[Snorlax94]

Or, the true numbers are 20-35x (!!!)

https://www.sfgate.com/bayarea/article/C...196799.php

If true, that would push the cfr down to .08-.14 percent.

The transmissibility would be scary but the lower cfr would be great news.

I personally don’t expect anything *this* big, especially since ~90% tests were coming back negative.

Can’t wait to read the results of the recent Stanford study in SCC. I read they were supposed to release results late last week, so maybe the result was wildly unexpected?

[Snorlax94]

Or, the true numbers are 20-35x (!!!)

https://www.sfgate.com/bayarea/article/C...196799.php

If true, that would push the cfr down to .08-.14 percent.

The transmissibility would be scary but the lower cfr would be great news.

I personally don’t expect anything *this* big, especially since ~90% tests were coming back negative.

Can’t wait to read the results of the recent Stanford study in SCC. I read they were supposed to release results late last week, so maybe the result was wildly unexpected?

[BostonCard]

Would be great news if true.  Like you I would be a bit surprised if it was quite that high.

BC

[BostonCard]

Would be great news if true.  Like you I would be a bit surprised if it was quite that high.

BC

[OutsiderFan]

It would be awesome if everyone who has been infected and had an opportunity to develop antibodies is safe from the virus. 

Do we have any such evidence? All I have seen on the subject is that this is an assumption. I have read some research reports that show reinfections do occur and that particularly younger people don’t develop enough antibodies to fight off a second exposure after recovering from initial infection.

The other thing we don’t know is what will happen to people who recovered from first infection but don’t have enough antibodies to fight off another infection? Will they have just as easy of a time with it as the initial exposure, or will a second one do more damage?

[OutsiderFan]

It would be awesome if everyone who has been infected and had an opportunity to develop antibodies is safe from the virus. 

Do we have any such evidence? All I have seen on the subject is that this is an assumption. I have read some research reports that show reinfections do occur and that particularly younger people don’t develop enough antibodies to fight off a second exposure after recovering from initial infection.

The other thing we don’t know is what will happen to people who recovered from first infection but don’t have enough antibodies to fight off another infection? Will they have just as easy of a time with it as the initial exposure, or will a second one do more damage?

[M T]

I have to assume Dr. Scott Morrow is a reasonable physician and did not pull this number out of the air.  He calls it a "guess".  Is this a WAG or a SWAG?  He gives no reason for his number.

Until he gives a reason, I'm skeptical.

[M T]

I have to assume Dr. Scott Morrow is a reasonable physician and did not pull this number out of the air.  He calls it a "guess".  Is this a WAG or a SWAG?  He gives no reason for his number.

Until he gives a reason, I'm skeptical.

[BostonCard]

Do we have any such evidence? All I have seen on the subject is that this is an assumption. I have read some research reports that show reinfections do occur and that particularly younger people don’t develop enough antibodies to fight off a second exposure after recovering from initial infection.

I think the big question on the reinfection is whether they are true reinfections.  A lot of times they are framed as a patient who tested positive after having tested negative, which could just as well represent an intervening false negative test in a patient who is continuing to shed, which we know happens somewhere between 5 and 10% of the time (even two false negative tests would be expected to happen some proportion of the time).  To me, the most important thing is whether these reinfections are symptomatic, resolve their symptoms and test negative and then have symptoms again and test positive.  That would probably be a true reinfection, and I haven't seen that described yet.

BC

[BostonCard]

Do we have any such evidence? All I have seen on the subject is that this is an assumption. I have read some research reports that show reinfections do occur and that particularly younger people don’t develop enough antibodies to fight off a second exposure after recovering from initial infection.

I think the big question on the reinfection is whether they are true reinfections.  A lot of times they are framed as a patient who tested positive after having tested negative, which could just as well represent an intervening false negative test in a patient who is continuing to shed, which we know happens somewhere between 5 and 10% of the time (even two false negative tests would be expected to happen some proportion of the time).  To me, the most important thing is whether these reinfections are symptomatic, resolve their symptoms and test negative and then have symptoms again and test positive.  That would probably be a true reinfection, and I haven't seen that described yet.

BC

[M T]

Is it possible that some, perhaps many, of asymptomatic cases (with reported fewer antibodies) never really completely kill off the virus in 2 weeks and become low rate infection sources?  Maybe their R0 is 0.1 or so, but they continue being infectious longer than those that got sicker & got more antibodies.  I could imagine a scenario some of the asymptomatic might never develop the virus in the airways (for nasal swabs or CT scan detection) but carry them somewhere else.   (But, then, wouldn't they infect their own airways?  Maybe they've got enough antibodies to discourage that.  Maybe that's what happens in some of the delayed onset cases.)

A paper that I probably wouldn't have paid much attention to, except that it fit Santa Clara County's data, is
A Very Flat Peak:Exponential growth phase of COVID-19 is mostly followed by a prolonged linear growth phase, not an immediate saturation

While the transition out of an exponential phase is relieving, the roughly constant number of daily new infections differ widely, range from around 50 in Singapore to around 2000 just in Lombardy (Italy), and 7600in Spain. The daily new infection rate of a region seems to depend heavily on the time point in the exponential evolution when the restrictive measures were adopted, rather than on the population  of  the  region.  It  is  not  easy  to  point  the  critical  source  of  these  persistent infections.  We  attempt  to  interpret  this  data  using  a  simple  model  of  newer  infections mediated  by  asymptomatic  patients,  which  underscores  the  importance  of  actively identifying any potential leakages in the quarantine.

Sorta like neutrinos, we (currently) only see the asymptomatic by the effects they cause.

[M T]

Is it possible that some, perhaps many, of asymptomatic cases (with reported fewer antibodies) never really completely kill off the virus in 2 weeks and become low rate infection sources?  Maybe their R0 is 0.1 or so, but they continue being infectious longer than those that got sicker & got more antibodies.  I could imagine a scenario some of the asymptomatic might never develop the virus in the airways (for nasal swabs or CT scan detection) but carry them somewhere else.   (But, then, wouldn't they infect their own airways?  Maybe they've got enough antibodies to discourage that.  Maybe that's what happens in some of the delayed onset cases.)

A paper that I probably wouldn't have paid much attention to, except that it fit Santa Clara County's data, is
A Very Flat Peak:Exponential growth phase of COVID-19 is mostly followed by a prolonged linear growth phase, not an immediate saturation

While the transition out of an exponential phase is relieving, the roughly constant number of daily new infections differ widely, range from around 50 in Singapore to around 2000 just in Lombardy (Italy), and 7600in Spain. The daily new infection rate of a region seems to depend heavily on the time point in the exponential evolution when the restrictive measures were adopted, rather than on the population  of  the  region.  It  is  not  easy  to  point  the  critical  source  of  these  persistent infections.  We  attempt  to  interpret  this  data  using  a  simple  model  of  newer  infections mediated  by  asymptomatic  patients,  which  underscores  the  importance  of  actively identifying any potential leakages in the quarantine.

Sorta like neutrinos, we (currently) only see the asymptomatic by the effects they cause.