Corona virus general questions mega thread

[J.C.MacSwell]

Seems like China has the Covid 19 virus down to a 0.1%/day growth rate. (Though that is based on total cases including those recovered, if I read it correctly): 80,651(+0.1%)

https://en.wikipedia.org/wiki/2019–20_coronavirus_outbreak_in_mainland_China

Edited March 7, 2020 by J.C.MacSwell

[Sensei]

Deja Vu...

Grand Princess cruise ship staff has been infected by coronavirus. If they had easy access to meals and/or guests, in one or two weeks USA will be in top 5, in the greatest number of confirmed infected people..

https://edition.cnn.com/2020/03/08/health/us-coronavirus-sunday/index.html

"There are at least 21 people with coronavirus aboard the Grand Princess cruise ship, which is expected to dock sometime Monday in Oakland, California, Gov. Gavin Newsom said in a news conference Sunday"

"The Grand Princess has been in limbo since Wednesday, when officials learned a California man who traveled on the same ship last month later died of coronavirus. On Sunday, the US Centers for Disease Control and Prevention said four people from that February Grand Princess voyage have been diagnosed with coronavirus."

 

Edited March 9, 2020 by Sensei

[Prometheus]

Thought this was an excellent video introducing the maths of exponential growth and logistic growth and applying to the virus.

 

https://www.youtube.com/watch?v=Kas0tIxDvrg

[J.C.MacSwell]

Assuming you have caught a lesser coronavirus or cold, are you more or less likely to catch Covid-19 if exposed?

Same/different for other virus's? Bacterias? Fungi?

Does the timing matter? Is there a "crowding out" effect in place sometimes vs a "rundown" effect other times?

 

[StringJunky]

1 hour ago, J.C.MacSwell said:

Assuming you have caught a lesser coronavirus or cold, are you more or less likely to catch Covid-19 if exposed?

Same/different for other virus's? Bacterias? Fungi?

Does the timing matter? Is there a "crowding out" effect in place sometimes vs a "rundown" effect other times?

 

I've read before that the hep c virus can outcompete the hep b virus in a host and put it into dormancy.

[CharonY]

I think the whole infection process is sufficiently complicated so that there is not clear answer. At the onset of infection your body ups its response. At this time some pathogens may have a harder time to get in, while others may use the inflammatory cascade to their advantage. Malaria, for example was actually used as a treatment of neurosyphilis in order to induce fevers. Then, as String mentioned, there are interactions between pathogens.

With respect to respiratory infections, folks have detected frequently co-infections with multiple respiratory viruses, but their effect on disease outcome are unclear. Conversely viral and bacterial co-infection seem to be more commonly related to the development of pneumonia and other severe illnesses. This is why COVID-19 infections are often treated with antibiotics. And of course in severe stages of illnesses the immune system can be weakened to such a level that opportunistic infections can happen with a higher likelihood. So in other words, precise answers are unlikely to be forthcoming, especially not with a disease whose pathophysiology is not fully explored yet.

 

Edit: Quite unrelated to that, but I think it is a bit worrisome that the US seems to be fumbling the response a bit. There was time to prepare and normally the CDC is quite on top of things.

[J.C.MacSwell]

Thanks SJ, CY.

[Sensei]

Viral infection (e.g. HIV) can cause that microorganisms which are normally co-existing in the body, and in healthy body are harmless, that they will start being troublemakers for organism..

[CharonY]

5 minutes ago, Sensei said:

Viral infection (e.g. HIV) can cause that microorganisms which are normally co-existing in the body, and in healthy body are harmless, that they will start being troublemakers for organism..

Yes, they are called opportunistic pathogens. However, it is not specific to viral infections but can be any situation that negatively affects host defense mechanisms or otherwise create situations that are allows certain pathogens to strive. A famous example of a genetic disease is cystic fibrosis, which creates a lung environment allowing Pseudomona aeruginosa to cause harmful opportunistic infections.

[Externet]

Good day to all.  A couple more questions...

Is it known if a patient that survives this new virus, remains immune to it or can contract it later again ?

What happens to donor antibodies on a blood transfusion into the recipient patient ?  Die, stay or start renewal/multiplication ?

 

[dimreepr]

57 minutes ago, Externet said:

Is it known if a patient that survives this new virus, remains immune to it or can contract it later again ?

I think it's safe to say, you'd be far far far less susceptible...

57 minutes ago, Externet said:

What happens to donor antibodies on a blood transfusion into the recipient patient ?  Die, stay or start renewal/multiplication ?

None of the above...

It's my (limited) understanding that blood has little to do with it, other than transport. 

 

Edited March 14, 2020 by dimreepr

[iNow]

58 minutes ago, Externet said:

Is it known if a patient that survives this new virus, remains immune to it or can contract it later again ?

They’ll be mostly immune unless/until the virus mutates. Once they’re sick and recover, it will generally be safe for them to go out and socialize again... unless/until the mutation occurs. 

[J.C.MacSwell]

What about exposure at a level where you don't "catch" it, or it doesn't take root? Will this have given you at least a head start on reducing susceptibility if exposed to a greater extent later?

Or if you do catch it, is a lesser exposure still consistent with a better outcome? (all other factors being equal)

How about exposure to the dead remnants of the virus, say from the a surface that has been exposed to sunlight? Any potential for positive effect going forward?

I'm sure I have some misconceptions leading to these questions and would be interested in where they are.

 

[druS]

Like Externet I am curious on a couple of issues:

How do you "kill" a virus given that they are not life forms? Why would a period of time render them redundant?

Is not the common cold a corona virus? Have they not been trying to develop a vaccine for decades? If that is the case, what  is the basis for confidence that a solution (vaccine) to Covid-19 will be achieved in months? (Given this needs to happen for a vaccine to be available in 12-18 months).

I have read somewhere that Covid-19 is not mutating (rapidly like flu anyway). How do they determine that?

China looks well to have caught the situation. I understand that secondary transmissions can be expected in epidemics and indeed I see that this happened for Spanish flu. How does that work and what is the likelihood in, say China (but anywhere really), while there is no vaccine?

What rate of exposure and adaptive immune response is required in a population to have the matter under control? I refer here to vaccines for things like measles which require a certain level of immunisation to control the disease - which is not 100%.

Cheers

[iNow]

55 minutes ago, druS said:

have read somewhere that Covid-19 is not mutating (rapidly like flu anyway). How do they determine that?

You sample an early patient. You sample a later patient. You compare them. You see how much it’s mutated. You do the same for flu.  You see if covid mutates as quickly as flu. How is this a question for you?

57 minutes ago, druS said:

How does that work and what is the likelihood in, say China (but anywhere really), while there is no vaccine?

Depends on human behavior 

[CharonY]

12 hours ago, J.C.MacSwell said:

What about exposure at a level where you don't "catch" it, or it doesn't take root?

This is the basic idea for attenuated vaccines. However, ascertaining how is not trivial. 

 

12 hours ago, J.C.MacSwell said:

Or if you do catch it, is a lesser exposure still consistent with a better outcome?

That is unclear. If the dosage is too low it may not result in disease, but may also not trigger immune responses.

 

12 hours ago, J.C.MacSwell said:

How about exposure to the dead remnants of the virus, say from the a surface that has been exposed to sunlight? Any potential for positive effect going forward?

Again, same idea for attenuated vaccines, but without studying what levels of inactivation and required dosages, it is rather risky (or useless).

 

3 hours ago, druS said:

How do you "kill" a virus given that they are not life forms? Why would a period of time render them redundant?

You can think in terms of inactivation. If you destroy their structure they become ineffective.

 

3 hours ago, druS said:

Is not the common cold a corona virus? Have they not been trying to develop a vaccine for decades?

As discussed before, cold is a not a specific disease and given the wide range of viruses causing such mild symptoms there was little incentive to develop a vaccine for each of these viruses. However, there have been work on SARS and from what I remember it was difficult but they were close. But funding effectively dried up as outbreaks were small and there was no sufficient economic incentives, I imagine. 

 

3 hours ago, druS said:

What rate of exposure and adaptive immune response is required in a population to have the matter under control? I refer here to vaccines for things like measles which require a certain level of immunisation to control the disease - which is not 100%.

Any level of immunization as well as immune population reduces the transmission rate. Even if no perfect herd immunity is achieved it would make other measures (such as contact tracing) more effective.

[J.C.MacSwell]

Thanks CY.  

One more:

I can understand why older individuals with compromising health issues would be more at risk, but why would the the very young with underdeveloped immune systems not be more at risk than those still young and healthy but with fully developed immune systems? Covid-19 seems to, thankfully, have spared the very young for some reason, compared to other viruses and flus relatively speaking. I believe the Spanish flu was relatively hard on the middle group that normally would be in the optimal range.

 

[michel123456]

Posted in the Lounge as it is simply a thought.

A method to test many people with few tests:

say for a probability of 1% of infection cases, take a set of 7 samples from 100 people. Mix all the 1st samples in 2 groups of 50 people. Statistically, one group will be positive, one group negative. With 2 tests, you have already eliminated 50 people who have been tested negative. Separate the Pos. group in 2 groups of 25 people & use their 2nd samples. Again 1 group will be pos. the other neg. You have eliminated another 25 people with so far 4 tests (total 75 people). Continue like this until finding the single positive. You will need 14 tests for testing 100 people if my calculations are correct.

What do you think?

[swansont]

How does a 1% probability apply? Is that based on anything valid?
How have you eliminated anyone you haven’t tested?

[Sensei]

28 minutes ago, swansont said:

How does a 1% probability apply? Is that based on anything valid?

It depends on country. e.g. until 13 March 2020 South Korea made 210k coronavirus tests to find out 8k infected individuals which gives ratio 1:26 = 3.8%.

 

I proposed similar method to locals to mix samples and use of binary search algorithm.. Analogy, if you have one black paint can and nine white paints cans, you can mix them together (just tiny bit of each). If result is not white anymore, but slightly greyish, there had to be one black in them, but you don't know which, so there is needed to split cans by half and repeat with new samples. Instead of O(n) operations it will be done much faster. It has sense only if there is many negatives..

An analysis of money delivered every day to banks from shops and individuals can reveal whether there are any unaware infected people in the community.

Edited March 15, 2020 by Sensei

[michel123456]

1 hour ago, swansont said:

How does a 1% probability apply? Is that based on anything valid?
 

No, I took it for simplicity.

1 hour ago, swansont said:

How have you eliminated anyone you haven’t tested?

I haven't. But with this method in 20 steps (40 tests) you have tested more than 1 million.

56 minutes ago, Sensei said:

I proposed similar method to locals to mix samples and use of binary search algorithm

Exactly. Where did you propose that?

[Prometheus]

This sounds like the poisoned drinks problem. Unfortunately it won't work here. In the idealised case where we there is say, exactly 1 in every 100 people infected then it could apply. But for every 100 hundred people we take there is no guarantee of the number of infected people. Sometimes there are none. Most times there will be one. Occasionally there will be 10. It is a random variable itself. Also, the tests themselves have a number of false positives and false negatives which will likely be significant.

[J.C.MacSwell]

7 minutes ago, Prometheus said:

This sounds like the poisoned drinks problem. Unfortunately it won't work here. In the idealised case where we there is say, exactly 1 in every 100 people infected then it could apply. But for every 100 hundred people we take there is no guarantee of the number of infected people. Sometimes there are none. Most times there will be one. Occasionally there will be 10. It is a random variable itself. Also, the tests themselves have a number of false positives and false negatives which will likely be significant.

Agree. Also, wouldn't it dilute the samples to make false negatives more likely?

[swansont]

37 minutes ago, michel123456 said:

No, I took it for simplicity.

I haven't. But with this method in 20 steps (40 tests) you have tested more than 1 million.

But you haven’t actually done that. If you have a false negative, and the ones with the virus who have mistakenly been cleared will be able to more easily pass the virus along.

16 minutes ago, Prometheus said:

This sounds like the poisoned drinks problem. Unfortunately it won't work here. In the idealised case where we there is say, exactly 1 in every 100 people infected then it could apply. But for every 100 hundred people we take there is no guarantee of the number of infected people. Sometimes there are none. Most times there will be one. Occasionally there will be 10. It is a random variable itself. Also, the tests themselves have a number of false positives and false negatives which will likely be significant.

OK, I was taking “a set of 7 samples” to mean you test 7 people. Still, the false negatives will be amplified, and testing needs to be more sensitive to come up positive since they’re diluted, as J. C. has pointed out.

[CharonY]

Iirc the Spanish flu put the immune system on overdrive, resulting in massive inflammation, which caused damages. 

Personally, I think with Covid-19 the issue is less about immune responses alone, but comorbidities. Preexisting conditions are highly correlated with worse outcomes and my guess is that those in conjunction with Covid-19 mediated lung damages are what is causing the fatalities. I.e.younger folks with those issues might also be vulnerable.