What should a convalescent patient be on the look out for in terms of a possible second phase/late rebound? Any sign of age or preexisting conditions as rush factors for this?
Dear TWIV contributors,
Thank you so much for all that you are doing to publicize the latest information on Covid-19 and virology in general!
I was listening to ep.631 with Daniel Griffin, and he mentioned that he’s starting to see some cases of reinfection now, which is obviously a troubling prospect. I’ve also been hearing anecdotes about people having positive PCR tests and later testing negative for IgG. So my question is, do we know if the patients coming in with reinfections are also testing positive for antibodies?
If they are IgG negative, that would seem to suggest that some people aren’t forming proper immune responses to the disease itself, but could a future vaccine in theory do a better job of getting them to produce antibodies than the disease?
If they are IgG positive, does that mean that their antibodies are simply ineffective at blocking the virus?
And I guess that leads to a broader question that I’ve been having over the past few months. When different people make antibodies for a disease, are they always the same chemical compound? Are some people’s antibodies more effective than others?
Ofer from Houston
Here is a link to an article titled “Coronavirus May be a Blood Vessel Disease, Which Explains Everything” by Dana G. Smith. This is in the health magazine Elemental, which is published on Medium. Smith is also a “health” writer for Scientific American. She is writing about the damage to endothelial cells in blood vessels. The title is click bait, but the article is responsible and well sourced. She writes…
A respiratory virus infecting blood cells and circulating through the body is virtually unheard of. Influenza viruses like H1N1 are not known to do this, and the original SARS virus, a sister coronavirus to the current infection, did not spread past the lung. Other types of viruses, such as Ebola or Dengue, can damage endothelial cells, but they are very different from viruses that typically infect the lungs.
I was wondering if you could comment on this. Is this correct? She links to journal articles including an article in The New England Journal of Medicine by Ackerman, et al. and in The Lancet by Varga, et al.
Maybe Daniel Griffin would weigh in? Would infected blood vessels in the lungs account for symptoms like “silent hypoxia,” for the multitude of small clots found on autopsy, and for what Dr. Griffin described in an earlier episode as symptoms more akin to altitude sickness than pneumonia?
Hi, TWIV Team. I’m a lay person but an avid TWIV listener. It’s reassuring to hear you talk in clear, practical terms about public health in such uncertain times. Plus, there’s always a surprise. I admired Peter Daszak’s artful descriptions of bat populations and the fragility of both frame and ecosystem in episode 623, and ep 609, where Susan Weiss talked about her history of studying coronaviruses.
My question is medical, and I guess because COVID-19 is new, there may not be an answer yet, but I will try anyway. I have an autoimmune disease–Graves’–and genetic markers, though asymptomatic, for antiphospholipid syndrome and lupus anticoagulant. I’ve never had a thrombotic event, but worry that if I get COVID-19, the virus will trigger APS and I will quickly become critical. Should I be concerned, or is this another case of late-night Internet-induced medical terror? Also: what exactly happens in the body when one talks about an autoimmune disease “trigger” and a virus?
In my reading on APS, I was struck by how similar it sounds to symptoms some COVID patients experience after the cytokine storm. It’s all a fascinating puzzle, albeit one that sometimes keeps me up too late.
I’ll keep washing my hands, wearing a mask, and listening each week. Thanks!
The Singing Bone: A Novel (Regan Arts, March 2016)
I was listening to Daniel Griffin on episode 621 and in the section where he was talking about the early advice from Chinese docs to use ventilators early, he mentioned that this turned out to be probably bad advice because the outcomes for people on ventilators are so bad. I’ve heard the same from other healthcare sources, too.
My question is this: Is it the chicken or the egg? Does being on a ventilator itself cause problems or is it that in normal practice people are so sick when they are put on ventilators that their outcomes would be terrible anyway? In an earlier stage of the illness, before the patient actually requires a ventilator to live, why will it make someone worse?
Hey Twiv. It’s just been hailing here and now it’s stopped. I don’t think the temperature matters when it’s sunny one moment and hailing the next.
I thought I’d bring this study to your attention! This Wuhan study was first posted back on March 16th on medRxiv and interestingly found Blood Type O has decreased odds ratio, in agreement with the Italy/Spain data. They also claimed A had an increased odds ratio, though this wasn’t true of both their study populations so it wasn’t so clear…
Keep up the great work. Microbe.tv is my #1 source for Sars-CoV-2 information and it’s been super helpful.
Just listening to your newest podcast and hearing the question how vaccines will be delivered so that everybody in this world is able to get vaccination.
Interestingly, yesterday the European Union put forward an announcement that it will try to make sure that everybody has access to vaccination once available. So hopefully we can make sure that poorer countries also get access.
I hope you will go on producing this interesting Podcast. A lot to learn from there!
Many greetings from Germany,
Hello Vincent & the Viral Clan,
First, I want to thank y’all for the fantastic coverage that you folks are doing at covering this Covid thing from the many angles that you have. I first came to this podcast from listening to Vincent & Nils’ This Week in Evolution Podcast. I do my best to stay focused while listening to those podcasts but admittedly pass out from lack of intellectual oxygen when you do those deeper dives. I work in the practical side of health and the education I got for that, by nature, only skips stones off of evolution and viruses on its way to hands on work; I’m a Registered Massage Therapist. The colloquial nature of the This Week in Virology podcasts leaves me with not only enough breathing room to follow along for the whole thing but has also sparked some thinking of my own.
Here in Canada, there has recently been a [*bleep*]storm created by a politician for outing a doctor as being the catalyst for an outbreak of Covid19 in a community that had none. While the doctor was in the wrong for breaking isolation rules, sadly xenophobia is also rearing its Hydra-like head and making the situation even uglier. (This is the home of the TrailerPark Boys after all, and now it looks like they’re taking Meth; no doubt your POTUS is their current dealer.)
So . . . . the doctor hires an investigator . . . . who says he can’t be Patient 1 in this case because yada, yada, yada (you tell the story) . . . . but I can see weakness in the investigators argument too.
In the end it’s going to cost the people of that province gobs of money for all the lawyers and financial payment to the doctor should he be found not be the spark for the outbreak. All because some politicians can’t help but speak their minds before actually having a thought in them.
My question is: Would it be possible, by getting the unique genetic sequences from all of those in the infected cluster, to know if the doctor was patient A, who passed on the virus to B and then C and then D, etc? Or is the genetic timeline not distinct enough to stand up in court?
Thanks and please keep on doing what you’re doing; with your help one day I would like to be able to count myself as being a smarty-pants on this subject.
Hello TWiV team,
Thank you so much for all you do to discuss COVID and viruses from a critical and analytical perspective with simultaneous charisma. I am an alumnus from the University of Florida. I got both my bachelor’s and PhD from UF, and my PhD was in Microbiology and Cell Science. I spent almost all my time working at the Whitney Laboratory studying mosquito molecular biology and physiology. I remember seeing Dr. Condit during someone’s committee meeting or department seminar, and I remember thinking he was quite intimidating. This podcast has shown me that he is really funny and an amazing scientist. I hope I can meet him in person someday, even though he now lives in Texas.
My question is this: I want to have a career in science. I have no idea what I want to do. I would love to be a professor for the rest of my career but not need to run a lab and write grants, just teach. I know adjuncts do that, but I don’t want to be that for too long, just long enough to get a little experience. I would also like to stay in Gainesville. Do you guys have any insight on that?
If that is just a pipe dream, what would you recommend I do to get hired as a faculty? I worked for mosquito control for three years after getting my PhD, and am currently working with the USDA as a post-doc. Again, I don’t want to leave Gainesville. Any suggestions on how I can get myself noticed by the university to start working there?
Thank you so much for reading this. I deeply appreciate your wisdom and will hopefully get to hear back from you soon.
I was invited to an outdoor social distancing birthday party for my 70 year old father who is in cancer remission and has a weakened immune system. Any advice on whether non-essential gatherings like this are OK to attend or not? It will be outdoors, around 10 people or less keeping distance (not sure if everyone will be wearing masks though). Thanks!
Scott from Massachusetts
sorry about sending so many emails recently, the podcast is just engaging and I feel the need to participate sometimes. I am writing to ask about the global Virome Project, and my question is can citizen science/ non virologist help? In particular I know there many hunters who bring in several million wild animals annually that could help reduce sampling cost for the project. Additionally there are MANY scientists with animal samples in their freezers that they would be glad to part with. For example I know several people in my department with marine mammal tissue, bird blood samples and countless invert samples, is there a way we could contribute some of our old/spare samples to the project? lots of hands can make for light work, so please let me/ your listeners know if we could contribute and what samples they would want. For example my lab has several thousand bivalve (clam, oyster, scallop etc) samples from the last decade but i’m not sure if the global virome project would want invert samples or how many they would want. I Hope I can help!
School of Marine and Atmospheric Sciences,
Stony Brook University
Hi Vincent et. al.
Have been listening to TWIV and TWIM for about a year now and really enjoy the shows. You and your team are doing a great service for the wider scientific community.
Just finished listening to TWIV-621 this morning. I appreciate that there are not great studies to back up the efficacy of general mask wearing by the public to reduce SARS-CoV2 spread. However, I believe the anecdotal evidence is strong enough that I wish your team would more strongly urge listeners to wear masks rather than saying “it can’t hurt, and it may help” as was stated in response to a letter on that show.
I think some recent incident that occurred in Springfield, MO just after our state started relaxing the shelter-in-place orders suggests that masks can be highly effective. In case you are not familiar with the story, two hairstylists reported to work at a Great Clips salon while symptomatic with COVID-19. Between them, they exposed ~140 customers. More than 2 weeks later, none of the exposed patrons have tested positive. Both stylists were wearing masks as were the customers. Here’s a link to a news story about the incident.
Granted, we don’t know what kind of masks, although very few were probably N95s, or what the distancing guidelines were used in the salon, but it seems that even the simple cloth masks can be quite effective if 70-80% of the public wear them.
p.s. I drink out of my TWIM coffee mug every day.
Maureen Donlin, Ph.D.
Director, Master’s Program in Bioinformatics and Computational Biology
Biochemistry and Molecular Biology
Saint Louis University School of Medicine
Hi team TWIV,
I’m a PhD student finishing a dissertation in philosophy of science where I study the transfer of mathematical models across disciplines. Whenever Rich says “all models are false” it makes me squirm in the way I’m sure Vincent does when someone says “killing a virus.” I always respond in my head, “but that’s not a very precise way to use the word ‘false’!”
A classic problem in my area of expertise is “what is the relation between model and world, and how do scientists exploit that relation to learn about the world?” It seems that by definition models have to be unrealistic. Completely realistic representations of phenomena are useless for modeling – a classic analogy is how a one-to-one scale representation of England would be useless as a navigational map. So in one sense of false (where it means ‘unrealistic’), Rich is right. However, unlike with the sort of things we normally take to be ‘false’ (assertions, propositions, sentences), a model’s unrealisticness is a necessary condition for being useful for knowing something. By leaving out detail, a model is able to be especially useful, perhaps by highlighting the essential mechanism for producing some phenomena, or by showing only the relevant detail for navigating across England. Paradoxically, the more ‘false’ a model is in the sense of ‘realistic’, the more ‘true’ it is in some other sense; ‘explanatory’, ‘salient’, ‘understandable’. For this reason, us philosophers of science have (mostly) abandoned using the words ‘true’ or ‘false’ when theorizing about how models contribute to the growth of scientific knowledge.
If you all can get Rich to change his word usage I promise to correct my family whenever they tell me some disinfectant can “kill viruses”.
Hope that was insightful rather than pedantic, love your podcast!
There have been some questions about the scalability and stability of mRNA-based vaccines for SARS-CoV-2. This manuscript, which is from a couple of years ago, offers helpful information about the two: https://www.nature.com/articles/nrd.2017.243#ref-CR9
According to the article, mRNA production has a yield of about 2 g/L in multi-gram scale reactions. One of the major benefits of using bacterial expression systems to carry out production is that you don’t have the issues with immunogenicity that production of biologics using a mammalian cell line can cause. But, stability is a major problem – which one of you commented on. Formulations to improve stability are appearing, but they are not great. Once encapsulated in a lipid nanoparticle, the stability improves, but the drug still doesn’t have a great shelf life (6 months according to the article) and requires low temperatures to maintain it.
Veronika A. Szalai, PhD
Leader, Biomedical Microtechnologies Group
Microsystems & Nanotechnology Division
Physical Measurement Laboratory
National Institute of Standards & Technology
Hello TWIV, I am not a virologist or a physician, but just a neuroscientist. However, I have been listening to TWIV for quite some time, because my virologist wife made me. Your show is a true treasure and has even gotten me excited about viruses and not just as reagents for my neuroscience research. Your shows on COVID-19 have become essential listening for me, I especially like hearing from the frontlines from Daniel Griffin. I was curious about something. At least in some patients, COVID-19 seems to promote strokes, perhaps through infection of endothelial cells. I am wondering if this is an underappreciated aspect of all coronoviruses that use ACE2 as a mode of entry? Perhaps such an association could be pulled out of Jeff Shaman’s dataset?
Dear Professor Racaniello and Team,
I have been listening to “This Week in Virology” since the episodes that were in the 580s. I do hope that you will answer my question.
My question is….if heat is so important in the transmission of droplets and aerosol, then how can you explain what is happening in Arizona right now?
It is 108-degrees in Phoenix right now: https://www.google.com/search?q=phoenix%2C+arizona+temperature&oq=phoenix%2C+arizona+temperature&aqs=chrome..69i57j0l7.10158j1j7&sourceid=chrome&ie=UTF-8
Why is Arizona still seeing hundreds of deaths per day? https://www.google.com/search?sxsrf=ALeKk03ZnxLz9fJyecsIEaDG0cpR980Lww%3A1591911763704&ei=U6XiXtjNKsiVwbkPiP2ugA8&q=coronavirus+deaths+by+state+usa&oq=coronavirus+deaths+by+state&gs_lcp=CgZwc3ktYWIQARgBMgQIIxAnMgUIABCxAzICCAAyBQgAELEDMgcIABAUEIcCMgIIADICCAAyAggAMgIIADICCAA6BwgAEEcQsANQgu4JWPjzCWDXhApoAnAAeACAAUaIAacCkgEBNZgBAKABAaoBB2d3cy13aXo&sclient=psy-ab
No, I do not live in Arizona. I live in New Jersey, where about 3 of the 5 panelists live. I love the podcast.
a few months back you guys had a clinician (I think from TX) that couldn’t seem to understand pooled testing and dismissed them. Other countries have used them, and now it looks like they are finally getting imported into the US: https://marginalrevolution.com/marginalrevolution/2020/06/fda-allows-pooled-tests-and-a-call-for-prizes.html
AFAIK they date back to the 40s, but I’m too lazy to track down the citation 🙂
Hey Vincent, Kathy, Rich, Brianne et al,
What do you think of this paper? https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30937-5/fulltext
It suggests that SARS-COV2 might induce an endothelial cell infection and not just a respiratory infection.
Also this article https://www.nature.com/articles/d41586-020-01692-z says that, if it were indeed a vascular disease, it would explain why children seem to be less affected than adults.
Regarding this, I have some questions:
1. Do you think that this is possible?
2. If so, do you think it makes sense?
3. What should we be doing differently if COVID19 was indeed a blood vessel disease?
4. What other diseases behave like this?
I’m a CS student, and even though I’m a jack of all trades at heart, I don’t have the medical knowledge to tell if these articles make sense, therefore I ask.
It caught my attention; I guess that is because we all want there to be order and an explanation for the horror of this virus.
Anyway. Thank you for your time guys.
Keep doing the good work,
and please don’t follow Daniel’s example and get some sleep, okay? 🙂
We all are aware that people are more affected/infected with the seasonal flu and the common cold during the fall and winter months. My question is: Where are these viruses “hanging out” during the spring and summer?
I understand they are not alive but that under certain conditions, will disintegrate. For example, let’s say someone sits on a park bench during optimal conditions – his hands come in contact with the virus and he touches his face and contracts the virus. During less active conditions, another person sits on the bench, hands come in contact with the virus and he touches his face/mouth/nose. will he not get the virus??
Thank you for an explanation.
Fort Worth, TX
Given the importance of dendritic cells to antigen presentation, the tissue localization of dendritic cells and the normal route of exposure for many viruses through mucus membranes, wouldn’t cutaneous, subcutaneous, or mucosal inoculation be better than intramuscular injection in eliciting an effective immune response for viruses like Sars CoV2 and Influenza?
On a related note, Flumist was suspended for a couple of years because of its failure to produce a large increase in antibody titers vs intramuscular injection used in the standard flu vaccines. Could this lower antibody titer in serum samples be misleading?
Perhaps there is a tissue-specific immune response that makes serum antibody titers high against muscular injection (to protect against viremia) but relatively low against mucosal antigen challenge which would elicit some sort of other strong immune response in mucosal tissues which would not be as strong in serum antibody titers.
[vr: The ACIP voted to drop FluMist from the list of recommended vaccines starting in the 2016-2017 flu season after studies conducted by the CDC showed that the vaccine component that targets H1N1 flu viruses was not protecting people who got the vaccine. That decision was later extended to cover this flu season as well.
MedImmune believes it traced the problem to the virus used in the H1N1 component. It has replaced it, and testing in ferrets and in cells from human nasal passages suggests the new virus is more effective.] from https://www.statnews.com/2018/02/21/flu-flumist-vaccine/
A few episodes ago you talked about some patients with Covid19 (confirmed w/ a positive PCR), who then tested negative for IgG antibodies.
How do these individuals clear the virus from their system? Do you think it’s simply a matter of a faulty antibody test (even though some tests like Abbott are supposed to be 99.7% accurate)? Or, are they using some other part of the immune system like a combo of IgM and T cells? If so, what would you infer for these individuals in terms of future ‘immunity’/ability to fight off the virus? My understanding is that T-cells are actually longer lasting than antibodies?
(Asking b/c my husband and I were both very ill in March with classic Covid symptoms. He fought off the virus more quickly and produced antibodies (confirmed with an Abbott test). I took about 7 weeks to clear my virus, but tested negative for antibodies).
I understand that most if not all of the vaccines under development are using techniques that have never been used in vaccines in widespread use in humans previously. I find this fascinating and a wee bit worrisome.
First, am I incorrect in my assessment of the vaccines — virus vectors, mRNA/DNA, etc. Have they been developed and used previously?
Second, if it is the case that the vaccine form is novel for humans, should I be worried? 🙂
I am so happy to have found your podcast, even if 2/3 of every podcast soars over my head.
Hi TWIV team,
I especially enjoy learning about the immune system and how it works. My question is (for SARs-CoV-2 and in general), if the innate immune system effectively fights off an infection, and doesn’t need to “pull in” the active immune system in any substantial way, would that mean that there wouldn’t be any antibody production? Or at least antibodies that are specific to a given infection?
Not asking from the perspective of future “immunity” implications but rather understanding seroprevalence testing.
Dear TWIV team,
Hello from the UK! I’m a GP (primary care physician) working in Oxford. I’ve been listening to your podcast for a few years now since the initial SARS outbreak, and I’m extremely grateful to you all for doing such a great job keeping us informed about the current SARS-2 outbreak around the globe. As I’m sure you’re aware, the initial UK response to the COVID outbreak was pretty widely criticised both inside and outside of the UK, for being too slow to introduce lockdown measures, distribute PPE and ramp up antigen testing. We have only just today started to introduce contact tracing measures – more than a week AFTER the lockdown has started to be lifted. Sigh.
Daniel has done a great job keeping everyone up to date with the situation in hospital, and I thought I would add my experience as a non-hospital doctor. At the peak of the outbreak in the UK, I would estimate I was triaging 5 patients a day on average over the phone with COVID19 symptoms, and as far as I’m aware the vast majority never received confirmatory tests. As the weeks have gone on, this has dropped dramatically, which makes me wonder if the peak was many times higher than officially recorded (almost certain), but also if the decline in cases is steeper than officially recorded.
As the outbreak has gone on, we have seen the phenomenon of persistent symptoms including fatigue, myalgia, shortness of breath, chest pains, headaches and “soft” cognitive dysfunction (foggy but not overtly confused) often still troublesome more than 6 weeks after first getting ill. My observation of who we send to hospital is that it’s probably more based on frailty and co-morbidity than on the severity of the disease itself. I suspect we have quite a few young, fit and healthy patients who have stayed at home despite moderate or severe disease because their physiology can cope with it (and I suspect these are the ones we are seeing 6 weeks later still feeling bloody awful). We are also seeing a few patients who turn out to have pulmonary emboli but only presenting 6 weeks later with persistent breathlessness – unfortunately, the only way to find out is a CTPA scan, which has one of the largest doses of radiation of any of the scans that we do and I shudder to think how many lung cancers we are iatrogenically causing 10, 20 or 30 years down the line
The letter you read out about the difference between sensitivity, specificity, PPV and NPV was interesting – I’d like to point out that PPV and NPV are not only dependent on timing but on place too. A fact that we have to deal with in primary care constantly is that the PPV of any clinical symptoms or sign or investigation is considerably lower than for medics working in other settings. See someone in A&E with a headache? There’s a fair chance it might be a brain haemorrhage. See someone in primary care with a headache? 99.9% chance its benign. I’m sure its the same for COVID. Similarly the risk/benefit ratio of treatments is usually much worse. If you anticoagulate your COVID patients in ICU, you’re probably stopping many thromboses for every one haemorrhage you cause, but if we do the same for our community patients, the opposite is probably true. Anyway, enough rambling – I’d love to hear you actual experts talk now
One of the things I always wondered was why it is that people are so infectious in the pre-symptomatic stages? My common sense would think that coughing would be the most important factor in spreading virus, but by definition patients wouldn’t be coughing when pre-symptomatic. Is this because viral secretion is higher in the pre-symptomatic stages, or for some other reason?
We have also started to reopen schools here based largely on research out of UCL that showed that children were less susceptible to the illness and therefore less likely to spread it. I have to admit that the only place I have heard this stated is on the BBC news, and nowhere else. What’s your view on this?
Apologies if you’ve answered those questions already – I’m afraid I’m a few episodes behind. Keep up the great work and stay safe
Dr. Charlie Luo
Thank you so much for doing this podcast! I started listening to you guys a few months back when my wife suggested i take a listen. She is currently an immunology fellow and has been listening for quite a while, I’m an electrician and it become clear i may have missed a calling in my life. After a few of the letters read on the last couple of episodes being a bit targeted towards the information you’re putting out and somewhat on the brash side of things, i just wanted to write in with a Thank you!
You all do such a fantastic job of explaining what’s happening with this pandemic in a way that most lay people can understand, like myself. Lucky for me though, when its not broken down fully, to a way that i like to call “Barney Style”, i have my wife to fall back on to translate and obviously the world of Google when she’s busy doing Dr. things and ignoring my texts!
Whenever there is an episode with a ton of relatively easy information, i share it throughout my social circle to do my best to offset the spread of Covidiots. But being that i am a tradesman and former grunt in the Army, my circle tends to be a little less scientific and a little more conspiracy/MAGA! I really don’t know how you all are able to keep your cool demeanor when explaining off some of the conspiracy talk that comes up, it amazes me. My blood boils when i see that crap spreading like wildfire, so kudos!
Anyway, ill quit my rambling on and i look forward to the future topics of the show after the pandemic. Learning from you all has been a blast!
May I commend you on fantastic evidence-based coverage of the pandemic and a fantastic podcast in general. I was into Twiv before it was popular, I won’t use the above phrase with “cool” because Twiv was always cool.
I would like to suggest re-covering the news of the CDC mixing coronavirus PCR and antibody tests at an earlier time-stamp in a future podcast, perhaps after Daniel’s clinical updates. This way listeners who may not stay till the end will get to hear how an agency that is supposed to protect everyone (poor and rich, regardless of political party) is being run in such a way as to mislead and endanger the health of its citizens.
This is not about politics, this is plain and utter bullshit scientifically-speaking. Would you mix white and blue paint and call the original paint colour light blue? No. Would you mix water with motor oil and then use it in your engine? No. Then why are two separate tests being treated as the same thing?
If any business was run this way the executives would be fired and prosecuted, don’t believe me? Look up Theranos.
A lot of the political heat over the past decade is because people are angry. I get it, there has been a sense of stagnation in many people’s personal lives for a long time. Wage growth runs behind inflation, life is getting harder and more complex for most people. Values-systems are being challenged like never before. And now many jobs have been lost and society has been turned upside down.
None of the above negates the truth. If you die, you are dead. If you live, you are alive. The same for those around you, no person nowadays is an island. Verified evidence and understanding the truth are more important now than ever. Literally thousands may or may not die from decisions made now and evidence is the best available tool we have with which to make those decisions.
There is a virus, it spreads worse than wildfire, it has killed and may kill many more people depending on the actions we take. A virus does not care who you are, what ambitions you may have, because it doesn’t have a brain. The virus is selected for or against depending on its environment.
Who has the power to select against this virus? We do. Social distancing and Tetris work.
I live in Australia and cannot be prouder of how my countrymen have banded together to stop the spread of Coronavirus despite political differences and personal costs. The extent of outbreak has been much smaller than in the US and our country is beginning to open up with the sense that secondary outbreaks can be controlled, a semblance of normal life is getting closer. Our response has been by no means ideal but I can say I’m certainly happier here than in the US, even with my wife (also primary breadwinner in our household) soon to lose her job. Our economy will recover soon enough and she will be able to find work without fear of Coronavirus.
I am also a US citizen and have been appalled at the misinformation and willingness to let people die unnecessarily for the sake of political and economic gain. Economies may open up but people can still get infected, this is a biological fact.
You do not need a degree to be able to think critically, I should know, I used to be a labourer. Ask the question: What does this person have to gain if I believe what they say?
Being angry at change is normal, why not direct it at the cause of your anger and do something about it rather than let misinformation sway you to deeper anger? Would you let an unqualified builder build your house? Didn’t think so. Then why do we have number-fudgers in charge of an agency tasked with keeping you and I safe?
Be kind to Dickson!
Stay safe, stay healthy,
John from Melbourne
Hi TWiV team,
I found this short report from the JAMA Network: https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2765654?utm_source=Global+Health+NOW+Main+List&utm_campaign=d0fcb69ba6-EMAIL_CAMPAIGN_2020_05_26_01_24&utm_medium=email&utm_term=0_8d0d062dbd-d0fcb69ba6-3081125
In it, the authors report that they detected SARS-CoV-2 present in 6/38 patient semen samples collected during a cohort study in Shangqiu, China. However, they only seem to report performing qPCR on the samples. We know from TWiV that positive PCR results does not indicate the presence of virus. Am I missing something here?
What especially concerned me from the report was that the authors seem to cite the WHO as a reference for the support of their use of PCR to define the presence of SARS-CoV-2 in semen. (reference: World Health Organization. Clinical management of severe acute respiratory infection when novel coronavirus (nCoV) infection is suspected: interim guidance, 25 January 2020. Accessed April 14, 2020. https://apps.who.int/iris/handle/10665/330854.)
However, as far as I can tell, the cited WHO reference only recommends that laboratory confirmation of COVID19 diagnosis in the clinic should be done via PCR on nasal/pharyngeal swabs. Applying this recommendation to test whether virus (not RNA) is present in a sample appears to me to be a misapplication/misunderstanding of the WHO guidelines. While I’m aware that there is confusion regarding what positive PCR results mean (ie, presence of viral genetic material vs. replication competent virus), do you think that the WHO and other public health authorities need to clarify this when issuing guidelines?
Would appreciate to hear your thoughts on this. Thanks for all you do!
Recently discovered your podcasts and I am loving them!
Your latest podcast on bats and coronaviruses was of special interest to me as it vindicated my refusal to explore a cave in Guinea which was densely inhabited by bats. This was nine years ago and I still remember vividly entering this cave that was so full of guano that I promptly said – I don’t think this is a good idea I’ll wait for you outside – too much batshit in here.
Valerie (from Montreal)
I just wanted to say thank you for answering my questions. It is hard to find sources that will tell you the truth these days. The media is sugar coating everything so much it’s a miracle our phones aren’t in a diabetes pandemic.
P.S. That memorial day pool party in Lake of the Ozarks you were talking about wasn’t in Arkansas. It was in Missouri…about 50 miles from me. There were several venues on the lake that had pool parties that weekend. The largest one that had all the photos in national media was called Backwater Jack’s. I kid you not, the name of the pool party was “Zero Ducks Given” I’ve attached a picture of their advertisement for the party, along with a notice that my county’s health department informed them an attendee of the party did test positive for SARS-COV-2.
Hi Twiv team,
Thanks for your excellent work. Along with Christian Drosten’s podcastand the reporting in a select few publications capable of science journalism, this podcast has become a must-listen for me during the pandemic.
Just wanted to respond briefly, albeit as a science layperson. Daniel in his as usual excellent clinical update and Q&A briefly discussed a question about vitamin D and said even if it boosts immunity, boosting immunity might turn out to be problematic in the postviral stage of severe illness. I do not make any claims here, but would appeal to Brianne and ask whether this global picture of an immune response either being boosted or not might not be misleading.
For instance, promoters of vitamin D as an immune system regulator argue that it promotes both other-immunity and self-tolerance, and there is some suggestion vitamin D levels may negatively correlate with autoimmune inflammatory responses. Whether such claims are true or not (there does not seem to be enough evidence to make definitive claims), the point here is that the immune response is complex and manifold and it’s not necessarily accurate to conceive of it being boosted as a whole. I wonder if “immunomodulation” might not be a more general and appropriate term than “boosting”. And whether other immunomodulators that are widely used (cannabinoids, benzodiazapenes, etc.) might not have either welcome or deleterious effects.
There’s a brief layperson-oriented discussion of claims about vitamin D and COVID-19 in the most recent Guardian Science Weekly podcast (which is now twice weekly).
Re: Sweden responses. As this discussion appears bound to continue, can I make a plea for only reading contributions to the debate that cite evidence and omitting those that baldly say “so and so made a lot of false claims” without supporting justification?
Thanks again for the terrific contributions to science education,
I live in Wakayama JP with a population of 900,000!
Here all restaurants limit the number of customers and have seating and tables at a distance. City hall every other seat is blocked…folks bow no hand shaking and the culture emphasizes keeping distant.
The emergency announced by the PM Abe was met with thankfulness and as a result our numbers are very low nation wide. Wakayama 63 infected…3 deaths population as stated 900,000.
Your podcast is beyond wonderful and is a cool spring of wisdom in a desert of confusion and misinformation!
BTW Japan’s population is 126,000,000!
Again I wanted to say thanks for spending your time to share your expertise and help inform (and entertain) us non-virologists. It really is much appreciated.
I was just listening to TWIV617 and felt my heart sink when the letters about Sweden were being read out. I’m not going to try to second guess the politics or motivation of these contributors but it suddenly sounded very similar to the debate around Climate Change.
This is a subject I’ve followed since the mid-1980s and learnt a huge amount about the science (and I subsequently went back to Uni to do an Open University degree in Environmental Science) but probably just as much about politics :0(
I’m sorry to say your science of Virology is about to change forever. It has made the heinous mistake of supporting policy that impinges on those of a libertarian bent. They do not take this kindly and I can absolutely guarantee that huge sums are being spent by extreme political lobby groups and ‘think tanks’ to ensure that the general public are confused about the science of virology and even worse, confused about scientists’ motivations for trying to communicate it. There is a lot of bad reporting about science but there is also a lot of deliberately manipulated reporting about science.
You probably know about this but when it becomes personal it can be tough, as scientists like Michael Mann and Phil Jones (who had his email server hacked) discovered.
Love the podcasts (been listening to Twievo too).