18 February 2021

m_d_h: (Default)
You've heard of DNA, the genetic code inside each cell that is used to replicate proteins, the genetic code that we pass down to our children via the sexual combination of female egg and male sperm.  RNA is a simpler version of DNA that can also replicate proteins, but with a much higher error rate.  RNA lacks the ability to proofread the replication process, whereas DNA has a proofreading function.  Think of the "D" in DNA as standing for "Double-checking NA", although that's not what it really stands for.  Think of the "R" in RNA as standing for "Reckless NA".

With DNA's double-checking proofreading function, it makes replication errors in one step per 100,000,000 on average.

RNA makes replication errors in one step per 10,000 on average.  That's 10,000x as often as DNA's error rate.

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The COVID virus variants use RNA to copy themselves after they've successfully infected a human cell.  Creating a new copy of a COVID virus requires about 10,000 replication steps.  As RNA makes mistakes in one step per 10,000 on average, the average new copy of a COVID virus contains a mistake.  On average, each COVID virus that is produced looks slightly different from the previous one.

In other words, most COVID virus particles contain mutations.  In the universe of RNA viruses, mutations are the rule not the exception.

As a result, most COVID virus particles don't work.  This is typically true for viruses in general -- most virus particles don't work.  They're born broken, unable to infect new cells, destined to disappear rather quickly as they erode under environmental pressures (heat, light, hungry neighboring cells, etc.).

This is why a single virus particle is unlikely to cause an infection.  To get infected, you need to be exposed to a large number of virus particles.  Sometimes dozens, sometimes hundreds, sometimes thousands.  When your coworker sneezes on you, the vast majority of those virus particles ejected from her mouth and nose are duds.

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Although viruses are mutating all the fuckin' time, the vast majority of these mutations produce broken copies that don't work.  A small fraction of these mutations don't affect the functioning of the virus -- think of them as different color paint jobs -- a purple virus instead of a green virus -- virus particles that otherwise work exactly the same as their parent.  An even smaller fraction of these mutations somehow improve the functioning of the virus.

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With respect to the Original COVID-19 that emerged from China, there are countless variants that work pretty much the same as the original -- they differ only with respect to their "color".

Each person who is infected with COVID-19 carries around 10,000,000,000 functioning virus particles at peak infection, on average.  Each of these functioning virus particles creates thousands of copies of itself before its host cell bursts, releasing these new copies into the body.  Most of these copies are broken, but enough of them work well enough to infect more cells, using those cells to create thousands of copies until they burst, etc.  Without our immune systems, COVID-19 would kill us every time, bursting and infecting and bursting its way through our body until we're dead.

Currently, on any given day, tens of millions of humans around the world are actively infected with COVID-19.  This means the active population of COVID-19 virus particles at this moment is somewhere around a quintillion, and each of these virus particles is in the midst of creating thousands of copies of itself.

This huge population of virus particles, making mostly mistaken copies of themselves, is bound by the laws of statistics to come up with some random mistakes that actually work better than their parent virus particles.

This has now happened at least three times.

Once in the UK by September 2020, once in South Africa by December 2020, and once in Brazil by January 2021.  These three variants of COVID are each some combination of more infectious and less susceptible to antibodies/vaccines than the original China variant discovered in December 2019, and they've each gone global thanks to continued air travel.

You could call the UK variant COVID-20a, the South African variant COVID-20b, and the Brazilian variant COVID-21a.

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Scientists are working to figure out how much more infectious and how less susceptible to antibodies/vaccines these new COVID variants might be.

In general, they seem to be 50% more infectious, and 50% less susceptible to antibodies/vaccines.  But we do not know precisely yet.

We know that some people who have already been infected with COVID-19 have been reinfected with one of these three variants.

We know that the vaccines we've already approved are less effective against some of these variants.

As a result, the vaccine manufacturers are already working to update their vaccines to match these variants.

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Meanwhile, a quintillion COVID particles are busily making thousands of copies of themselves at this moment, and most of these copies will be mutations.  Most of these mutations will not work.  Some of them will work just the same as their parent, but with a different "color" coat.  Occasionally, one of them will work better than their parent, and a new variant will have emerged.  Maybe the next new variant will appear in the US, maybe in India, maybe in Sweden, maybe in Mexico.  Who knows, the process is entirely random.  But there's no reason to think we're done with COVID mutations after three new global variants have emerged in a matter of months.

This is why COVID is not going away anytime soon.  This is why even if you've had COVID before, or even if you've been vaccinated, you may get COVID again.  This is why we're probably going to need annual booster shots for COVID like we do for influenza.  This is why I wonder whether we'll ever go back to the old normal, or whether we'll just get used to some average number of daily deaths from COVID, like we're used to an average of 100 daily deaths from influenza in the US.

The chances are you'll get COVID someday, or you'll get COVID again someday.  So what will our new normal look like?  And for how long will you remain in Quarantine?
m_d_h: (Default)
It's a good thing I skipped the weight lifting in favor of snow shoveling because trying to shovel these two inches of frozen sleet was impossible.  I tried, I really tried, but I started feeling like my hands were going to form blood blisters from trying to scrape this frozen shit off the sidewalk.  Not to mention the stress on my arms and shoulders.  I couldn't finish, and I've felt sorta sick ever since.  I think if I'd continued, I would've ended up with painfully swollen hands for a couple days.

I completed the work I had to complete today, and then I quit at 4pm, I'll take two hours of sick leave.

T didn't even try to shovel this crap.  Usually we split the job of shoveling and it doesn't take that long, except for that 2016 Snowpocalypse when we had two feet of snow and I paid somebody to come over with his snowblower.

This winter we're not really getting snow, we're getting freezing rain and sleet with a bit of decorative snowfall in between the layers of ice.  But today we didn't get any snowflakes, it was all freezing rain, then sleet, then it all froze together like that shit on your freezer coils that requires you to unplug the thing and let it defrost.  You cannot shovel it, you can only pound and scrape it an inch at a time.

It will be above freezing for a while tomorrow afternoon, but I was hoping to be downtown by then.  And I'm not sure having the air a few degrees above freezing will help with shoveling that crap anyway.  But then it's gonna be cold cold over the weekend.  This neighborhood is gonna take a while to melt out of this sleetstack.
m_d_h: (Default)
He said, "I studied how this stuff works for 10 years and you want me to explain how it works in 5 minutes,"

Yes!

Here was my question:  Why do we need a flu vaccine every year, but we only need the measles vaccine once as kids?  Doesn't the measles virus mutate as often as the influenza virus?

It took awhile for Public Health Friend to get to my point.  Yes, the measles virus mutates as often as any other RNA virus.  But he wanted to explain the different survival strategies and host populations of the two viruses.  He felt I was using his field's terminology too loosely.

But I'll get to my point.  Both measles and influenza are RNA viruses and they both mutate a lot, on average once per new virus particle.  But measles is built like a precision missile -- it is super infectious against human cells -- and so each copy of the measles virus either works the same or it doesn't.  There's not really any room for mutations to make measles even better, or to change how it looks.  It's too precisely-well designed for infecting human cells.  Most measles copies don't work, because of mutations, but the minority of true copies are fuckin' powerful weapons.

But with influenza, it's more like spam.  Not nearly as infectious, but there are lots of ways for influenza mutations to result in different-looking versions of still-effective influenza.

With influenza, changing its coat every season to avoid last year's antibodies is its well-evolved survival strategy.

With measles, having a super-effective precision infection skill is its well-evolved survival strategy, so it can't change its coat every season or it stops working.

So there are viruses that have a stable set of working copies, that we can easily vaccinate against, and there are viruses that have a potentially endless variety of working copies, that we cannot easily vaccinate against.  Influenza and most of the common cold viruses -- some of which are coronaviruses, distant relatives of COVID -- have a potentially endless variety of working copies.  COVID may end up being like influenza and most common cold viruses, with potentially endless varieties that can evade last season's antibodies.

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So what about HIV, why don't we have a vaccine for HIV, I asked Public Health Friend.

HIV is a retrovirus, a completely different category of virus -- "retro" meaning backwards, retroviruses work backwards compared to normal viruses, making them difficult for your immune system to fight.  And HIV also specifically targets the immune system's cells, so when your T cells come sniffing around for HIV, the HIV infects them before the T cells can do anything about them, and blows them up.  It's like HIV always wins the initiative roll against T cells and strikes first with a critical hit.

An RNA virus like COVID invades a cell and uses the cell's machinery to make new virus copies until the cell bursts from all these byproducts, releasing all the virus copies into the body.  Retroviruses invade a cell and then copy themselves permanently into the DNA of the cell -- where they either lie dormant for a while, or they continually produce copies of themselves without destroying the host.  Instead of bursting their host cells, new copies of HIV "bud" through the cell walls and then go looking for new hosts.

Your immune system cannot fix this embedded HIV DNA inside your cells.  Your immune system is not designed to edit your own DNA.  When your T cells look at an HIV-infected cell, it looks fine to them, there's no "virus" inside, only some updated DNA inside the cell nucleus.  And your antibodies can chase after the new HIV viruses that are floating around in your blood, but they can't get to the embedded DNA inside your cells that keep producing new HIV.  So antibodies for HIV cannot get rid of the source of the HIV infection.  So a vaccine that produces HIV antibodies doesn't help much.  HIV antibodies cannot cure you of, or even protect you from, an HIV infection, so producing HIV antibodies via an HIV vaccine is pointless.

HIV is also a slow burn infection.  It can take years to ramp up inside your body.  You can have this equilibrium where your HIV antibodies are cleaning up nearly all the HIV viruses that your HIV-infected cells are making, but over time a few of these new HIV viruses slip through the antibody net and infect new cells.  Until finally, after years of this game, so many of your cells are making HIV that they overwhelm your antibodies and then wipe out your T cells, leaving you defenseless against secondary infections -- the stage of HIV infection known as Acquired Immune Deficiency Syndrome (AIDS).

Scientists found other ways to stop HIV, via antiviral drugs.  They can block HIV from entering new cells, they can block HIV from creating new slices of HIV DNA, they can block HIV from updating your cell's DNA with slices of HIV DNA, and they can block new HIV copies from budding out of infected cells.  They can do everything to stop HIV from infecting and replicating except -- to cure your already-infected cells.  There's no drug that can edit the HIV DNA out from the inside of your cells.

BTW, this is how Prep works --> by blocking HIV from entering new cells, and if that fails, blocking HIV from creating new slices of HIV DNA to insert in your cells, and if that fails, blocking HIV from updating your cell's DNA with slices of HIV DNA.  But Prep doesn't kill HIV, it just blocks it from working until it dies a natural death.  Viruses usually don't live for long inside the human body if they can't infect a cell.

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It is possible to design antiviral drugs that block other kinds of viruses.  We already have antivirals that block influenza, and plenty of scientists are working on new antivirals that would block COVID.  But there's always the danger that viruses will mutate around specific antiviral drugs, that's why for HIV infection you have to take a triple-drug cocktail for the rest of your life, to block HIV from having any chance of replicating inside your body, so that it cannot even mutate.

Fun stuff!

But it is way more complicated than my description.  This is the 5-minute version.  Go study immunology for 10 years if you want to know how it all really works.

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