"As you said, being airborne makes it very dangerous and that is why it's exponentially difficult to contain."

It isn't airborne in the sense that matters, it is airborne droplet - just like H1N1. Containment is fundamentally no different from a process/procedure perspective.

"Some victims were frequent travelers: did they consider what the consequences will be?"

So, story time. Back in the 80s I was part of an agency that prepared/planned for stuff like this. The primary thing we talked about regarding broad transmission was what we called "super carriers" - people who travelled frequently and to high traffic/population areas. The modeling showed that if we, when faced with an outbreak the most important thing you could do to stop it was to lock down most of the "super carriers". Absent them more than 90% of outbreaks would be contained/eliminated.

Had we had the data/tech we do today, I have no doubt we'd have used it in our planning. Even then we knew the names of the vast majority of the American "super carriers".

That said, essentially we're talking Pareto Principle in regards to the "super carriers". But the effect is/was to drop that r0 value below 1. If you can do that, you've got it beat. However, realizing this the question of curtailing movement switches.

It is one thing to shut down travel broadly - such as all flights in/out of a hot zone - and another to stop that tiny minority from travel. Now here I kinda need to clarify just a bit about the work I was involved in in the 80s. While the basic principles and processes are the same, bioweapons are a bit different than natural viruses. However, IMO if you want to know the best way to stop something, consult the people who figure out the best way to spread it.

An alternative is mandatory quarantine/isolation. From a "freedom" perspective it can be thorny to consider travel limitations and/or physical quarantine. The sticky wicket is the post-operational period. Don't do enough or target the wrong population and you decrease confidence and justification for it. Go too far and you build resentment. The catch there is in the beginning you don't know how hard to go, and if you go hard enough it will look like you overreacted.

re: r-naught, my pleasure, glad to help. :)

On the social changes, Texas govt. offices have been working on remote-work capabilities and coincidentally just completed a WFH test run, determining that, yes, they could do it. I think the other area will be remote-schooling. My daughter's district just cancelled next week and is exploring "distance learning". I wonder just how much of a push this is going to give to that.

Anyway, related to the r0 info is a subset. Looking at the (still limited, but you deal w/what you have ;) ) data on PUI (Person Under Investigation) and "clinically confirmed" that result in lab-confirmed is interesting.

We have a "high" level of "clinal confirmation" because that, perhaps oversimplifying here, means presented with certain symptoms and had contact w/someone confirmed or a PUI". Basically the pipeline (for those not aware, which may not include you ofc) is:

go to hospital -> cough cough wheeze -> PUI (I know so and so and they know so and so who was on a cruise ...) -> lab test.

We are seeing an expected drop in each phase of the pipeline, and this isn't reaching the public's eyes and ears. But what I find interesting is how drastic of a drop we see from PUI/clinical confirmation to lab confirmation. For example, if we take the study from Illinois in the Lancet ( https://www.thelancet.com/journals/la... ) we see that we had a confirmed case from travel with:

A total of 347 contacts
44 conversion to PUI
1 lab confirmed case

Note that this study did the analysis for both from onset of symptoms and from confirmed source infection. The other thing to note is just who that 1 lab confirmed case was: the spouse.

Again, this is a singular case but it was conducted in Illinois, not China, and the results are stark. I wouldn't take it as broadly representative just yet. But it does provide grounds for it not being crazy infectious.

To me it highlights the main* risk factors are poor health (heart disease, diabetes, and pulmonary such as COPD), age, and prolonged close contact. It is also why I am cautious, but not terribly concerned.

And on being busy while WFH, I hear yah! I've been a remote guy for a very long time and it is a huge adjustment. But I can say that once you do ... it becomes almost zen-like at times.

The Spanish flu had about a 2.5% death rate while covid-19 seems to be in the 2 to 3 percent death rate of those infected. The Spanish flu had spread to something like 20% of the world's population and thus killed hundreds of millions. Perhaps all the control methods now available will keep it from killing less than 100,000.
H1N1 had a lesser death rate than covid-19 appears to have but infected tens of millions.

Yeah, I understand. I don't think 34,000 have died from flu this year - have they? Don't know.

CDC and WHO...Uh, have your grains of salt ready.

I'm not going to parse through your message bit-by-bit. But, at first glance your R0 doesn't match the numbers I received. But, I haven't listened for R0 numbers lately. In short, I read every study I can get my hands on. That's why I get a headache every Friday. My initial, and early, conclusion that this was airborne was based on CDC recommendations on how to deal with this virus. Since then, I have heard a few reports supporting the conclusion. Your chances of getting a normal flu after sitting three feet from an infected person for eight hours is very low. Not so with this.

But, I just read and think. Everybody takes in different information. I'm not going to shovel out my sources. And, everybody can think whatever they want to think. It's somewhat possible this thing may fade away in a month or so, then show up again in the next "cold and flu season", based on a collection of conditions. We'll see. I appreciate your commentary.

Thank you, excellent video.I will definitely start taking vitamin D.

How many tests must a person take to be sure of the correct outcome of the test.? All test have a certain probability of giving a false positive or a false negative. It is not just the false positives to be concerned about, but the false negatives which allow the disease to continue to be transmitted with only the disease becoming semptomatic to indicate the negative was a false negative. False positives are usually weeded out by giving the test over a couple of times, but is the test repeated for a negative result?

I agree the exclusion of schools was unwarranted. Granted, kids are not terribly at risk of getting or carrying it, but I suspect the driving factor was what would happen if all of those kids had to be watched by someone who normally would be at work, and/or possible political fallout from the teacher's union.

Thank you for the addition data on the R-naught. I have not had a chance to check recently. Ya know: I am working from home right now and am as busy as the proverbial cat in the rocking chair room. You'da thought that I would have time hanging heavy on my hands...

I think you are correct about the social changes too.

Jan

I'd take that claim with a pallet of 50lb bags of salt. The claims made in the article are explicitly countered by the paper they claim to base it on.

For example:

From the linked article:
"Further, the science paper finds that there is no known viral ancestry to the CoVid-19 coronavirus, meaning it did not evolve from nature."

From the source paper:
"Based on its genome sequence, 2019-nCoV belongs to lineage b of Betacoronavirus (Fig. 1A), which also includes the SARS-CoV and bat CoV ZXC21, the latter and CoV ZC45 being the closest to 2019-nCoV. 2019-nCoV shares ~76% amino acid sequence identity in the Spike (S)-protein sequence with SARS-CoV and 80% with CoV ZXC21 (Chan et al., 2020)."

and the full context of the cherry-picked quote from the article:
"This furin-like cleavage site, is supposed to be cleaved during virus egress (Mille and Whittaker, 2014) for S-protein “priming” and may provide a gain-of-function to the 2019-nCoV for efficient spreading in the human population compared to other lineage b betacoronaviruses. This possibly illustrates a convergent evolution pathway between unrelated CoVs. Interestingly, if this site is not processed, the S-protein is expected to be cleaved at site 2 during virus endocytosis, as observed for the SARS-CoV."

So no, the authors of the paper are not implying in any way this was bioengineered to kill humans. Indeed, reading further they indicate that this is nothing new and is possibly a route to treatment as it has been in other cases. I will also note that the implication the article's authors make is that because a new virus pops up and we don't know its ancestry, it must be a bioweapon engineered by man is absurd and unsupportable.

Scaremongers and conspiracists tend to only read abstracts - to the extent they even bother. But here, even the original paper's abstract makes no such claims:

"In 2019, a new coronavirus (2019-nCoV) infecting Humans has emerged in Wuhan, China. Its genome has been sequenced and the genomic information promptly released. Despite a high similarity with the genome sequence of SARS-CoV and SARS-like CoVs, we identified a peculiar furin-like cleavage site in the Spike protein of the 2019-nCoV, lacking in the other SARS-like CoVs. In this article, we discuss the possible functional consequences of this cleavage site in the viral cycle, pathogenicity and its potential implication in the development of antivirals."

Note that this paper is over a month old, and since it was published the actual virus has been named SARS-CoV-2 because it is not different enough genetically from SARS-COV (-1) to get its own classification.

The article plays slight of hand with selective quoting and letting the reader fill in the blanks with fear. The article author clearly wants you to think it is unique, but the original paper shows it isn't. For example the article reads “The spike glycoprotein of the new coronavirus 2019-nCoV contains a furin-like cleavage site absent in CoV of the same clade.”

But they fail to point out that, as the original paper clearly shows, the cleavage site is present on a bit more than half of CoV overall. Further the article adds emphasis around a claim that the virus is efficiently spread among humans, insinuates this is demonstrative of engineering. But here is the lie: if the virus was not "efficient" in spreading in humans would we be having an epidemic? Of course not.

Something important to keep in mind in all this is that corona virus is a family of viruses that exists across species. Sometimes these viruses mutate and "jump" species. This isn't new or unique. The genetic lineage of SARS-COV-2 indicates a bat origin.

For example a related paper still awaiting peer review indicates:
"At the whole genome level, the sequence identify of SARS-CoV-2 was 50% to MERS-CoV, 79% to SARS-CoV, 88% to two bat-derived SARS-like coronaviruses, Bat-SL-CoVZC45 and Bat-SL-CoVZXC21 (collected in 2018 in Zhoushan, China), and 96% to Bat-SARSr-CoV RaTG13 (collected in 2013 in Yunnan, China)"

"According to random drift hypothesis (15), these nucleotide mutations among different SARS-CoV-2 strains now available are still determined by neutral evolution. In short, there has no powerful factor to force SARS-CoV-2 to evolve in a certain direction by far. However, we should take strict precautions against the strong factors that may cause directional variation of SARS-CoV-2 both in natural environment and infection treatment."

TL;DR: no, the analyses we have so far are not indicative of it being a human engineered bioweapon.

I would like to see some real data:
1) By age group, what percentage of the people exposed actually dont get sick at all.
2) Of the remaining group, what percentage get sick, but recover without problems.
3) Of the people who do get sick, how what percentage actually are very sick and need hospitalization, and
4) Of the people who require hospitalization, what percentage actually die

These answers would be a lot more useful to assess my chances of dealing with this.

Besides Vitamin D and reduced starches/sugars for prevention, my family and I are also taking N-acetyl Cysteine, which studies show helps fight off viruses and protects the lungs. https://www.lifeextension.com/magazin...

Thanks for the info Real Bill.

Abaco and jlc, I would love to get an informed opinion on whether the genetics of this virus support the claims by some that it originated as a bioweapon. https://www.naturalnews.com/2020-02-2...

"I'm missing something here. I understand that it's airborne and contagious."

Sort of to the former, and yes to the latter. It is transmitted by droplets. This means you have to not only come into contact with the droplets but do so at a place they can ingest - it doesn't absorb via the skin. Th general public is not well educated on airborne vs airborne droplet transmission. The movies tend to go for actual airborne displays and scientists report "airborne droplet so that doesn't help.

An airborne droplet is a droplet that can cover short distances suspended in the air for short periods of time. Think of someone sneezing or coughing. By contrast an airborne virus is floating in exhaled breath.

As to contagion, the data and research we have so far puts the range of average transmission in the 1.3 to 3.3 range. Which means on average one person will infect 1.3 to 3.3 other people. So yes to contagious, but with the caveat that it isn't super contagious as some claim. It is presently less contagious than whooping cough, for example, which is also spread via droplets and airborne droplets and has an r0 of about 5.5.


You can always say we were not as prepared as we "should" have been - for something new. Those kind of claims are generally done to deflect blame - which isn't always warranted but still thrown.

The WHO delayed recognizing it as a pandemic well beyond their own published standards. It had met the criteria for stage 6 for weeks before they did. The reality is there really isn't much actual news so they all-"news"-all-the-time companies glom onto something they can scaremonger with because the human brain is wired to pay more attention to danger signs.

It makes me remember a Bill Engvall(?) bit:
"This doll looks safe enough doesn't it" like we're all at home going "uh-huh!" "But what if Barbie skated through a pool of gasoline*?!" -- https://youtu.be/rISEOKSbcko?t=195

Okay, thanks.

"Every carrier infects X number of other people (and we do not know what X is yet or what all of the means of transmission are)"

So far the data and calculations are showing 1.3 to a max report of 3.3 (that was later revised to 2.2 IIRC).

"H.sapiens is actually making a surprisingly good showing of rationality in terms of low-granularity decisions to self-isolate and to close public events."

Indeed, and this may be a major contributor to reducing the spread. I'm also curious as to the longer term effects of this. By way of example, many companies are doing full-time work from home now - and not just tech people. This will, in my experience, open people up to that notion more and show the company that yes, they can actually do that and be fine. So I wonder how much of a boost remote-work will get out of this. One tech conference I know went virtual this year as well.

No, wmiranda, it is not the flu - though some types of flu are due to a related species. We know this because we test for the genes of the virus...that is what the Covid-19 test kits to: they test for unique genetic sequences that this particular virus has.
Whatever other decisions you make, please do not base them on the idea that this 'may be just the flu'

Jan

I contracted an apparent cold three-and-a-half weeks ago. It began in the middle of the night with a mild sore throat. I took a certain brand of echinacea for a few days, and on day 5 was feeling much better. I doubt that this bug was COVID-19 because I healed so rapidly, had a very drippy nose, my temp never exceeded 99.3, had no aches or pains, and no difficulty breathing. BTW, has the Thieves study been replicated? I've always been skeptical. Thanks for any input you may have.

As you also probably know, I am a Medical Technologist - though I have not worked at the bench for ~27 years now. I started working at home and self-isolating this Monday past. Here is what I know:
-Every carrier infects X number of other people (and we do not know what X is yet or what all of the means of transmission are)
-Of those X people, Y become sick enough to go and be tested and turn out positive for Covid-19. If we artificially make Y = 100...
-Then, of that 100, ~20 become significantly ill
-And between 1-3 people die

We originally hoped that the X population was not infective, but it looks like many of them are. That means that the community contagion is spreading rapidly through our general population: your own immune system, age and general health will determine your personal risk.

H.sapiens is actually making a surprisingly good showing of rationality in terms of low-granularity decisions to self-isolate and to close public events. People are not waiting for the authorities to do this, eg HIMSS (big medical show) voluntarily canceled last week.

I admit that I have felt a bit like Cassandra, talking to my co-workers about this, though I was able to get some of them to a position of less risk.

Jan

I've been taking 4,000 IU Vitamin
D-3 with K-2 daily since last fall. Perhaps I should up it a bit. I also use 7,500 IU of a multi-carotene product at least 3x each week. I also suspect that the virus may be airborne because of the increase in community transmission.

I'm curious as to how you justify your expression of its contagiousness. From all of the data I've seen its current estimated r0 value is lower than most of the pandemics in the last decade, and the second lowest of the corona virus family pandemics in recent history as well. With an r0 of even 3 that would still put it in the range of the previous SARS, which ranged from 2-5.

Note for those not versed in it: r0 can basically be understood as the base rate of infection. Put simply an r0 of 1 means that, on average, a person with it will infect one other person. On average someone with a contagion with an r0 of, say, 12 will infect a dozen people. So, if something has an r0 of less than one it will have a strong tendency to just die out naturally in the outbreak. Calculating the r0 value is complex, even complicated. It is also population dependent and based on the population having no immunity. So a given virus may have higher or lower r0 values based on things such as age ranges, geographical location, and treatment or avoidance measures.

MERS was surprisingly low, but the rest of the major human corona virus based outbreaks have been in the 2-5 range. This would put the SARS-CoV-2 virus at the lower end of that scale with it's current range of 1.3 to 3. Comparing this to others puts more doubt to the claim of more contagious than anything we've seen in your lifetime. Seasonal influenza r0 ranges from 0.9 to 2.1 with a mean of 1.3 - the lower end of this one. Zika: 3-6.6. Norovirus: 1.6-3.7. Whooping cough (Pertussis) is ~5.5, Mumps is 4-7.

Even with a 1.3 r0 - the low end of the range so far - it won't just die off, but that doesn't mean it is one of the most contagious things we've seen in the last, let's say four decades.

As to airborne status, I'd expect one in the field to be more precise in terminology. It is airborne droplets (like influenza, SARS-COV, MERS, etc.), not airborne (like measles). While to some it may seem that is no different, it is critically different. An actual airborne virus is much, much, more difficult to contain than a droplet based one.

In that regard SARS-CoV-2 is no different than SARS-CoV, MERS, Influenza, or whooping cough, so again I wonder what your justification is for claiming "Early on I said I thought this was airborne. I'd, more specifically, now say it's the more airborne flu-like illness I've ever heard of. This makes it very dangerous.".

For those who do not know the key differences between airborne and droplet: if it was an actual airborne virus washing hands and surfaces would make no difference, neither would avoiding touching your face. Airborne viruses require significant isolation - down to the atmosphere in the quarantine rooms - and gloves and masks don't help. For droplet spread ones, as SARS-CoV-2 is, gloves, high quality masks, and cleaning does make a difference and you can contain by avoiding physical proximity even while in the same atmosphere. An actual airborne virus gets into you by you breathing it in. A droplet based transmission means you have to have physical contact and ingest via ayes, mouth, nose, etc. droplets containing the virus.

Now to be clear, I'm not questioning you personally, just asking how you justify your claims when they are contrary to all of the available data and virus biology. You may have valid reasons for some of them, but they aren't being presented; and some of your claims go against well known virology. As such I am asking on what evidence and data you base these claims.

Thank you Abaco. Please keep posting any information you have.

A man in his 30s died recently in Poughkeepsie who drove an Asian car. If that happens at least a few hundred times more - preferably a lot more than that - we might have a statistic. For now, you and I have both cited events. I understand your point, but I disagree that shutting down a few avenues of travel - say, international flights - would stop a virus which is already here, and even locking every civilian in their own personal clean room would still require people moving to service their needs, every movement of which could move the virus.

I was referring to the fact that some people will not heed any precautionary measures and carry on as usual with their travels.

I woman in her forties just died recently in CA who was a frequent global traveler, her last trip to an Asian country.

I am far from advocating government regulating travel of people but some sort of measure is absolutely necessary. Relying on people to control their own moves did not seem to work in the past.