discussions. I got to know about the podcast after the plug in from science vs.
Kindly
Kavinda
Andrew writes:
Have you any insight on this?
Thank you.
Andrew
Montreal QC Canada
“However, there are different findings on how the coronavirus spreads. Experts from the US Institute of Health CDC and NIH had come to the conclusion that the virus can survive 24 hours on paper, three hours in aerosols and up to three days on plastics and stainless steel. As the Robert Koch Institute states on their website, however, scientific studies like this are realised under experimental conditions, which is why they are not very representative for the risk of transmission in daily life.”]
Bijan writes:
Hi TWIV gang,
I’m a physician by training – Columbia P&S class of 1999, and i still fondly remember Dickson’s lectures on tropical diseases! I am a healthcare venture capital investor these days so I’m using all of that Columbia learning in a different way.
I’m a huge fan of TWIV and the education and service you are all providing. Thank you. So many incredible episodes from Ralph Baric to Mark Denison to Jon Yewdell to Christian Drosten.
Heres my question:
There is lots of talk about serology testing for prior exposure to SARS-CoV-2 and even the concept of “Antibody Passports” that would indicate if it was safe for those who are serology positive to possibly go back to work.
Given the low population prevalence of COVID-19 (single digit percent perhaps – right Rich?), and the currently imperfect serology tests, aren’t we just asking for high false positive rate?
See below for an illustration from Lucas Wheeler on twitter using the current Cellex serology test data from FDA EUA showing 30% false positive rate at 10% population prevalence of prior infection. That number is 82% false positive at 1% population prevalence! That seems unacceptable real world test performance to drive policy from
Second question: isn’t an “antibody passport” actually penalizing people who did keep very good social distancing and did not get the virus? Why should they be penalized and not be allowed to work? Lots of ethical and biostatistical questions to work through.
Keep up the great work.
Best,
Bijan
Kevin writes:
I was just listening to ep.597 with Jon Yewdell and loved the discussion of innate vs. adaptive immunity. I was struck with the discussion of “inapparent viruses” as they relate to an appropriately functioning immune system. I’m not sure if this is something we can know right now the way that SARS-CoV2 attacks humans, but I had a thought and wanted to bounce it off your panel:
As SARS-CoV2 seems to hit some people “harder” than others, can any part of that distribution be attributed to the presence of concurrent “inapparent” viruses? In other words, sort of an agonist effect of a co-present virus that the immune system would otherwise be able to fight off without symptom development, yet causes a cytokine storm in those that acquire SARS-CoV2?
Incidentally, practitioners are seeing interesting responses to COVID-19 in their patients, such as increases D-Dimer levels and decreased Procalcitonin (common in a classic Sepsis presentation), yet relatively low levels of C-reactive protein (CRP) which is usually seen in septicemia patients in extremis. That coupled with the “dry” nature of the respiratory presentation in the face of ARDS leads me to wonder if it is more of a systemic immune response that circles back around to the lungs (though originally seeming to be acquired via the upper airways), causing the inflammatory respiratory arrest.
That might have been alot to wade through. Thanks again for your podcast.
Wilmington, NC is warming up today in the mid 70s with an increased SW wind, some dropping barometric pressure and some good storms rolling through tonight.
Cheers to you all.
—
Kevin Keller
Associate Clinical Researcher
Catawba Research, LLC; Charlotte, NC
Tuomas writes:
wrt TWiV #598, in the 3/26/20 White House Coronavirus Task Force press briefing,
at around 58:24, Tony Fauci says that the U.S. government is working with a variety of companies to manufacture vaccines at risk before completion of phase 3 trials.
Cheers,
Tuomas
Marcin writes:
Dear TWiV Team,
Dear Prof. Racaniello,
Thank you for your recent wonderful coverage of COVID-19 on TWiV.
Could you please have The Team comment on this paper:
also covered here:
https://medium.com/@andrewt3000/covid-19-and-hypoxemia-697bc8a19bae
Could this explain the severity of hypoxemia and “non-standard” response of COVID-19 to ARDS ventilatory treatment? Could the lung involvement indeed be a form of iron toxicity-driven inflammation?
I am a long time TWiV listener, MD, PhD, pediatrician from Poznan, Poland, I work in pediatric pulmonology, allergy and immunology department.
Best regards,
Marcin
Frank writes:
Bill and Melinda Gates Foundation is pre-funding 7 different pathways of manufacturing facilities and prepared to waste billions to save a few months’ time.
Thanks for the great program you have. Very informative!
Frank
Volker writes:
Dear Twivsters,
Let us assume that we find out that it is possible to get an intestinal infection with COV 2 without getting lung disease and without being contagious. Might this lead to immunisation? Might this be a temporary solution as long as a proper vaccine is not available? Like a mixture between the original intentional infection with smallpox as practised in ancient China and the OPV? Do you know if anybody is looking into the effects of intestinal COV 2 infections or even an approach to use it for immunisation?
Greetings from Bavaria where it is still possible to go hiking in the mountains.
Best regards,
Volker
Alex writes:
From my research about the 1918 flu pandemic, I thought I remembered reading that cytokine storm was something that tended to happen to people with young, strong immune systems, which is why they thought young people were among the worst hit. Now, though, I’m hearing about cytokine storm with covid-19, which hits older people preferentially.
Does cytokine storm frequently happen to older people with weak immune systems after all? Or is it more a factor in severe disease in the young, when that does occur (less frequently)? Help me understand. As a person with nearly everything on the list that supposedly makes covid-19 worse (over 60, diabetic, high blood pressure, type A blood, immune compromised, autoimmune issues, etc.) I’d love to hear any reason to hope I can survive, if I get it.
Thanks so much, I really love your podcast. So glad I discovered it last month. Keep up the great work!
Alex
Ben writes:
Good Afternoon,
I wanted to note that your podcast has inspired me to take a closer look at the virology amd immunology world for graduate school. I currently work as a lab manager doing high throughput neuroactive drug testing on zebrafish with the Department of Defense.
On to my question: at the moment, it looks like there are very few animal models for the study of SARS-2, yet the virus seems to grow readily in cell culture. Many cell lines have been successfully grown in Zebrafish including cell lines that express ACE2 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6482513/). In previous high throughput drug testing it has been found that simply having some sort of liver to metabolize drugs has a significant impact on the outcome (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2834185/). Do you know of anyone who is running high throughput drug trials using zebrafish xenografts of cell lines infected with SARS-2 or other coronaviruses? And given the relatively unpredictable nature of drug metabolism, how helpful do you think having a very basic model of the drug-liver-virus interactions would be?
Thank you for taking the time to read this, and hopefully to answer it!
Best,
Ben
John writes:
Dear Vincent and Rich:
Is there any evidence to indicate that COVID-19 may be transmissible from toilet plume aerosols like SARS was reported to have spread throughout the Amoy Gardens apartment complex in Hong Kong in 2003? Does putting the toilet lid down before flushing help stop the spread of germs in general from toilet plume aerosols?
Also is there any evidence to suggest that people with certain blood types are more or less susceptible to COVID-19 infections?
Sincerely,
John
Zach writes:
Hello all,
First of all, thank you to each of you for everything you have been doing before, and currently doing with the SAR-CoV-2 pandemic. A thanks to all your extremely knowledgeable guests as well.
While I am not a professional scientist, and do spend a lot of my time studying a range of science topics for the purpose of increase my own understanding and knowledge. Virology has always been a fascinating interest to me, which is how I came across Vincent and his Virology lectures on YouTube. Over the last couple years have watched each lecture, and currently are watching the 2020 lecture series. They are what subsequently led me to find TWiV, after this pandemic began.
Anyway I have 2 questions for episode 602. The first question is slightly unrelated to the pandemic.
1. Stanley Perlman spoke about laboratory mice and the problems that came with giving mice human ACE-2 receptors in SARS 1 studies. The mice being readied for SARS 2 studies have a change of 1 amino acid in their ace-2 to allow for infection. How is this modification generally done? Is it gene manipulation at the embryo level, or later on?
2. Stanley also talks about researchers likely needing to adapt the virus to allow it infect mice, or manipulate the virus to allow it to compensate and use the mouse ace-2. What are the key differences between those 2 strategies? And do any of those strategies possibly affect how the findings in the animal model translate to human infection?
Thank you again, and any response is very much appreciated!
Zack
Chesterfield, Virginia
Daniel writes:
Dear prof. Racaniello et al.,
I know you are swamped with questions, and this may have already been asked. An engineering post doc sent me this paper
“Relationship between the ABO Blood Group and the COVID-19 Susceptibility“
https://www.medrxiv.org/content/10.1101/2020.03.11.20031096v2
From looking at their graph (page 17 of PDF), their data is mostly statistically indistinguishable from 1x risk, and looks like their differences are probably statistical flukes, but if there are correlations with genetic markers and the ABO antigen, I haven’t heard of them.
An anecdote that might be of interest: in Canada the blood service agency put out a call for donors, fearing a shortage, and when I was donating yesterday they said that there was no known shortage in western Canada. The CBS has just rolled out an online sign up of donors for convalescent plasma this week, but only those who have tested positive by the nasopharyngeal swab rt PCR, for trials to start up in Ontario and Quebec, our hardest hit provinces (outbreaks in senior care homes). Alberta is starting to test all patients with flu-like symptoms this week as lab testing capacity has caught up, but Ontario is still way behind.
great to hear the interview with Christian Drosten for #601!
Cheerio,
Daniel.