OT: COVID-19 Presentation from CROI Meeting

[pj]

If PJ is right we all die.

Heh, no, that's not the case. To summarize the high points:
- There are two versions of the virus circulating in the world, one that is extremely deadly and first entered the world in Wuhan in November, and has accounted for the major death clusters in Wuhan, Iran, Kirkland Life Care Center, etc, and another that is much less deadly and was introduced in China in December or January, that differs by two significant mutations but is otherwise highly homologous, and thus acts as a weakened live virus vaccine which can establish immunity against the lethal virus.
- The second virus was probably intentionally developed as a vaccine/defense by the Chinese. And thank goodness they had that and shared it with the world.
- Whereas the lethal virus may kill 5-20% of people infected, the weakened one kills 0.1-1%.
- The apparently schizophrenic response of the authorities is because they need "panic" in the form of quarantines, event cancellations, etc, to stop spread of the lethal virus, but they need the weakened vaccine-like virus to spread widely through the population in order to generate immunity.
- Timing of spread may be important, if the weakened virus spreads in winter alongside cold and flu it may kill 1%, if it spreads in summer it may kill 0.1%.
- So, we need a few months of "panic" to stop the lethal virus and to delay spread of the vaccine to a safer period, but we need the vaccine to work its way through the population in a timely manner (generating "herd immunity" by the fall).
- If the authorities decide that the lethal virus cannot be quarantined, they will try to spread the vaccine virus as rapidly as possible. This appears to be what the UK is doing. That is why unlike here they are encouraging large sporting events, which are good opportunities to introduce and spread the weakened vaccine virus. Something similar may be happening in the US on a local level, e.g. after the lethal virus outbreak at Kirkland we soon had a mysterious "community outbreak" of the weaker vaccine virus in the Seattle area, and similarly wherever the lethal virus has appeared, community spread of the weaker virus has soon followed in that local area.
- Meanwhile there should be crash programs to develop routine detection, good therapies, better vaccines, sufficient production of N95 masks, etc, so that we're prepared for next winter and for re-emergence of the lethal strain.

If everything goes well we will be able to hold mortality in the US down to 0.1%, almost all elderly, and eradicate the lethal strain as we eradicated smallpox. I am hoping things go well, and am optimistic they will.

 

[don356]

Conspiracy Kitty says:
Or are they?

I'm relying on the advice of the guy at the car wash.

 

[ctchamps]

"The overall sequence 120 similarities between 2019 -nCoV spike and SARS -CoV spike (isolated from human, civet 121 or bat) are around 76% -78% for the whole protein, around 73% -76% for the RBD, and 50%-53% for the RBM (Fig. 3A, 3 B )" Source: https://jvi.asm.org/content/jvi/early/2020/01/23/JVI.00127-20.full.pdf. There is enough similarity to show that SARS-CoV-2 uses ACE2 as its receptor, but not much similarity.



At this point, it is just a hypothesis that the bats could be a pool for such a large variety of viruses that one of them might evolve to be a perfect infectious agent in humans. This is very much like the idea of monkeys typing randomly on typewriters and hoping they'll produce Shakespeare: it takes more monkeys than the numbers of atoms in the universe billions of years to have a chance. The chance of SARS-CoV-2 evolving in such a bat pool is hardly "perfectly plausible," it is statistically akin to the monkeys writing Shakespeare. There just aren't enough bats in the world to make a large enough reservoir for this to work.

Meanwhile the classic model, while it does rely on a series of rare events, is known to have happened many times in human history - most pathogens enter humans this way. It will generate pathogens regularly - but not pathogens as super-adapted to humans as SARS-CoV-2. The classic process can and no doubt did generate the 2002 SARS, but it cannot have generated SARS-CoV-2.

Debating whether Dr. Baric's hypothesis is plausible based on statistics is not necessary, because we can go to animals and search for viruses. If the hypothesis that SARS-CoV-2 was one of a diverse pool of randomly varying bat viruses is correct, we'll see a huge range of viruses in bats ranging in genomic similarity from 98% to 100%. In fact, we don't see any closer than 96%. The hypothesis is being disproven by ongoing research.



The fact that SARS-CoV-2 is related to previous SARS (at a low level) does not tell us its origins, because a bioengineer would also begin working from the SARS-CoV sequence. What is key is that the SARS-CoV-2 has improved human binding compared to all those others, but worse animal binding -- yet it did no evolution in humans. There is no natural process that can bring that about (apart from the gazillion monkeys typing hypothesis).

As we use to say "when you see a potential mate, if you don't connect you can't inject". Or, "keep in mind you need to bind".

Having the ability to attach to a receptor site is still only the first step in what's required to get a problem from viruses. For a molecule that's just considered passive, viruses have several parts to their molecular makeup in order to subvert any cell. Nature really is fascinating. Thanks for your information.

This virus ultimately has to be airborne in order to get to the lungs. We have to breathe it in. We don't breathe in droplets. We have to release the virus from those droplets into the air when we contact those droplets. Am I wrong?

 

[pj]

As we use to say "when you see a potential mate, if you don't connect you can't inject". Or, "keep in mind you need to bind".

Having the ability to attach to a receptor site is still only the first step in what's required to get a problem from viruses. For a molecule that's just considered passive, viruses have several parts to their molecular makeup in order to subvert any cell. Nature really is fascinating. Thanks for your information.

This virus ultimately has to be airborne in order to get to the lungs. We have to breathe it in. We don't breathe in droplets. We have to release the virus from those droplets into the air when we contact those droplets. Am I wrong?

I'm not sure exactly what you are asking, but:
- When people exhale, cough, or sneeze, the virus comes out in droplets that can remain in the air for up to ten minutes and travel up to 20 feet.
- Then the droplets fall in surfaces and can last for up to several days, where they can be touched and picked up by fingers, which then infect a person when the fingers touch nose, mouth, or eyes.
- Humidity and warmth protect against viral transmission. Masks protect, both by preventing breathing of aerosol viruses and preventing touching of nose or mouth. Washing hands with hot water and soap, or alcohol, protects.
- Drinking water protects, as viruses are digested and destroyed if swallowed. They have to reach the lungs.
- Once in the lungs they enter cells via the ACE2 receptor on epithelial cells and replicate. The inflammatory response to the viruses can cause the air sacs of the lung to fill up with fluid and mucus, causing suffocation. That is why in severe cases you need oxygen, to make up for the loss of lung capacity.

 

[JustbrewitMan]

"The overall sequence 120 similarities between 2019 -nCoV spike and SARS -CoV spike (isolated from human, civet 121 or bat) are around 76% -78% for the whole protein, around 73% -76% for the RBD, and 50%-53% for the RBM (Fig. 3A, 3 B )" Source: https://jvi.asm.org/content/jvi/early/2020/01/23/JVI.00127-20.full.pdf. There is enough similarity to show that SARS-CoV-2 uses ACE2 as its receptor, but not much similarity.



At this point, it is just a hypothesis that the bats could be a pool for such a large variety of viruses that one of them might evolve to be a perfect infectious agent in humans. This is very much like the idea of monkeys typing randomly on typewriters and hoping they'll produce Shakespeare: it takes more monkeys than the numbers of atoms in the universe billions of years to have a chance. The chance of SARS-CoV-2 evolving in such a bat pool is hardly "perfectly plausible," it is statistically akin to the monkeys writing Shakespeare. There just aren't enough bats in the world to make a large enough reservoir for this to work.

Meanwhile the classic model, while it does rely on a series of rare events, is known to have happened many times in human history - most pathogens enter humans this way. It will generate pathogens regularly - but not pathogens as super-adapted to humans as SARS-CoV-2. The classic process can and no doubt did generate the 2002 SARS, but it cannot have generated SARS-CoV-2.

Debating whether Dr. Baric's hypothesis is plausible based on statistics is not necessary, because we can go to animals and search for viruses. If the hypothesis that SARS-CoV-2 was one of a diverse pool of randomly varying bat viruses is correct, we'll see a huge range of viruses in bats ranging in genomic similarity from 98% to 100%. In fact, we don't see any closer than 96%. The hypothesis is being disproven by ongoing research.



The fact that SARS-CoV-2 is related to previous SARS (at a low level) does not tell us its origins, because a bioengineer would also begin working from the SARS-CoV sequence. What is key is that the SARS-CoV-2 has improved human binding compared to all those others, but worse animal binding -- yet it did no evolution in humans. There is no natural process that can bring that about (apart from the gazillion monkeys typing hypothesis).

@pj

I really appreciate your tenacity to try and adapt information to support your main contentions that it's a bioengineered situation and that there are 2 viruses "released" on the world.

But you continue to fundamentally NOT understand that when it comes to the process of infectivity, it's the end product receptor binding characteristics that ultimately determine whether a virus can infect a host efficiently. NOT achieving some arbitrary "very high" sequence similarity...

There are many ways to construct a protein with amino acids that can contain crucial sections (binding domains) in the proper 3D orientation to bind to and interact with a host receptor (in this case, the ACE2 receptor).

Two proteins, if the right amino acid residues are used in the right sequences, can have very very low overall genetic sequence homology, yet both will strongly bind to the same receptor. The 50-75% numbers for SARS-CoV-2 vs SARS-CoV-1 are fine because, as shown quite elegantly in the article you cited, the crucial binding residues for both are 3-dimensionally IN THE RIGHT SPOTS.

Let me use another analogy to try and emphasize the point I'm trying to make:

• Penicillin and Cephalosporin antibiotic work by inhibiting trans- and carboxypeptidase enzymes (also known as Penicillin-Binding Proteins, or PBPs), that help to synthesize bacterial cell wall. They inhibit PBP function by binding to the site of the PBP enzyme where the peptidoglycan precursor (used to make cell wall) would bind to...this inhibits the ability of the enyzme to do its job, cell wall production stops, and the bacterial cell will eventually "die".
• Penicillins ans Cephalosporins are not even proteins and they have quite dramatically different chemical structures than peptidoglycan. Yet 3-dimensionally, they are still able to bind to the same site (and in fact, the penicillins bind better to the site on the PBP enzyme, which is why they are antibacterial).

The rest of your contentions are not well-thought-out, disingenuous, or both. There are myriad publications that show that there are many bat species with many different coronaviruses within them. I don't have the exact numbers, but there are thousands of different bat species in the world. We've only tested a tiny subfraction of them for presence of viruses. Even Dr. Zheng-Li (the "bat lady") has only tested a small number of the bats endemic to China. But the data thus far definitively indicates many different types of coronaviruses in bats. And its' definitive that they can recombinate their genetic material with ease. And there is ample evidence of strain evolution over time.

How China's 'Bat Woman' Hunted Down Viruses from SARS to the New Coronavirus

Wuhan-based virologist Shi Zhengli has identified dozens of deadly SARS-like viruses in bat caves, and she warns there are more out there

www.scientificamerican.com

Cheers,
JBM

 

[JustbrewitMan]

Are there two epidemic strains (one highly-virulent, one designed to stop the spread, a.k.a the "pj theory")?

At this point, there is no strong evidence to support this contention.

(1.) As of 3/15/2020, there have been almost 500 genomes sequenced from samples obtained around the world with the evolving spread of the COVID-19 epidemic:

auspice

nextstrain.org

There is definitely some small genetic variation amongst these strains, but given the known mutational frequency characteristics of coronaviruses during replication as well as their known ability to do recombination (combining sections of two "parents" genetic materials to form a new progeny), it is well within the expected ranges of "genetic drift" and there is nothing to suggest that, so far, it is any more different that what is observed from the spread of the original SARS events 2002-2003 or the yearly influenzae spread.

Although I cannot definitively rule out that there may be some important rare mutations that could have occurred so far that made certain strains less or more virulent (due to things like single-point mutations in the right regions of the genome that could then decrease or increase its binding to the human ACE2 cell receptor (needed as a first-step to human cell invasion), or do something like increase other enzymes that could increase its virulence, I could find no evidence so far from experts that indicate that some of these mutations have been documented in the strain variants. But I'll be continually monitoring this!

For further reading for those so inclined, there are a couple of discussions from experts at the two links below that argue (convincingly) that the "...recent paper [that] has claimed that SARS-CoV-2 has split into two strains, “L” and “S”, with the “L” strain causing a more severe version of COVID-19. This theory was used to try to explain the higher case fatality ratio that has been seen in Wuhan, China, the epicenter of the outbreak as compared to other parts of China." - is inaccurate.

Response to “On the origin and continuing evolution of SARS-CoV-2”

Response to “On the origin and continuing evolution of SARS-CoV-2” Oscar A. MacLean*, Richard Orton, Joshua B. Singer, David L. Robertson. MRC-University of Glasgow Centre for Virus Research (CVR). *To whom correspondence should be addressed: Oscar.MacLean@glasgow.ac.uk. Introduction An...

virological.org

(2) As the pandemic has evolved, it has become clear that the mortality observed has also evolved over time. For example, in Wuhan, the mortality for people who became symptomatic from December 2019 through January 10th was ~15%. From 1/11-1/20 it was 6%, 1/21-31 it was 2%, and its been 1% since February 1st:

Why The Death Rate From Coronavirus Is Plunging In China

And what that means for the rest of the world. Researchers have found three likely reasons for the drop in the fatality rate.

www.npr.org

The VAST majority of deaths were in the early phase of the epidemic...when healthcare providers were woefully unaware of what it was, how it was transmitted, how to diagnose it properly, how to provide care, and there were significant delays in care due to the overwhelmed healthcare facilities. Since the identification that COVID-19 is caused by a SARS coronoavirus, things have dramatically gone in a positive direction wrt clinical management of infected patients. The very low mortalities in MANY areas of the world that were the later countries to see COVID-19 (and thus, could have appropriate measures in place early on in the disease spread) support this fairly logical concept.

We've witnessed the same thing happen in other countries like Italy, Iran, etc. with high initial mortality rates.


3.) As mentioned by @auror , morbidity and mortality is MULTIFACTORIAL and research is rapidly being published to provide some insights.

• Some factors are patient-specific (like comorbid illnesses, genetic and/or comorbid factors that could make them more susceptible to infection via variation in cell-surface ACE2 amounts (male>female, smokers>non-smokers, active hypertension>no hypertension, perhaps race, etc.)
• Some factors are public-health related (quarantine effectiveness for positive cases, social distancing measure implementation time and amounts, numbers of hospital beds and types of equipment available)

EVERYONE please continue to be safe, patient, try not to over-react/panic, do healthy things, go enjoy a nice walk outside today (going to be a really nice day!).


Best,
JBM

 

[DCUconnfan]

I have learned more from reading the boneyard/this thread in an hour than I have from reading the news for a week. Lost productivity from the inter web? I think not!

 

[pj]

JBM, I have no idea why you think I don't understand infectivity and the molecular biology of binding. I am a PhD scientist with decades of experience in molecular biology and therapeutics. The reason I pointed to gene sequence similarity is because it addresses the question of virus origins. I was not discussing virulence at all.

As for the data in bats, there is no evidence at all of strain evolution in bats toward or anywhere near SARS-CoV-2. There is no evidence of a bat pool of coronavirus diversity that encompasses any of the key genetic components of SARS-CoV-2, much less the whole virus.

Obviously, I was persuaded by the Tang et al report that there are two strains, a lethal strain that first appeared in November in Wuhan and is responsible for the high early death rate and the high death rate in places like Iran that received the lethal strain, and a weakened strain that first appeared in China in December or January. I think that aspect of the paper is highly likely to be correct, as it is hard to imagine another explanation for the extreme variations we've seen in lethality by outbreak, some outbreaks at 5-20% lethality and some at 0.1-1% lethality. The critique of Tang et al you point to makes some reasonable objections to issues with the Tang paper (which I think cannot be totally honest due to constraints from the Chinese government), but they don't refute the idea that there are L and S strains. I think Tang et al know more than they have said and have highlighted for us two key mutations which, as time will show, greatly weaken virulence and turn the virus into a de facto "vaccine" against the lethal version.

All of these questions will be resolved as we get more sequences from patients in the West and correlate them with outcomes, and observe whether and in what circumstances re-infections occur.

As for your idea that most deaths were early and now there is some health care response that is mitigating death -- no, not in Italy. The healthcare response is not substantially better now in Europe than it was in Wuhan in January. If more people died in Wuhan, it is because the strain they contracted was more lethal. That lethal strain still has the potential to grow and spread. We are not yet safe from it.

 

[Stinger92860]

We cant trust the China numbers, why would that government start being truthful? Let’s see if their supply chains reopen AND the virus does not boomerang back. This will take a few weeks. I’m watching Italy who is probably 3 weeks ahead of us. They made a number of mistakes, not banning travel fast enough, especially from China. Hindsight is 20/20 but they should have locked down sooner.

 

[phillionaire]

We cant trust the China numbers, why would that government start being truthful? Let’s see if their supply chains reopen AND the virus does not boomerang back. This will take a few weeks. I’m watching Italy who is probably 3 weeks ahead of us. They made a number of mistakes, not banning travel fast enough, especially from China. Hindsight is 20/20 but they should have locked down sooner.

Can we trust our government to be truthful?

 

[JustbrewitMan]

JBM, I have no idea why you think I don't understand infectivity and the molecular biology of binding. I am a PhD scientist with decades of experience in molecular biology and therapeutics. The reason I pointed to gene sequence similarity is because it addresses the question of virus origins. I was not discussing virulence at all.

As for the data in bats, there is no evidence at all of strain evolution in bats toward or anywhere near SARS-CoV-2. There is no evidence of a bat pool of coronavirus diversity that encompasses any of the key genetic components of SARS-CoV-2, much less the whole virus.

Obviously, I was persuaded by the Tang et al report that there are two strains, a lethal strain that first appeared in November in Wuhan and is responsible for the high early death rate and the high death rate in places like Iran that received the lethal strain, and a weakened strain that first appeared in China in December or January. I think that paper is highly likely to be correct, as it is hard to imagine another explanation for the extreme variations we've seen in lethality by outbreak, some outbreaks at 5-20% lethality and some at 0.1-1% lethality. The critique of Tang et al you point to makes a few objections that would be reasonable in ordinary circumstances but in this instance are, in my view, not convincing. I think Tang et al know more than they have said and have highlighted for us two key mutations which, as time will show, greatly weaken virulence and turn the virus into a de facto "vaccine" against the lethal version.

All of these questions will be resolved as we get more sequences from patients in the West and correlate them with outcomes, and observe whether and in what circumstances re-infections occur.

As for your idea that most deaths were early and now there is some health care response that is mitigating death -- no, not in Italy. The healthcare response is not substantially better now in Europe than it was in Wuhan in January. If more people died in Wuhan, it is because the strain they contracted was more lethal. That lethal strain still has the potential to grow and spread. We are not yet safe from it.

Hey pj,

Similar evolution towards less-virulent strains has occurred with many human-infecting viruses including influenzae, and the original SARS virus (Strains in the few cases post 2002-3 were much less virulent). I think that there's evidence that this is already happening again naturally.

In perusing bioRxiv.org this AM, there are a couple new non-peer-reviewed articles that, through skimming the abstracts, are suggesting this in some strains within and outside of China. Haven't read them completely though.

There's also another non-peer-reviewed article I'm going to dive into later that seems to show that through protein structure modeling, that the SARS-CoV-1 and SARS-CoV-2 viruses, though only showing 72.8% sequence identity of receptor-binding domains, had 97% structural similarity of those areas.

https://www.biorxiv.org/content/10.1101/2020.03.10.986398v1.full.pdf

Agree that we all may interpret things quite differently in as shortly as 2-4 weeks as new data furiously emerges.

I'm a little worried and fascinated about some of the new VERY PRELIMINARY suggestive concerns for relationships between people with higher-ACE2 states (hypertension, poorly-controlled diabetes, possibly obesity, as well as people receiving various cardiovascular/kidney disease with ACE inhibitors and/or Angiotensin Receptor Blockers (ARBs) and more severe COVID-19 infections / higher mortality

It's a bit too early to say whether people should stop taking these medications yet / switch to some other class of antihypertensive medication (so people, PLEASE PLEASE don't do this on your own!) in the face of the COVID-19 pandemic...but its something to watch closely.

 

[ClifSpliffy]

Hey pj,

Similar evolution towards less-virulent strains has occurred with many human-infecting viruses including influenzae, and the original SARS virus (Strains in the few cases post 2002-3 were much less virulent). I think that there's evidence that this is already happening again naturally.

In perusing bioRxiv.org this AM, there are a couple new non-peer-reviewed articles that, through skimming the abstracts, are suggesting this in some strains within and outside of China. Haven't read them completely though.

There's also another non-peer-reviewed article I'm going to dive into later that seems to show that through protein structure modeling, that the SARS-CoV-1 and SARS-CoV-2 viruses, though only showing 72.8% sequence identity of receptor-binding domains, had 97% structural similarity of those areas.

https://www.biorxiv.org/content/10.1101/2020.03.10.986398v1.full.pdf

Agree that we all may interpret things quite differently in as shortly as 2-4 weeks as new data furiously emerges.

I'm a little worried and fascinated about some of the new VERY PRELIMINARY suggestive concerns for relationships between people with higher-ACE2 states (hypertension, poorly-controlled diabetes, possibly obesity, as well as people receiving various cardiovascular/kidney disease with ACE inhibitors and/or Angiotensin Receptor Blockers (ARBs) and more severe COVID-19 infections / higher mortality

It's a bit too early to say whether people should stop taking these medications yet / switch to some other class of antihypertensive medication (so people, PLEASE PLEASE don't do this on your own!) in the face of the COVID-19 pandemic...but its something to watch closely.

hehe...u said 'ace2' again. hehe.. cool.

 

[navery12]

JBM, I have no idea why you think I don't understand infectivity and the molecular biology of binding. I am a PhD scientist with decades of experience in molecular biology and therapeutics. The reason I pointed to gene sequence similarity is because it addresses the question of virus origins. I was not discussing virulence at all.

As for the data in bats, there is no evidence at all of strain evolution in bats toward or anywhere near SARS-CoV-2. There is no evidence of a bat pool of coronavirus diversity that encompasses any of the key genetic components of SARS-CoV-2, much less the whole virus.

Obviously, I was persuaded by the Tang et al report that there are two strains, a lethal strain that first appeared in November in Wuhan and is responsible for the high early death rate and the high death rate in places like Iran that received the lethal strain, and a weakened strain that first appeared in China in December or January. I think that aspect of the paper is highly likely to be correct, as it is hard to imagine another explanation for the extreme variations we've seen in lethality by outbreak, some outbreaks at 5-20% lethality and some at 0.1-1% lethality. The critique of Tang et al you point to makes some reasonable objections to issues with the Tang paper (which I think cannot be totally honest due to constraints from the Chinese government), but they don't refute the idea that there are L and S strains. I think Tang et al know more than they have said and have highlighted for us two key mutations which, as time will show, greatly weaken virulence and turn the virus into a de facto "vaccine" against the lethal version.

All of these questions will be resolved as we get more sequences from patients in the West and correlate them with outcomes, and observe whether and in what circumstances re-infections occur.

As for your idea that most deaths were early and now there is some health care response that is mitigating death -- no, not in Italy. The healthcare response is not substantially better now in Europe than it was in Wuhan in January. If more people died in Wuhan, it is because the strain they contracted was more lethal. That lethal strain still has the potential to grow and spread. We are not yet safe from it.

This makes your posts in this thread even more terrifying

 

[ctchamps]

I'm a little worried and fascinated about some of the new VERY PRELIMINARY suggestive concerns for relationships between people with higher-ACE2 states (hypertension, poorly-controlled diabetes, possibly obesity, as well as people receiving various cardiovascular/kidney disease with ACE inhibitors and/or Angiotensin Receptor Blockers (ARBs) and more severe COVID-19 infections / higher mortality

It's a bit too early to say whether people should stop taking these medications yet / switch to some other class of antihypertensive medication (so people, PLEASE PLEASE don't do this on your own!) in the face of the COVID-19 pandemic...but its something to watch closely.

It's definitely something to watch.

The following study demonstrates that ACE inhibitors and ARBs are the most effective treatments for hypertension to prevent new-onset diabetes mellitus (NOD) and possible cardiovascular disease.

Journal of Cellular and Molecular Medicine - Comparing six antihypertensive medication classes for preventing new‐onset diabetes mellitus among hypertensive patients

It's a particular concern for the U.S. considering a bulletin posted on the World Health Organization site claims that 17.2% of Americans between the ages of 35 to 49 years of age and 34.5% of Americans between the ages of 35 to 84 years were diagnosed with hypertension. In individuals with hypertension aged 35 to 84 years, the age-standardized percentage whose high blood pressure was diagnosed, treated or controlled was highest in the United States at 85.3%

Who - Control of hypertension with medication: a comparative analysis of national surveys in 20 countries

 

[ctchamps]

I'm not sure exactly what you are asking, but:
- When people exhale, cough, or sneeze, the virus comes out in droplets that can remain in the air for up to ten minutes and travel up to 20 feet.
- Then the droplets fall in surfaces and can last for up to several days, where they can be touched and picked up by fingers, which then infect a person when the fingers touch nose, mouth, or eyes.
- Humidity and warmth protect against viral transmission. Masks protect, both by preventing breathing of aerosol viruses and preventing touching of nose or mouth. Washing hands with hot water and soap, or alcohol, protects.
- Drinking water protects, as viruses are digested and destroyed if swallowed. They have to reach the lungs.
- Once in the lungs they enter cells via the ACE2 receptor on epithelial cells and replicate. The inflammatory response to the viruses can cause the air sacs of the lung to fill up with fluid and mucus, causing suffocation. That is why in severe cases you need oxygen, to make up for the loss of lung capacity.

I really wasn't asking. I was highlighting the weak link to what has been developing in this country - droplets can remain in the air for up to ten minutes (That's a consensus number. I linked a study in another thread that indicated 45 minutes is possible).

Yes people should wash and sanitize frequently. That is something effective we can do to reduce infection. However based on the above point we have no protection against viruses in the air. We have no idea if anyone traveled in any community space up to ten minutes prior to our arrival and whether they sneezed or coughed within that window. That is why various organizations and communities have taken action to stop public gatherings.

Unfortunately this generalized draconian action had to be taken because we did not take immediate action to ramp up testing for the virus. Had we done so we might have had the opportunity to isolate which communities and events needed to be on hold. Just to be clear. Having taken that action would not have definitively prevented a wide spreading of the problem. Having not taken action however guaranteed it.

 

[Hi-Low]

I'm not sure exactly what you are asking, but:
- When people exhale, cough, or sneeze, the virus comes out in droplets that can remain in the air for up to ten minutes and travel up to 20 feet.
- Then the droplets fall in surfaces and can last for up to several days, where they can be touched and picked up by fingers, which then infect a person when the fingers touch nose, mouth, or eyes.
- Humidity and warmth protect against viral transmission. Masks protect, both by preventing breathing of aerosol viruses and preventing touching of nose or mouth. Washing hands with hot water and soap, or alcohol, protects.
- Drinking water protects, as viruses are digested and destroyed if swallowed. They have to reach the lungs.
- Once in the lungs they enter cells via the ACE2 receptor on epithelial cells and replicate. The inflammatory response to the viruses can cause the air sacs of the lung to fill up with fluid and mucus, causing suffocation. That is why in severe cases you need oxygen, to make up for the loss of lung capacity.

Question about the droplets with the virus that are exhaled....does the infected person need to be symptomatic to expel the droplets?

What I'm getting at is since the droplets can remain in the air for 10 minutes when out in public at grocery, pharmacy do we need to at this point be wearing a mask since infected could unknowingly be spreading the virus if not symptomatic just by breathing?

 

[pj]

Question about the droplets with the virus that are exhaled....does the infected person need to be symptomatic to expel the droplets?

What I'm getting at is since the droplets can remain in the air for 10 minutes when out in public at grocery, pharmacy do we need to at this point be wearing a mask since infected could unknowingly be spreading the virus if not symptomatic just by breathing?

No, people can transmit the virus while asymptomatic.

Wearing a mask in public would be helpful. Really, there ought to be masks distributed to everyone, and everyone ought to wear them. We ought to manufacture billions of them.

 

[unother]

Interesting how we can go years of talking basketball and never really know some other posters are flipping morons, whackos or conspiracy theorist until a pandemic occurs.

the things you discover once you discuss another topic...

 

[Letsgohuskies11]

I'm glad Gov. Pritzker is speaking out and making a scene about the lines at airports and just the miserable job the white house is doing

 

[Leebo]

This makes your posts in this thread even more terrifying

He's gonna take that the wrong way.

 

[LIuconn]

“Dear leader” needs to step down

 

[Dream Jobbed 2.0]

Pray to Jim Calhoun that Lamont shuts bars and restaurants down.

 

[Stinger92860]

Can we trust our government to be truthful?

Are you suggesting that the Johns Hopkins numbers which come from the states is not truthful? Let me ask, do you think this is serious or a hoax?

 

[Dream Jobbed 2.0]

Cases, recoveries, death rates, etc mean nothing until more than a handful of Americans are tested.

 

[Stinger92860]

Mistakes have been and will be made. Our government needs to fix any issues quickly as they arrive when possible. I get the sense that some people want our government agencies to fail.