What exactly is Government of India doing?

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Red Dragon, since seemingly you know more about this than what I do I will ask the question that I am unable to comprehend. The serological surveys showed that 23% in Delhi have developed antibodies. Does this mean that over time almost 45L-50L have been infected and cured. Does this mean the actual fatality rate is more like 0.1%. If yes, and since there are smart people making decisions at various bodies, why are lockdown measures still being so strictly enforced while the economy suffers despite the fatality rate being much lower than the earlier assumed number of 2%. Every life lost is a tragedy but the question is why the decisions that were taken at a data of 2% still in place when the new data says 0.1% which is probably in line with regular flu.

I am a noob with these things but what am I missing with these calculations.
 
icysmoke said:
Red Dragon, since seemingly you know more about this than what I do I will ask the question that I am unable to comprehend. The serological surveys showed that 23% in Delhi have developed antibodies. Does this mean that over time almost 45L-50L have been infected and cured. Does this mean the actual fatality rate is more like 0.1%. If yes, and since there are smart people making decisions at various bodies, why are lockdown measures still being so strictly enforced while the economy suffers despite the fatality rate being much lower than the earlier assumed number of 2%. Every life lost is a tragedy but the question is why the decisions that were taken at a data of 2% still in place when the new data says 0.1% which is probably in line with regular flu.

I am a noob with these things but what am I missing with these calculations.
Click to expand...
Since I "seemingly" know a little bit of epidemiology, will try to answer your rather interesting questions:
1. Regarding serological surveys,
There are 2 types of serological studies
a. Antibody ( IgG and IgM) based
b.Antigen based assays
Antibody based tests are easiest, fastest, cheapest but have very low specificity and low sensitivity ( varies wildly depending on the duration of viral entry, which is not to be confused with incubation period IP) since we are still not sure of even the IP of the virus, they are of very little practical value.
Antigen based assays are usually of 2 types
a. Truenat
b. Gene Xpert
The truenat machines are rather crude and not fully automated.
I believe in India serology test is truenat based tests which seek out specific proteins only found in the virus, which the body’s immune response recognises as 'foreign'. Most COVID-19 antigen tests target the 'spike protein' that studs the surface of the coronavirus.
Since it's swab based, there are 2 big issues with it
1. Faulty sample collection ( since no amplification, it's more technique dependent than RT-PCR)
2. It will only be positive in "current" infection,
since we don't know how long a patient remains infective, it doesn't really help in breaking the transmission chain
This test merely represent a very gross estimation of current load of the disease ( and every symptomatic with negative antigen should be tested with RT PCR)
I'm not sure of Delhi's ( any part of India/ world, for the matter) situation statistically anymore.
And to be very honest, these test results don't matter at all, given the current situation in India.
Yes, it helps to decrease public panic to certain extent, but that's all these data are good for.
If you really interested in useful data,
I can suggest you one...look out for infection per million in countries who have gone through the first wave of the epidemic, compare it with India's present infection per million.
Now if you want I can post a VERY COMPLEX equation to predict the approximate infection per million depending upon the population density , mean age, mean incubation period etc. But it's extremely complex.
I do not want to comment on mortality rate and spread fear, just use common sense and data from other countries.
Indian doctors are finally agreeing with long term.lung damage after the primary infection, so calculating mortality during the ascending limb of epidemic curve is not very wise.
 
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red dragon said:
Since I "seemingly" know a little bit of epidemiology, will try to answer your rather interesting questions:
1. Regarding serological surveys,
There are 2 types of serological studies
a. Antibody ( IgG and IgM) based
b.Antigen based assays
Antibody based tests are easiest, fastest, cheapest but have very low specificity and low sensitivity ( varies wildly depending on the duration of viral entry, which is not to be confused with incubation period IP) since we are still not sure of even the IP of the virus, they are of very little practical value.
Antigen based assays are usually of 2 types
a. Truenat
b. Gene Xpert
The truenat machines are rather crude and not fully automated.
I believe in India serology test is truenat based tests which seek out specific proteins only found in the virus, which the body’s immune response recognises as 'foreign'. Most COVID-19 antigen tests target the 'spike protein' that studs the surface of the coronavirus.
Since it's swab based, there are 2 big issues with it
1. Faulty sample collection ( since no amplification, it's more technique dependent than RT-PCR)
2. It will only be positive in "current" infection,
since we don't know how long a patient remains infective, it doesn't really help in breaking the transmission chain
This test merely represent a very gross estimation of current load of the disease ( and every symptomatic with negative antigen should be tested with RT PCR)
I'm not sure of Delhi's ( any part of India/ world, for the matter) situation statistically anymore.
And to be very honest, these test results don't matter at all, given the current situation in India.
Yes, it helps to decrease public panic to certain extent, but that's all these data are good for.
If you really interested in useful data,
I can suggest you one...look out for infection per million in countries who have gone through the first wave of the epidemic, compare it with India's present infection per million.
Now if you want I can post a VERY COMPLEX equation to predict the approximate infection per million depending upon the population density , mean age, mean incubation period etc. But it's extremely complex.
I do not want to comment on mortality rate and spread fear, just use common sense and data from other countries.
Indian doctors are finally agreeing with long term.lung damage after the primary infection, so calculating mortality during the ascending limb of epidemic curve is not very wise.
Click to expand...

The equation please..
 
Let's start with within host model:
Let's consider a virus that causes an acute infection. The virus replicates with a rate r to an intrinsic carrying capacity KV and is removed by innate immunity I, non-specific memory cells N and specific memory cells P. Thus, we model three components of immunity based on the observed biology concerning acute viral infections such as influenza. Specifically, innate immune defences are the first to respond to viral infection, whereas non-specific memory cells begin being effective on the time scale of several days post infection. With these principles in mind, we assume that I grows at a baseline rate of bI(1 − I/KI, where bI is a constant rate of growth and KI is the carrying capacity for I, and increases in proportion to viral abundance with rate constant aI. On the other hand, production of N is delayed and grows in proportion to viral abundance with rate constant aN. We can model this delay using the Heaviside step function, Θ(t). Θ(t) = 0 for t < 0 and Θ(t) = 1 for t ≥ 0.

Specific memory cells arise from naive memory cells with a constant lag of τP and grow in proportion to the product of viral abundance and pre-existing P-cell abundance with rate constant aP, and in proportion to naive memory cells with rate constant c. N decays with rate constant dN, while P reaches an asymptote once N and V are cleared completely. We do not implement waning of specific memory cells since we do not consider reinfections here. Since the viral load does not drop until T cells are produced to fight the virus, we assume that the innate immune response is less effective at lowering the viral titre than the T cell response, i.e. kI < kN < kP, where kI, kN and kP are the rate constants of removal of virus for I, N and P, respectively.

The equations governing the within-host dynamics are:
Sorry, I can't type it from a phone..will try to upload an image later ( it's possibly available somewhere online, type equation governing within host transmission)
Just apply the same between host models ( growth matrix to keep it simple) and then extrapolate the value in population under study ( India's population/ state population)
Yes, it's complicated and tedious, but doable. 20200810_210207.jpg Sorry for my terrible handwriting.
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Really sorry for going off topic and turning it to a medical statistics thread!!
But,I love statistics, though in the present situation it does not have much role, but once this thing slows down, everyone in my field will jump into the enormous data this has generated and keep themselves happily busy for months, if not years.Looking forward to that eagerly.
Anyone from Indian Statistical Institute/ AIIH&PH here? Please send me a PM, I am stuck with few things a hardcore statistician can solve easily.
 
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Wow. Thanks for the detailed post. Gives a lot of stuff to delve deeper into. Coming weekend's deep dive topic is sorted :).
The "seemingly" wasn't meant to be a jibe, I didn't know that you are an epidemiologist.
 
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@red dragon A question.

Suppose an infected person with high viral shedding coughs right in your face (worst case scenario) and you're wearing a perfect p100 or whatever mask, but your eyes are completely unprotected, what are the chances of getting infected through that route. Realistically. We know theoretically it's possible, but practically.
 
I'm not sure mate. Yes, theoretically possible as you mentioned, but...conjunctiva and sclera are not similar to skin/ mucous membrane.
Conjunctivitis is a very common early symptom, but I'm not sure if it's the point of entry even in those patients as sclera is really tough structurally.
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Duration of contact is very important, unlikely to catch it if both the individuals are using surgical masks and coming in close contact for less than 10-15 minutes.
I faced similar situation hundreds of times.
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And to be very honest, I'm not a virologist. So don't know much about the virus itself. But since I treated a lot of patients with the infection, possibly know few things about the clinical manifestations.
The latest problem seems to be the residual significant lung/ myocardial damage.
Receiving lot of calls from previously treated patients developing fresh symptoms after 2 months!!
Except three, none got infected again ( RT PCR negative) but a lot of them are having exertional dyspnea, pluritic chest pain etc.
Most of them have developed an obstructive pulmonary disease ( lung function tests are s/o obstructive> restrictive issues) few developed RWMA on echo.
This was one of my biggest fears, returning of symptoms without evidence of new infection.
Everything we know about the virus ( including the pathogenesis) can be wrong.
 
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No need to reach the sclera, if it somehow penetrates the mucous layer into the conjunctiva, could it spread into the circulatory system via the conjunctival blood vessels?

Longer duration of exposure simply means the total viral load in the recipients body keeps increasing till the immune system is no longer able to easily fight it right?

And yes, so many reports coming out of heart and lung issues months after 'recovery'. People are taking it too lightly assuming they have 'immunity'. Even kids are manifesting symptoms similar to Kawasaki.
 
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Bulbar conjunctiva is supplied by ophthalmic artery, palpebral conjunctiva by branches from external carotid.
If there is blood stream invasion through carotids, the virus should be able to enter internal carotid eventually meninges and brain's anterior circulation.
Sure it's causing encephalitis and strokes ( septic embolic) but those are mostly affecting posterior ( vertebro basilar) circulation.
This defies logic.
Higher viral load means the mask's mechanism is failing. Masks don't act like sieves.
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It's really heartening to see techies developing such keen interest in medicine...love you guys...
 
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And you're not like some of the asshole doctors out there who think information is proprietary trade secret meant to be kept out of the hands of lesser mortals!

It's only by sharing knowledge that true progress can happen.

Meanwhile, mask research:

news.sky.com

Coronavirus: Which face covering works best? Scientists test 14 masks - and find one actually increases risk of infection

Scientists have tested 14 different types of face-covering and found that one of them actually increases the risk of coronavirus infection.
news.sky.com news.sky.com
 
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Heard a news that schools in India are opening in September. Is this true?
Don't know right or wrong , but a very bold decision indeed.
 
Looks like semi-fake news. No decision taken either way actually.

www.oneindia.com

Fact check: Govt has taken no decision to keep schools shut till December

A website has claimed that schools in India will not open until December 2020 owing to the coronavirus pandemic.The website attributes the decision to the Union Government and said that schools will remain closed until December.
www.oneindia.com www.oneindia.com

www.india.com

School Reopening News Updates: Centre Says no Timeline Has Been Decided to Open Schools

Issuing a statement, the Centre said that the opening of schools will depend on the situation of COVID-19.
www.india.com www.india.com

www.india.com

Schools Not to Open Before December? Here is The Truth

Neither there has been any decision to reopen schools from September, nor has there been any decision to not open schools before December.
www.india.com www.india.com

What's funny is none of the major media outlets are talking about it so there's probably something brewing.
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Meanwhile, kerala govt. : Privacy? What privacy???
 
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This news is from Feb.

Anything is possible with these guys given that they used various excuses from black money to terrorism to counterfeits to justify demonetisation.

They will use 'health benefits to the poor and economically vulnerable' to make more blanket sweeping surveillance tools to control the sheep.
 
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Julian said:
This news is from Feb.

Anything is possible with these guys given that they used various excuses from black money to terrorism to counterfeits to justify demonetisation.

They will use 'health benefits to the poor and economically vulnerable' to make more blanket sweeping surveillance tools to control the sheep.
Click to expand...

He introduced insurance based health services for public.
Now he is gifting health-history of individuals to those insurance companies (obviously at the expense of tax-payers' money).

Indian-corporate has never seen such a loyal servant.
 
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