SARS-CoV-2; CoVID-19; Coronavirus; Updates and Information

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[FONT=&quot][h=1]Phylogenetic network analysis of SARS-CoV-2 genomes[/h][h=2]Peter Forster, Lucy Forster, Colin Renfrew, and [FONT=hwicons !important][/FONT] View ORCID ProfileMichael Forster
PNAS first published April 8, 2020 https://doi.org/10.1073/pnas.2004999117


Significance[/h]This is a phylogenetic network of SARS-CoV-2 genomes sampled from across the world. These genomes are closely related and under evolutionary selection in their human hosts, sometimes with parallel evolution events, that is, the same virus mutation emerges in two different human hosts. This makes character-based phylogenetic networks the method of choice for reconstructing their evolutionary paths and their ancestral genome in the human host. The network method has been used in around 10,000 phylogenetic studies of diverse organisms, and is mostly known for reconstructing the prehistoric population movements of humans and for ecological studies, but is less commonly employed in the field of virology.
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[FONT=&quot][h=2]Abstract[/h]In a phylogenetic network analysis of 160 complete human severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) genomes, we find three central variants distinguished by amino acid changes, which we have named A, B, and C, with A being the ancestral type according to the bat outgroup coronavirus. The A and C types are found in significant proportions outside East Asia, that is, in Europeans and Americans. In contrast, the B type is the most common type in East Asia, and its ancestral genome appears not to have spread outside East Asia without first mutating into derived B types, pointing to founder effects or immunological or environmental resistance against this type outside Asia. The network faithfully traces routes of infections for documented coronavirus disease 2019 (COVID-19) cases, indicating that phylogenetic networks can likewise be successfully used to help trace undocumented COVID-19 infection sources, which can then be quarantined to prevent recurrent spread of the disease worldwide.
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An interesting article by Peter Forster of university of Cambridge was published in PNAS a couple of days ago. He tried to trace the root of genome type based on genomes from 160 patients.
 
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Open access↓↓↓
Phylogenetic network analysis of SARS-CoV-2 genomes
https://www.pnas.org/content/early/2020/04/07/2004999117

https://www.cam.ac.uk/research/news...nalysis-provides-snapshot-of-pandemic-origins
Forster and colleagues found that the closest type of COVID-19 to the one discovered in bats – type ‘A’, the “original human virus genome” – was present in Wuhan, but surprisingly was not the city’s predominant virus type.

Mutated versions of ‘A’ were seen in Americans reported to have lived in Wuhan, and a large number of A-type viruses were found in patients from the US and Australia.

Wuhan’s major virus type, ‘B’, was prevalent in patients from across East Asia. However, the variant didn’t travel much beyond the region without further mutations – implying a "founder event" in Wuhan, or “resistance” against this type of COVID-19 outside East Asia, say researchers.

The ‘C’ variant is the major European type, found in early patients from France, Italy, Sweden and England. It is absent from the study’s Chinese mainland sample, but seen in Singapore, Hong Kong and South Korea.

The new analysis also suggests that one of the earliest introductions of the virus into Italy came via the first documented German infection on January 27, and that another early Italian infection route was related to a “Singapore cluster”.

"...type ‘A’, the “original human virus genome” – was present in Wuhan, but surprisingly was not the city’s predominant virus type.

...

Variant ‘A’, most closely related to the virus found in both bats and pangolins, is described as “the root of the outbreak” by researchers. Type ‘B’ is derived from ‘A’, separated by two mutations, then ‘C’ is in turn a “daughter” of ‘B’."

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https://www.tabletennisdaily.com/fo...amp-Tokyo-2020&p=307118&viewfull=1#post307118
 
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Current COVID-19 situation in Poland can be traced here: https://pokazwirusa.pl/ (Potwierdzonych zakażeń - confirmed cases, Osoby wyzdrowiałe - cured cases, Śmiertelnych zakażeń - deceased (this metric does not follow WHO metric though, If sick had for example heart disease, they are not included, "because they might have died from accompanied disease")).

I will try to make this as politics free as possible.
Since quite a few of my clients work at new Cracow's University Hospital I have firsthand information and opinions. Ladies working there descrived COVID-19 as a bizarre disease. Patients typically have one of 3 forms they observed.

First one is really severe, patients need medical attention, but they are typically under control. Second one is when the patients are 70+ y/o and have other diseases and they die real quick in vain. The third one is most common and patients have little to none symptoms. One of those from last group had positive test but only had lack of smell and taste for one day. Really bizarre indeed.

Current hospital situation is even more bizarre. Since our ruling party had limited budget we had to help our heroes without capes in hospitals. A lot of restaurants give food to hospitals for doctors quite regurarly. A very big chunk (I would even say the most in case of small medical facilities) of self security equipment (masks, faceshields and suits) were fund by us, ctizens directly. Lot of private parties (motorcycles, a farmer wifes associations (actual thing here), faceboog froups) organized fundraisers. Some companies (MGHM copper, PGG, some actors and football players) funded stuff too for hospitals. The weird side of the coin is due to the fact that hospital staff got infected too, there are hospitals without doctors in Poland currently. Also getting medication prescriptions is pain in the butt too.

The executive power (Police and such) are abusing their power giving giant fines as big as 2500$ for very puny stuff like changing tires in car or not owning a mailbox (we never needed one previously for 100 years+, mailman just gave us mail or left it on the counter). For a few days washing your car was prohibited with a fine of 100$, but people called carwashes as self disinfection stations. Also at the same time current ruling party is forcing president election (despite obvious dangers associated with it), not that money could spent on making sure hospitals are functioning, but let's not get too political.

TL;DR Currently in Poland we live in a live comedy, a real life comedy to be exact.
 
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The eggheads held a press conference on this "big-deal" finding just several hours ago. Doctor Yuen likened COVID-19 to a "ninja" where the human immune response, such as interferon and inflammatory cytokine, is suppressed, in stark contrast to SARS. That's why there are so many asymptomatic patients walking around. SARS was contained within 6 months by isolating those with fever, pneumonia and close contacts. That won't work with COVID-19. The measures of wearing masks, washing hands and social distancing etc. are only to help carry on our daily lives and keep the healthcare from getting overwhelmed, the fates that befell the US and UK. Therefore, it's not realistic to expect this pandemic to "magically disappear" this July.

Comparative replication and immune activation profiles of SARS-CoV-2 and SARS-CoV in human lungs: an ex vivo study with implications for the pathogenesis of COVID-19
https://academic.oup.com/cid/advance-article/doi/10.1093/cid/ciaa410/5818134?searchresult=1

Coronavirus that causes Covid-19 can produce more than three times as many pathogens than Sars strain, HKU study reveals
https://www.scmp.com/news/hong-kong.../coronavirus-causes-covid-19-can-produce-more
The findings also proved that a cocktail therapy by Hong Kong medical practitioners is going in the right direction to induce an immune system response, Yuen added. Doctors have been prescribing a cocktail of lopinavir and ritonavir along with interferon beta.

“It appears from our preliminary results that the beta-interferon is the backbone, the most important component of this therapy,” Yuen said.


Alternative video source:
https://www.facebook.com/RTHKVNEWS/videos/港大微生學系講座教授袁國勇團隊記者會現場直播/2630152153773219/
 
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The eggheads held a press conference on this "big-deal" finding just several hours ago. Doctor Yuen likened COVID-19 to a "ninja" where the human immune response, such as interferon and inflammatory cytokine, is suppressed, in stark contrast to SARS. That's why there are so many asymptomatic patients walking around. SARS was contained within 6 months by isolating those with fever, pneumonia and close contacts. It won't work with COVID-19. The measures of wearing masks, washing hands and social distancing etc. are only to help carry on our daily lives and healthcare from getting overwhelmed, the fates that befell the US and UK. Therefore, it's not realistic to expect this pandemic to "magically disappear" this July.

Comparative replication and immune activation profiles of SARS-CoV-2 and SARS-CoV in human lungs: an ex vivo study with implications for the pathogenesis of COVID-19
https://academic.oup.com/cid/advance-article/doi/10.1093/cid/ciaa410/5818134?searchresult=1

Coronavirus that causes Covid-19 can produce more than three times as many pathogens than Sars strain, HKU study reveals
https://www.scmp.com/news/hong-kong.../coronavirus-causes-covid-19-can-produce-more


Alternative video source:
https://www.facebook.com/RTHKVNEWS/videos/港大微生學系講座教授袁國勇團隊記者會現場直播/2630152153773219/

The issue of SARS-CoV-2 being able to evade immune surveillance in part by suppressing interferon production (which was suggested by other studies too) MAY be a reason why ivermectin could be useful clinically Also interferon beta infusion which is currently in clinical trial for Covid-19 and probably already done in a lot of hospitalized patients (as I think was already mentioned by passifid).

There are lots of other ideas out there for how to deal with seriously sick Covid-19 patients, including anti-TNF therapy and JAK/STAT inhibitors.

To Zeio, the "eggheads" as you call them are the ones who will find so,utions to coronavirus infections (and dont think this will be the last one that jumps into people). Im often amazed by how many languages you know, but this us a bit subtle. In English the term has always had a somewhat belittling connotation and was once widely used by corporate types who consider the scientists to be lowly hired help.
 
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The eggheads reference are by intention to differentiate them from the stable genius.
 
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Obesity is a high-risk factor for SARS, not surprisingly for COVID-19. I am not sure there have been studies to correlate obesity alone with poor prognosis of COVID-19 but I feel there will be a statistical significance. I do know BMI is a factor for triage plan for ventilator/ECMO in US.

US CDC stats for Mar 1-30: among 1482 hospitalized COVID-19 patients, 12% had data on underlying conditions, 50% with hypertension and 48% with obesity (BMI>30).
https://www.cdc.gov/mmwr/volumes/69/wr/mm6915e3.htm


A small cohort (24) of critically ill patients in Seattle, BMI 33.2+/-7.2
https://www.nejm.org/doi/full/10.1056/NEJMoa2004500

UK ICNARC report on Apr 4: out of 2621 ICU COVID-19 patients, 35.7% with a BMI between 25-30, 30.7% with a BMI between 30-40 and 7% with a BMI >40.
For the outcomes, discharged alive from ICU vs died in ICU, BMI <25, 106 vs 82; BMI 25-30, 127 vs 110; BMI >30, 84 vs 114

As for China, BMI analysis of COVID cases or deaths is lacking. Obesity is not among the most common underlying conditions of 44672 cases: 10.5% cardiovascular disease, 7.3% diabetes, 6.3% chronic respiratory disease, etc.
https://jamanetwork.com/journals/jama/fullarticle/2762130

Or from this analysis of 168 deaths in China in Jan: Hypertension 50.0%, diabetes 25.0% and ischemic heart disease 18.5%.
https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2764293


My musings were about Dutch statistics. Probably less obesity, and certainly less morbid obesity, than across the pond(s).

As for blaming the victim, I merely stated my mild surprise at a reported correllation — for the Dutch situation only, since I’ve found nothing of the sort mentioned elsewhere. I did not mean to suggest a strong relation - a causal one, for example.

And yes, I am aware of the strong relation between obesity and type 2 diabetes (and related). And yes, I do know about comorbidities; but I had not seen BMI isolated in a statistical correlation this directly.
 
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Are you still able to do your research now? My institution (Dallas) has shut down all non-essential research for weeks, me included :p Although Houston and Dallas being the hot spots in TX, things seem not too bad. The affiliated hospitals with my institution have quite a lot beds available.

Haven't checked TTD for a while. Hope that every one stays safe and healthy.

I'm not an MD. I am a PhD (in pharmacology) and I do medical research. I can't really advise you on that. Bear in mind that it is completely unproven.
 
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I didnt know you were in Dallas.

We are shut down too, for 3+ weeks now.

There is still hospital capacity in Houston, which is a little hotter of a Covid-19 spot than Dallas at the moment, but my colleagues are nervous that this could change quickly. As you know, in Texas testing is at best sporadic. Fortunately local authorities in Dallas and Houston took some earky actions on their own that have helped. Hopefully the governor won't do anything to overrule them.
 
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~10% tests in TX returned positive, much lower than NY (41%) and NJ (48%). But of course, more tests are better.


Dallas county has reported 1644 cases, 27 deaths, and 2 recovered while the neighboring Collin county 425 cases, 7 deaths and 194 recovered. I don't think Dallas has inferior healthcare system compared to Collin. The difference may come from (1) Dallas doesn't have enough public health workers to keep track of confirmed cases and don't know the outcomes (considering that most cases are self-isolating at home) (2) Collin has loose criteria for the recovered. They may consider one as recovered when symptoms are gone without actual testing. It takes quite long before a recovered person stops shedding viruses and it is not safe to think such patient not contagious. Nevertheless, TX needs to do a better job to test/trace/treat.


Now most people in US get 1 test (if any) and that's all. It is concerning to me. The experience from China said the detection of viral RNA from swabs (BALF much more accurate but invasive) relies on the timing and sampling. A negative result 3 days ago (my coworker did a drive-through test in Dallas and got the result 3 days later, which is quicker than avg turnover time in US) didn't guarantee a negative result today. Also not all hospitalized COVID patients in US get RNA tests before discharge (most countries use 2 negative tests 24 hours apart as the criteria). One of my friend in NYC got COVID; he was hospitalized for 10 days and then discharged without RNA test; he is doing well now but cannot take a flight because he was put on the no-fly list when he tested for COVID the first time. Another case I heard is in MN that a COVID patient died the same day after discharged from the hospital when the symptoms seemed reduced without RNA test.




I didnt know you were in Dallas.

We are shut down too, for 3+ weeks now.

There is still hospital capacity in Houston, which is a little hotter of a Covid-19 spot than Dallas at the moment, but my colleagues are nervous that this could change quickly. As you know, in Texas testing is at best sporadic. Fortunately local authorities in Dallas and Houston took some earky actions on their own that have helped. Hopefully the governor won't do anything to overrule them.
 
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The official numbers in Greater Houston area this morning are 5,293 cases, 81 deaths, 890 recovered. That encompasses several counties. In the city of Houston proper it is supposedly 2,124 cases, 16 deaths and 214 recovered.

In reality it is pretty much impossible to know how many people are walking around with this and I don't know what criteria are being used for recovered (or if there even is one consistently used). Are deaths being undercounted? Very possible. But at the moment it's not like NYC here. I also cant get a good feel for where we are in the progression of this epidemic here, i.e closevto the peak or not.

Edit added. Only 332 tests for every 100,000 people in Texas (49th of 50 states), so the # infected stats here are not to ge believed.
 
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Let's hope that is true everywhere, but I wouldn't minimize this. It's worth noting that 4,000 people died of this in the US in two days, and that is probably an undercount.
I don't think it is minimization but we need to be clear about what we are really doing here. Is there something extra that a lockdown is getting us over just social distancing, face masks and enhanced hygiene? If so what is it and how long should the lockdown last?

The virus is already all over America. If we lockdown until we get a vaccine, it may cost us way more in social issues and silent deaths than the people who have died so far, many of whom would likely have died anyways.
 
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Open up too soon and it comes back with a vengeance setting us back further by every consideration. The problem is that we are flying blind, at least in the US. We have no strong data on where we are just yet. How many people have or have had this virus? What are the rational criteria needed to decide when it is reasonable to relax the more severe social distancing guidelines? We need something other than the intuition of politicians who have financial interests at stake and who have very bad track records in responding to this so far. We obviously can't lock down until we get a vaccine, that's for sure. Nobody has or should suggest that.

But the decision on when to open needs to be made on the basis actual science. More analyses on the prevalence of SARS-CoV-2 antibodies in the general population would definitely help, and we need to get the overall case load down to the point where hospitals can cope and healthcare providers dont have to beg for protective gear the need. As of the time I am writing this, we are not at that point.

A lot of people minimized this from the start. I was never one of them. One guy at MyTT predicted there would be 1,000 fatalities in the US. We got that many in 12 hours yesterday.
 
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https://www.nih.gov/news-events/new...antify-undetected-cases-coronavirus-infection
NIH is working on a serosurvey for ~10k volunteers (confirmed COVID cases excluded) for ELISA test on IgM/IgG. Before this study is done, I don't see any scientific evidence that US is ready to think of "reopen".
Officials keep saying antibody test will solve the problem: who is ready to go back to work. Scientists don't say so but get ignored/twisted (4.10 Fauci CNN interview). Luckily my institution knows the situation and does not rush to reopen.
When is the time to reopen? It not only depends on massive and rapid testing, but also the measures to reduce exposure especially for those in essential jobs who contact many many people a day. Give them PPE not just home-made cloth facial coverings! Also more PPE to front line healthcare workers! I always don't get why CDC made those stupid guidelines like reusing masks after H2O2 sterilization and why hospitals follow... The trash bags are more protective than the gowns that NY nurses are wearing... T_T
 
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We're contingency planning on how to teach first year medical students this summer in case we need to still use some sort of social distancing.

I agree 100% with the previous post. State authorities should probably do similar screens on as big a scale possible once NIH proves the concept.
 
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