What’s behind India’s second wave? A simple model can help us understand what’s going on.
There’s lots of variation between cities, so it’s best to look at a single city like Bangalore. Why did cases in Bangalore start to dip in Oct 2020? Why did they start to rise in Mar 2021?
“R0” is the average number of new infections that would be caused by one infected individual, assuming nobody is immune. This depends both on behaviour and viral biology.
Let’s define the “level of caution” as the inverse of R0. Less cautious people cause more infections.
Let’s scale the y-axis from 0 to 1. In RED is the fraction of people who have recovered, and so are immune (measured from BOTTOM). In GREEN is the level of caution (measured from TOP).
When the red and green curves cross, new cases per day start to fall. This is “herd immunity”.
What happens if we drop our guard? The level of caution drops, so the standing level of immunity is not enough to stop infections spreading.
More people get infected, until we hit a second herd immunity threshold. This kind of second wave is usually smaller than the first.
After the first wave, broad immunity keeps new infections low even if people are less cautious, or if a more infectious strain arises.
But immunity fades. Someone who has recovered could be reinfected. The combination of less caution and less immunity drives a large second wave.
Fading immunity is why “natural herd immunity” won’t end the pandemic.
But we can increase immune protection through widespread vaccination. (We may need annual vaccinations to deal with new strains or fading immunity.)
So stay cautious, and if you are eligible, get vaccinated!
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"The term community transmission means that the source of infection for the spread of an illness is unknown or a link in terms of contacts between patients and other people is missing." [Wikipedia]
The novel coronavirus originated in Wuhan. So *every* case in India must have arisen, via a chain of contacts, from Wuhan. Therefore, *every* case in India involves an international traveller as part of the chain of infection. This is a matter of logic, not epidemiology.
2/5
Community transmission is a statement about the limits of our knowledge. It's not a statement about the virus.
In some cases we can establish the chain to an int'l traveller. This is not community transmission.
In some cases we can't. This is community transmission.
3/5
In coming days, it's important for the public to know that experts looking at the same data can legitimately disagree.
E.g. Consider the debate about whether community transmission has begun. Due to Bayes' Theorem, the answer depends on what you already believe.
Thread.
1/9
Assume the ideal case: don't consider asymptomatic carriers, let test results be instant.
We test 1,000 symptomatic cases and all are negative. This means there's no community transmission right?
Wrong. To interpret the result, we need to make a bunch of assumptions.
2/9
First we need to define some level of C.T. to look for. In the high-incidence group of symptomatic int'l travellers & contacts, about 2% are positive (283 out of 15,701 tested).
Let's assume that incidence due to C.T. among all symptomatic people is a tenth of that: 0.2%.
3/9
I was shocked to see such shoddy journalism from @the_hindu. They spun a 3-month-old *open-access* paper into a "secret" conspiracy theory, without even requesting a statement from the authors! The report, even the headline, contained many false statements.
A science journalist would have read the paper and spoken to the authors, rather indulging in speculation in the midst of a public health crisis. As @NCBS_Bangalore was not given a chance to respond, we have issued a clarification, covered by @1amnerd. thewire.in/the-sciences/c…
This thread explains the facts, and shows precisely how flawed the original report was. @the_hindu has been sent a formal statement from NCBS, but they are yet to issue a correction.
In dogs, three genes *independently* determine if the coat is short or long, soft or wiry, and straight or curly! science.sciencemag.org/content/326/59…
This kind of "gene-for-X" story is actually very rare, despite what the news headlines often claim. So why is it true in this case?
Knowing how cells work, it's not surprising most traits are "complex": they depend on 1000s of genes: quantamagazine.org/omnigenic-mode…. Conversely, mutations in most genes are "pleiotropic": they affect 1000s of traits.
So when would we expect a single gene to control a single trait?
Genes encode both "material" and "regulatory" proteins (as well as regulatory RNA and DNA elements).
Just like a tap controls the outflow of hot and cold water, regulatory proteins control the levels of the material proteins that give a cell its physical and chemical properties.
India has historically made large public investments in science. But now govt support is flat (in $) and decreasing per scientist (with PhD numbers as proxy). When government steps back, private entities will be able to set the agenda.
Thread
There are many reasons the nominal cost of research goes up:
1. More scientists. 2. Inflation raises costs of supplies, salaries. 3. Cost of new technologies.
We can't just track inflation rate for bunsen burners: we need cryo-EMs and DNA sequencers too. New tech is expensive.
For example, the Department of Biotechnology's annual budget from 2017/18 to 2018/19 is flat, at less than $400 million (see top of thread). The dollar exchange rate matters, because new technologies are often not locally available. Indigenization will help, but only marginally.