Jim writes:

Hi TWIVaria,

Love your shows. I’m a long time fan of TWIV and a devoted follower of TWIP. Your Coronavirus reporting provides a level of technical detail we just don’t get from the popular press. Love hearing from the experts. Thanks! 

Hopefully my question will be quick and easy so you can slip it between more complicated questions. It’s especially for Dr Griffin.

It would seem to me there are 2 general groups of cause of death from Covid-19. Sorry, if this sounds insensitive or an oversimplification.  

It is my understanding some people are dying of Covid-19 viral infection or its direct complications. By this I mean, their body is unsuccessful at mounting an immune response or the disease has crippled their immune defense to the extent they are succumbing to secondary infections – ie pneumonia?

And some people are dying after 6-7 days of infection, from the overexpression of their immune response, ie loosely described as “cytokine storm” and ARDS?

Can you give a rough estimate of the ratio: 60/40? 30/70?

It would seem to me that the pathologies are completely different and an important distinction for understanding the lethality of the disease. 

From Dr Griffin’s descriptions the treatments are very different. For example – convalescent plasma should work for people who’s body fails to muster sufficient immune response but useless for individuals with an over expression of immune activity. Are both groups progressing to the need for ventilators and ventilator use equality unsuccessful?

 Thanks!

 Jim “from upstate NY”

Charles writes:

I am assuming that you will be discussing the antibody testing that shows many more people have been infected by SARS CoV2 than previously thought or shown by testing for active disease. One take away has been that we now have enough data to calculate a real mortality rate. I have seen that rate being reported as around 0.57%. That is an underestimate, even taking the results of the tests as being reliable.

Bottom line, the rate is much closer to 0.76%, and I would bet it is higher, but I don’t know how much higher.

Taking data for New York state from the New York Times (link below) we see that estimated infections are about 10.5 times as many as confirmed cases (2,700,000 / 257,246 = 10.49579). Applying a factor of 10.5 to the confirmed infections gives us a daily estimated number of total infections. Doing a simple ratio from 04/22/2020 results in a 0.57% mortality. The problem is that we know that deaths lag infections. Taking today’s deaths and dividing by estimated infections from eight days earlier, the mortality rate averages 0.76% for 3/30/2020 through 4/22/2020. The mortality range over the same dates ranges from 0.71% to 0.81% using the eight day delay. I was surprised that the mortality range was that tight.

There is a problem with my method, well one big one I know about. The eight day delay is from confirmed infection to confirmed death. Confirmed infections lag real infections. I don’t know how to estimate the lag between the two infection values. I simply applied a simple scaling factor to get the estimated infections from the confirmed infections, which takes away the delay that is there and will result in a mortality rate that is low.

Bottom line, the New York antibody study does not change the 1% estimated mortality rate that the models have been using.  I wish it was really good news, but it is not.

Thanks again for the great work you, your co-hosts and guests have been doing,

Charles

PS, I can send you the spreadsheet if you want to check my data.

PPS, have you heard this one:

What’s the difference between an introverted scientist and an extroverted scientist?

An extroverted scientist will stare at YOUR feet.

Link to the Times daily data for each state:

https://raw.githubusercontent.com/nytimes/covid-19-data/master/us-states.csv

Link to the Times data for total New York state infections:

Link to the joke:

Barbi writes:

On Twiv I heard you mention the need for manuscript reviewers. While we cannot help with scientific reviews, we are currently providing language editing services of SARS-CoV-2 manuscripts at no charge. This is our way to contribute and may be helpful to you as your reviewers would need only to spend time focusing on the science.

Please see below for a description of our company and my background.

Best regards,

Barbi

Our company performs manuscript editing within the field of Immunology. We also edit a fair amount of virology papers, usually from scientists in Asia or Europe. I wanted to offer our assistance, free of charge, to any laboratories working on SARS-CoV-2. While our customers most frequently speak English as their second language, we can help streamline the submission process even for native speakers. We perform two rounds of editing on each manuscript. The first round focuses on grammar and during the second round we compare figures to descriptions and improve overall flow. 

We adhere to strict confidentiality standards and have been in business with a loyal group of customers for over 13 years

Immunology Science Editors

www.immunologyeditors.com

editors@immunologyeditors.com

Catherine writes:

It’s a clear 61 degrees Fahrenheit here in locked down Sonoma County, California.

Today we received the following Covid-19 briefing from President Trump: 

“So, supposing we hit the body with a tremendous – whether it’s ultraviolet or just very powerful light, and I think you said that hasn’t been checked but you’re going to test it. And then I said, supposing you brought the light inside of the body, which you can do either through the skin or in some other way. And I think you said you’re going to test that too. Sounds interesting. And then I see the disinfectant where it knocks it out in a minute. One minute. And is there a way we can do something like that, by injection inside or almost a cleaning? So it’d be interesting to check that. I’m not a doctor. But I’m, like, a person that has a good you-know-what.” 

Please let us know how you feel about President Trump, who only yesterday appointed a former Labradoodle breeder as the head of the Health and Human Services coronavirus task force, going on national television and suggesting that doctors ought to be SHINING POWERFUL ULTRAVIOLET LIGHTS INSIDE SICK PEOPLE and then INJECTING THEM WITH BLEACH.

Sound medical practice … or cutting edge research?

Inquiring minds want to know.

Catherine

Justin writes:

Inject bleach into your lungs or stand in the sun for 8 hours or bring powerful light into their body through uhm magic? Bloomberg: Trump’s Idea to Inject Disinfectant to Kill Coronavirus Alarms Medical Experts.

https://www.bloomberg.com/news/articles/2020-04-23/coronavirus-dies-fastest-under-light-warm-and-humid-conditions

Dennis writes:

How does a family protect themselves from a family member becoming sick? Lets just say in a standard suburban house.

Are things like positive pressure like the Blade relevant…. Like opening a bedroom window? And what about taping off doors? What can they do? This seems like a family killer.

I’m living alone, so I don’t have to worry much. Guess I’m thinking of friends

Listening now for two months. Good stuff you folks do.

I live in Miami. Our Mayor is opening Parks even though there are more than 10,000 infected. Cannot tell you where I work, but it rhymes with Parks.

All the best, and God Bless, Dennis

Michael writes:

Hi Cool Twiv I have been listening to your podcasts for the last five weeks and enjoying them very much.

It is so nice to hear intelligent no nonsense informed conversation. Its been reported here in the UK that there  is a higher rate of deaths from Covid 19 in the black and ethnic community, could this be due to low levels of vitamin D.  

Regards

Michael

CZ writes:

Hello there! 

I enjoy listening your podcasts very much. Thank you very much for providing this very informative resource for everyone. I am not a scientist but a communication scholar who is very interested in science communication. As it is probably very obvious, even though we are living in a technologically advanced society, science literacy is a major problem in our politics, culture and social relationships. So I appreciate your efforts.

Anyway, my question is about the vaccine that just started to be tried on human volunteers probably today. The vaccine was developed in under three months by a team at Oxford University. Sarah Gilbert, who is a professor of vaccinology at the Jenner Institute, led the pre-clinical research. And she says that she personally has a high degree of confidence in the vaccine. So basically stated to The Times of London that she is 80% confident that the vaccine would work. They also hoped about a million doses could be ready by September. What do we know about this vaccine and can we expect it to be available by September?

🙂

I have not listened to your podcast today. Hopefully maybe you have already talked about this. I decided email you anyway since I won’t be done with my teaching on Zoom until 5:30 today.

All the best,

CZ

Betsy writes:

Hi Twivsters!

I totally love your podcast, and am so grateful for a place to get clean, spin-free info about what’s going on.

Here in Glenview IL (Chicago ‘burbs), it’s cloudy and 50F.

Here’s my Q: On my local NPR affiliate, a guy from Harvard was asked about the possibility that SARS-CoV-2 could lie dormant and resurface every now and then, like Herpes or Hep C. His answer was basically, “we don’t really know,” and I am curious whether you all know if there’s any evidence of this being the case. That sounds like no fun at all….

Thanks for consistently presenting such a complex topic in a way that even I – an opera singing, skydiving MBA – can understand.

Thanks, and Blue Skies!

Betsy

Stephanie writes:

Dear TWiV folks,

Is there any evidence that those with existing blood clotting disorders are at higher risk for blood clots while infected by COVID-19?  I and (at least) four of my family members, have Protein S Deficiency.  Some of us are on anticoagulants for the duration and others of us are not.  What would you recommend to those with Protein S and C Deficiencies and Factor 5?  How do your recommendations change for those on anticoagulants vs. those who are not?

I hope you all are and remain healthy physically, mentally, and emotionally.

Thank you for all you do,

Stephanie

— 

Stephanie RiCharde, PhD

Assistant Professor

Psychological Sciences

University of Lynchburg

Jennifer writes:

Greetings to all:

Kostya Chumakov said:

1.The OPV may provide non-specific protection against SARS-CoV-2 AND

2.The MMR vaccine may provide similar non-specific protection

3. It is possible that kids may be a bit more protected against COVID-19 because their vaccines are more recent than the older population

It occurs to me that in the last year or so, a number of folks (born during or after 1957) got the MMR vaccine because they may never have received it as a child and because measles recently reappeared.

Question:

Would it be helpful for science purposes to look at the young-ish seniors who recently took the MMR series versus those who did not – and there are plenty who did not – to see if the recent MMR might have provided some protection against SARS-CoV-2?

While this may not be a true study, it may show some correlation that could be useful.  A simple questionnaire could be completed, possibly in the hot spot areas, to determine if these vaccines offered some protection.  While not everyone knows if they have contracted the disease, many certainly know if they DID and can say whether or not they had the MMR vaccine. 

Similarly, is there a place where people recently received the polio vaccine and would it be helpful to look at the numbers there too?

Please forgive if I have not asked this question in the best of scientific terms.  I am not a scientist…just a gal who listens and understands about 75% of what you are saying on your show but appreciates 100% of what you are saying and doing to promote understanding and to help find solutions.  God bless the nerds! 

Sincerely,

Jennifer W. (a nerd in her own kind of way) 

Ted writes:

Hi, virus experts – 

I listened to TWIV 604 with great interest. If I grasp the basic idea correctly, it is that attenuated-virus vaccines like OPV could provide some measure of protection against pathogens other than the ones they are designed for. Besides OPV, MMR was also mentioned.

So, let me ask a few naive questions about Zostavax, which I believe is an attenuated-virus product meant to convey immunity against shingles. Mightn’t this possibly do the same sort of thing?

Mightn’t there be data in existence which bear on this question, since (unlike OPV) Zostavax has been administered to large numbers of elderly people in the US (and where else?) in recent years? Might it not be possible to determine whether people who got it in NYC (say) are doing better with regard to COVID-19, controlling (yes I know this is necessarily imperfect) for other factors?

Would it be a good idea in taking medical histories of patients with COVID-19 to take note of whether and when they have gotten recent immunizations (yellow fever also comes to mind) and which? (Is this already being done?)

Naturally I suppose that probably there’s a reason known to experts why this goes nowhere, but since you are still accepting emails, I’ll take advantage. Thanks for all you are doing!! –

Ted 

Chicago

John writes:

Hello twiv crew.  

The hypothesis discussed in Twiv 604 regarding non-specfic innate immune boost from “live virus” OPV vaccination raise the question, what about “flu-mist” live virus flu. The study of flumist includes extensive controlled monitoring of respiratory infections in recipients. Does anyone know if Flumist induces non-specific resistance to “off target” viruses. Could Flumist reduce SARS-cov2 infectivity?  Just a thought.

John Terry MD

More OPV questions, answered by Kostya:

Mary Lu writes:

I’m not a health professional or scientist but I love your podcast and am learning so much! I listened to the recent one with Kostya Chumakov on the possibility that OPV could provide protection for SARS-CoV-2. I am wondering: is this possibly why India still has such a low amount of mortality due to this virus? That is a country of over a billion, the cities are very crowded and there is often little access for many to soap and water for handwashing. But they have had an aggressive campaign for years to eradicate polio there using types of OPV. Thanks! Mary Lu

Kostya’s answer

Indeed, this may be the case. A similar hypothesis was proposed to explain lower COVID-19 incidence in countries using BCG. However, another explanation that is also very likely is that in these countries, and India in particular, there is a higher prevalence of viral and bacterial infections, that continuously “train” innate immunity. One good example of this is the situation with polio eradication 10-15 years ago in northern Indian provinces of Bihar and Uttar-Pradesh. The seroconversion rate after one dose of OPV was as low as 8%, requiring repeated immunizations that produced additive effect. To reach the 85-95% population immunity needed for poliovirus to stop circulating they had to implement 10 sub-national immunization days on which they’ve immunized all children under the age of 5. Thus by the age of 5 children have received up to 50 doses!  The likely explanation is the so-called chronic tropical entheropahy caused by persistent bacterial diarrhea. Other live enteric vaccines such as rotavirus vaccine also have low efficacy in these populations. It is not unreasonable to think that living in the environments with poor sanitation has the unexpected benefit, and may protect against some pathogens. And of course we do not know what role the gut (and possibly respiratory tract) microbiome can play in susceptibility to these viruses. 

John Terry MD writes:

The hypothesis discussed in Twiv 604 regarding non-specfic innate immune boost from “live virus” OPV vaccination raise the question, what about “flu-mist” live virus flu. The study of flumist includes extensive controlled monitoring of respiratory infections in recipients. Does anyone know if Flumist induces non-specific resistance to “off target” viruses. Could Flumist reduce SARS-cov2 infectivity?  Just a thought. John Terry MD

Kostya’s answers

This is probably true for FluMist as well. There is a 2018 study from South Korea that claims that FluMist protects mice against respiratory syncytial virus, a completely unrelated pathogen. Inactivated Flu vaccine did not have this effect. It would be important to expand these observations to humans. If anyone at MedImmune or AstraZeneca as they are now called, is listening, they may want to consider this. 

David Spector writers:

I just finished listening to TWiV 604 with Kostya Chumakov and it blew me away!  

Given the general mechanism that he is proposing involving innate immunity, here are some questions:

Do you think that recent infections with other viruses could produce a similar protective effect?  

Might that explain some of the variability in people’s responses to SARS-Cov2 infections?  

If we knew that, would it identify another cohort of people among groups such as health care workers where such information could be useful in predicting who is more likely to be protected?

Is it worth doing retrospective studies to find out? Stay safe. Dave

Kostya’s answer

These are all very good points. Natural infections with wild viruses and bacteria could be expected to produce even stronger effect on innate immunity than live attenuated vaccines. So it may be that people who recently recovered from other infections could be partially protected against COVID-19. However this may be complicated by them being “weakened” by their disease. On top of that, some infections (such as wild Measles virus infection, but not live Measles vaccine) have immunosuppressive effect. But in general we know very little about population heterogeneity with respect to susceptibility to various infections. It would be nice to conduct a genetic association study among those who had severe, mild, or asymptomatic SARS-2 infection to identify genes responsible for different outcomes. I’ve seen a study on polymorphisms in ACE2 receptor gene that allegedly change the affinity for SARS-2 virus.