Go Back  FlyerTalk Forums > Miles&Points > Coronavirus and travel
Reload this Page >

Coronavirus / COVID-19 : general fact-based reporting

Coronavirus / COVID-19 : general fact-based reporting

    Hide Wikipost
Old Apr 4, 20, 5:06 am   -   Wikipost
Please read: This is a community-maintained wiki post containing the most important information from this thread. You may edit the Wiki once you have been on FT for 90 days and have made 90 posts.
 
Last edit by: username
Wiki Link
PLEASE READ BEFORE POSTING
This thread has become a valuable resource on Corona Virus/COVID-19 in general and no longer just about its impact on China travel. In order for the thread to remain fact-based and useful, posters are reminded to keep it free of speculation, conjecture and fear-mongering. Posts which do not meet these guidelines or which break the FT rules may be edited or deleted. Please observe the following FT rules in particular:

- be respectful and helpful
- stay on topic
- posts must be contributive to the thread
- inflammatory, inciting or unnecessarily provocative posts are not allowed
- repetitively posting comments of the same general theme is not permitted
- abusive, hateful, threatening, harassing or otherwise offensive posts will not be tolerated
- do not post comments on moderator decisions

FlyerTalk Senior Moderator Team

The following two links are updated daily:
IATA international transit / arrival policies Coronavirus Outbreak - Update
WHO Coronavirus disease (COVID-19) situation reports

Counters / Meters : Other Discussions on FlyerTalk Pertaining to COVID-19:

General (in this forum)
Location-specific
Airlines
Hotels
Other
Please add other discussions on FlyerTalk pertaining to COVID-19 not already been included in this WikiPost. Thank you.


Print Wikipost

Old May 30, 20, 9:50 am
  #5371  
 
Join Date: Mar 2005
Programs: Continental Onepass, Hilton, Marriott, USAir and now UA
Posts: 3,993
New article from the WSJ on the origins of the Covid virus. Unfortunately behind a pay wall but someone may know a work around.
https://www.wsj.com/articles/so-wher...om-11590756909

The Lancet article on hydroxychloroquin gets a correction but no change in the author's conclusions.

While I referenced a Buzzfeed article on the correction, I do recommend looking at the original correction for which there is a link in the journalist's paper. I would not rely on Buzzfeed's analysis of anything as the final word.
https://www.buzzfeednews.com/article...-letter-lancet

As I wrote in an earlier commentary about the Lancet report, it was a registration study, not a randomized controlled study and therefore would suffer the defects inherent in any registration study, which includes investigator bias, inaccurate registration and imbalanced participation groupings, to name a few.

There are always dangers in relying on incomplete studies to make treatment decisions. If the POTUS had never mentioned the drug, no one would have cared about it, TBH.
.

Last edited by NewbieRunner; May 31, 20 at 10:27 am Reason: Merge consecutive posts by same member
radonc1 is offline  
Old May 30, 20, 11:05 am
  #5372  
Suspended
 
Join Date: Oct 2004
Location: Bay Area
Programs: DL SM, UA MP.
Posts: 12,730
Originally Posted by radonc1 View Post
New article from the WSJ on the origins of the Covid virus. Unfortunately behind a pay wall but someone may know a work around.
https://www.wsj.com/articles/so-wher...om-11590756909
Summary?
wco81 is offline  
Old May 30, 20, 11:16 am
  #5373  
 
Join Date: Dec 2018
Location: PHX
Programs: Delta DM, Marriott Lifetime Titanium, HHonrs Diamond
Posts: 1,160
Originally Posted by wco81 View Post
Summary?
It is an opinion piece by a single author.
I read it and cannot find a free link, but here is the take home point....

The closest animal version of the virus remains a bat sample collected by scientists in 2013 a thousand miles away in Yunnan. Details of where and how that sample was collected have been sketchy, but a new paper by two scientists from the Agharkar Research Institute in Pune, India, show that it is the same as a published sample with a different name that was collected from an abandoned mineshaft in southern Yunnan in 2013, following an outbreak of pneumonia-like illness that killed three miners there the year before. But that virus cannot be the immediate source of Covid-19. Part of one of its key genes, coding for the “spike” protein that allows the virus to lock onto human cells, is distinct from the version that is causing the pandemic. In the human virus, this part of the gene, called the “receptor binding motif,” more closely resembles the virus found in smuggled pangolins, though the rest of the pangolin virus is less similar. Compared with the bat and pangolin viruses, the one now infecting human beings also has an extra 12-letter nucleotide sequence, called a “furin cleavage site,” in the spike protein gene; this greatly enhances the virus’s ability to get into and out of different types of human cells. Kristian Andersen of the Scripps Institute in La Jolla, Calif., and colleagues argue that this might have arisen by mutation during “a period of unrecognized transmission in humans” after the original transmission from an animal.
...
So what did happen? At present, the evidence is pointing tentatively to a chain of person-to-person infections occurring somewhere outside a city before somebody brought the virus to Wuhan, where the market acted as an amplifier. The first case could have been a rural farmer or possibly a bat researcher collecting samples for virologists. Or it is possible that another animal was involved in some way, with the virus bouncing between a farmer and his animals, or a wildlife smuggler and his poor pangolins.
MSPeconomist likes this.
FlyBitcoin is offline  
Old May 30, 20, 8:34 pm
  #5374  
 
Join Date: Aug 2014
Location: 42.1% in PDX , 49.9% in PVG & 8% in the air somewhere
Programs: Marriott Ambassador Elite, UA 1K, AS MVP GLD 75K, DL Pt
Posts: 1,051
Originally Posted by FlyBitcoin View Post
It is an opinion piece by a single author.
I read it and cannot find a free link, but here is the take home point....
Originally Posted by wco81 View Post
Summary?
1) The SARS-CoV-2 has very little genetic diversity compared to the SARS-CoV at the same early / middle stage of infection --> Implies when it came to Wuhan it had already genetically mutated to it's current state that made it highly effective for human-human transmission
2) The timeline for genetic evolution suggests a window from October - December --> The virus was mutating quietly before getting the features it needed for the highly contagious version we have.
3) Core of virus is closet to bat, the spikes are closely related to those from pangolins, but the core is NOT.
4) The current virus has another sequence very different from both the bat and pangolin

Model that there was a long chain of person to person outside of the city where the virus mutated to the current highly effective structure making it so suited for infections human-human. Then it was finally brought to Wuhan and the crowded market where that mutated / effective version soon became the Pandemic.
chipmaster is online now  
Old May 31, 20, 7:41 am
  #5375  
Ambassador: Emirates Airlines
 
Join Date: Sep 2004
Location: Manchester, UK
Posts: 15,056
This is frightening...

DYKWIA is online now  
Old May 31, 20, 5:27 pm
  #5376  
FlyerTalk Evangelist
 
Join Date: Jun 2005
Posts: 33,314
Originally Posted by DYKWIA View Post
The number of deaths doesn't matter. What matters is how much community spread--and from what she said it sounds like that is high, but there was no indication as to where those new cases were.
Loren Pechtel is offline  
Old Jun 1, 20, 8:52 am
  #5377  
 
Join Date: Mar 2005
Programs: Continental Onepass, Hilton, Marriott, USAir and now UA
Posts: 3,993
More data on efficacy of Remdesivir. From a Gilead press release
June 01, 2020
Gilead Announces Results From Phase 3 Trial of Remdesivir in Patients With Moderate COVID-19


" The study demonstrated that patients in the 5-day remdesivir treatment group were 65 percent more likely to have clinical improvement at Day 11 compared with those in the standard of care group (OR 1.65 [95% CI 1.09-2.48]; p=0.017). The odds of improvement in clinical status with the 10-day treatment course of remdesivir versus standard of care were also favorable, trending toward but not reaching statistical significance (OR 1.31 [95% CI 0.88-1.95]; p=0.18). No new safety signals were identified with remdesivir across either treatment group. Gilead plans to submit the full data for publication in a peer-reviewed journal in the coming weeks."

Hopefully, by Fall, we should have several treatments for the illness itself, even without a vaccine.
ajGoes likes this.
radonc1 is offline  
Old Jun 1, 20, 9:04 am
  #5378  
 
Join Date: Dec 2018
Location: PHX
Programs: Delta DM, Marriott Lifetime Titanium, HHonrs Diamond
Posts: 1,160
Convalescent serum works well, but is limited by supply: https://www.cbsnews.com/news/coronav...es-2020-05-31/

Also, graph of survival rates...
ajGoes likes this.
FlyBitcoin is offline  
Old Jun 1, 20, 11:19 pm
  #5379  
A FlyerTalk Posting Legend
 
Join Date: Aug 2002
Location: NY Metro Area
Programs: AA 2MM Yay!, UA MM, Costco General Member
Posts: 43,987
Originally Posted by FlyBitcoin View Post
Convalescent serum works well, but is limited by supply: https://www.cbsnews.com/news/coronav...es-2020-05-31/

Also, graph of survival rates...
https://twitter.com/EricTopol/status...92481072160771
They are working on supply. I had an antibody test done by a hospital system and part of the consent form was asking if we could be recontacted if positive for convalescent serum donation. It wasn’t required but I suspect most people in the NYC area are checking yes on the forms.
GadgetFreak is offline  
Old Jun 2, 20, 3:01 am
  #5380  
Hilton 5+ BadgeAccor 10+ Badge
 
Join Date: Nov 2012
Location: Rhineland-Palatinate
Programs: OW Sapphire (BA), *A Gold (A3), Le Club Accor Gold, HHonor Diamond
Posts: 2,916
A peer-reviewed statistical study from the RHEUM-COVID registry was published this week-end:
https://ard.bmj.com/content/early/20...is-2020-217871

Results: A total of 600 cases from 40 countries were included. Nearly half of the cases were hospitalised (277, 46%) and 55 (9%) died. In multivariable-adjusted models, prednisone dose ≥10 mg/day was associated with higher odds of hospitalisation (OR 2.05, 95% CI 1.06 to 3.96). Use of conventional disease-modifying antirheumatic drug (DMARD) alone or in combination with biologics/Janus Kinase inhibitors was not associated with hospitalisation (OR 1.23, 95% CI 0.70 to 2.17 and OR 0.74, 95% CI 0.37 to 1.46, respectively). Non-steroidal anti-inflammatory drug (NSAID) use was not associated with hospitalisation status (OR 0.64, 95% CI 0.39 to 1.06). Tumour necrosis factor inhibitor (anti-TNF) use was associated with a reduced odds of hospitalisation (OR 0.40, 95% CI 0.19 to 0.81), while no association with antimalarial use (OR 0.94, 95% CI 0.57 to 1.57) was observed.
Rather good news for people under biological therapy.
FAA1996 likes this.
fransknorge is offline  
Old Jun 2, 20, 6:09 am
  #5381  
 
Join Date: Mar 2011
Location: BDL, JFK
Posts: 619
Originally Posted by fransknorge View Post
A peer-reviewed statistical study from the RHEUM-COVID registry was published this week-end:
https://ard.bmj.com/content/early/20...is-2020-217871



Rather good news for people under biological therapy.
In our 200 plus HIV patients we have had illnesses but no deaths. This seems to be what others have observed anecdotally and it is being actively studied: https://www.fredhutch.org/en/news/ce...v-seattle.html
ajGoes likes this.
Robl is offline  
Old Jun 2, 20, 8:29 pm
  #5382  
Suspended
 
Join Date: Oct 2004
Location: Bay Area
Programs: DL SM, UA MP.
Posts: 12,730
Preprint of famotidine study available. Derek Lowe summarizes:

As this new work details, an initial hypothesis was that the compound had some effect on one of the viral proteases, and you can still find that rationale if you start looking around for comments on the drug’s MOA. That hasn’t held up, though – the compound does not seem to be an inhibitor of these enzymes. Moreover, it is not effective in a cell-based infection model with the virus, either – basically, it’s not an antiviral in any sense of the term.

What does that leave you with? The downstream effects of being infected – all the cytokine storm stuff, the inappropriate immune response that gets so many patients into trouble. And that brings the histamine receptor mechanism back around again. The paper confirms that famotidine is a much more potent H2 ligand than is cimetidine (technically, it’s more of an inverse agonist than a classic antagonist), and moreover it seems to have different consequences on receptor binding. It seems to stimulate beta-arrestin binding to the receptor and subsequent internalization (a mechanism that complicates all sorts of G-protein coupled receptor signaling), and it appears that cimetidine doesn’t do this, either. There is also a possibility that the compound acts on the CCR2L and CXCR3 chemokine receptors, which would certainly be of interest, but this needs to be firmed up.

But one of the biggest differences between famotidine and cimetidine is in their pharmacokinetics. As the preprint illustrates, the higher potency and better blood levels of famotidine mean that it has much stronger coverage of the H2 mechanism in general, especially at the dosages that seem to have an effect in coronavirus infections. So here’s the paper’s mechanistic summary:

The most straightforward explanation of the apparent famotidine activity as a COVID-19 therapy is that the drug acts via its antagonism or inverse-agonism of histamine signaling and via its arrestin biased activation—all a result of its binding to H2. If true, then it is reasonable to infer that a SARS-CoV-2 infection that results in COVID-19 is at least partially mediated by pathologic histamine release.
That’s an interesting and plausible idea – mast cells are what are involved in sudden histamine release – they’re sitting there loaded up with granules of the stuff, which can be dumped out on short notice. That’s an important part of a sudden anaphylaxis reaction, and mast cells are also involved in other immune response pathways, tissue permeability, and other processes. It’s certainly possible that they could be part of the inappropriate response to coronavirus infection and that inhibiting histamine release could be beneficial. The paper goes into details about lung physiology that tie the receptor’s action to some of the pathology seen in patients – for example, one thing that’s been noted is a lack of neutrophils and eosinophils in lung tissue samples, and both of these cell types have their activities inhibited by histamine release. In addition, the edema seen in coronavirus-affected lung tissue is unusual by the standards of viral infection, but makes more sense in light of a histamine-driven response. Mast cell degranulation also matches up with some of the other well-known symptoms (effects on smell and taste sensation, etc.)

The authors advance the idea, then, that many of the unusual features of the current virus in the clinic can be tied to histaminergic effects, and finish up this way:

If COVID-19 is partially driven by dysfunctional mast cell degranulation, then a variety of medical interventions employing marketed drugs useful for treating mast cell-related disorders may help to reduce death and disease associated with SARS-CoV-2 infection. Examples include drugs with mast cell stabilizing activity, other histamine antagonists (for example H1 and H4 types), leukotriene antagonists and leukotriene receptor antagonists, anti-inflammatory agents such as those developed for inflammatory bowel diseases, and mast cell activation inhibitors. If such repurposed drugs are used in combination with pharmaceuticals that directly inhibit SARS-CoV-2 infection or replication, it may be possible to rapidly develop potent, safe and effective outpatient treatments for preventing or treating COVID-19 until such time as a safe and effective SARS-CoV-2 vaccine becomes available.
https://blogs.sciencemag.org/pipelin...he-coronavirus

So no action on slowing or stopping viral replication as hoped. But it may suppress histamine release, which may account for the runaway immune response with the inflammation of the lungs, cytokine storms. Or prevent mast cell granules release, which can be associated with loss of smell and taste.

The actual preprint is here.

https://www.researchsquare.com/article/rs-30934/v1

They also talk about the case of a 47-year old hospital worker who complained of fever, feeling of chess pressure, cough, shortness of breath and other symptoms. He took famotidine for 30 days. On other occasions when his SpO2 was low, he was put on a canal to raise oxygen levels. But gradually his symptoms improved and by days 27 and 28 he tested negative on PCR tests for the virus. Returned to work at day 31 and by day 47 he considered himself "largely recovered" though "he continues to note a lack of ability to taste or smell."

Use of famotidine in this patient was recommended due to meeting FDA criteria for severe COVID-19 and his COVID-19 risk factors: male, 47yo, hypertension, obesity and diabetes mellitus Type 2. Although this is an anecdotal example, the patient experienced relief of symptoms overnight upon initiating use of famotidine. While not sufficient to demonstrate proof of cause and effect, this case does provide context for typical COVID-19 presentation and symptoms, as well as support for additional well-controlled famotidine therapeutic clinical trials in an outpatient setting.

The takeaway from the study is that there needs to be more investigation of whether "dysfunctional mast cell degranulation" partially drives C19, specifically investigate whether other drugs for mast-cell disorders could reduce the severity and deaths of C19:

other histamine antagonists (for example H1 and H4 types), leukotriene antagonists and leukotriene receptor antagonists 98, anti-inflammatory agents such as those developed for inflammatory bowel diseases, and mast cell activation inhibitors 99.
Then study whether such mast-cell disorder drugs could be combined with drugs which directly inhibit corona virus infection or replication to develop a safe and effective outpatient treatment before C19 vaccines become available.
MSPeconomist likes this.
wco81 is offline  
Old Jun 2, 20, 8:40 pm
  #5383  
Suspended
 
Join Date: Oct 2004
Location: Bay Area
Programs: DL SM, UA MP.
Posts: 12,730
Recent survey of repurposed drugs being studied as possible treatments, their status.

https://www.nature.com/articles/d41591-020-00019-9

Among them, here is a pair that I haven't heard of elsewhere:


Nafamostat and camostat are serine protease inhibitors both approved in Japan for use against pancreatitis in humans. Camostat was previously found in vitro to block the entry of SARS-CoV by acting as an antagonist to the serine protease TMPRSS2, and researchers believe both nafamostat and camostat could have a similar effect in inhibiting SARS-CoV-2. In vitro, both have been found to block the entry of SARS-CoV-2 into cells, although one preprint study reported that nafamostat inhibited viral cell entry with an efficiency roughly 15-fold higher than that of camostat.

These drugs are undergoing phase 2 and phase 2/3 clinical trials in the USA and Japan for their effectiveness against COVID-19, the primary outcome of which will be time to clinical improvement for nafamostat and reduced viral load after treatment for camostat.


“These drugs are quite old, they’re well studied, they have known targets that are exactly the same protease that the virus uses,” says Anton Yuryev, professional services director at Elsevier, who has done screenings for possible COVID-19 drug treatments.
wco81 is offline  
Old Jun 3, 20, 9:25 am
  #5384  
 
Join Date: Dec 2018
Location: PHX
Programs: Delta DM, Marriott Lifetime Titanium, HHonrs Diamond
Posts: 1,160
And now, the bigger health crisis as breast lumps and colon polyps continue to grow undiscovered and untreated...
From Washington Post, article behind paywall...
Note, even the white areas could be down, but less than 33%. Some of the white counties do not even have a hospital, which is the tragic reason why the county with the highest death rate in the USA (Early Co. Georgia) has 31 deaths but only 20 hospitalizations recorded.
MSPeconomist likes this.
FlyBitcoin is offline  
Old Jun 3, 20, 4:36 pm
  #5385  
 
Join Date: Oct 2007
Posts: 542
Originally Posted by FlyBitcoin View Post
And now, the bigger health crisis as breast lumps and colon polyps continue to grow undiscovered and untreated...
From Washington Post, article behind paywall...
Note, even the white areas could be down, but less than 33%. Some of the white counties do not even have a hospital, which is the tragic reason why the county with the highest death rate in the USA (Early Co. Georgia) has 31 deaths but only 20 hospitalizations recorded.
I'm having a hard time getting super worried because my colonoscopy on a five year recall is going to happen in August rather than the originally scheduled June, or that my mammogram (screening) recall will be in 15 months vs. 12 months, especially since professional organizations already disagree on the appropriate recall period for an asymptomatic woman of my age.

I'm more concerned about the drop in stroke victims and heart attack patients. Those seem like a much larger increase in mortality and morbidity.
lupine is offline  

Thread Tools
Search this Thread
Search Engine: