JUST ONE PERSON—UK 🇬🇧 scientists think one immunocompromised person who cleared virus slowly & only partially wiped out an infection, leaving behind genetically-hardier viruses that rebound & learn how to survive better. That’s likely how #B117 started. 🧵 https://t.co/bMMjM8Hiuz

2) The leading hypothesis is that the new variant evolved within just one person, chronically infected with the virus for so long it was able to evolve into a new, more infectious form.

same thing happened in Boston in another immunocompromised person that was sick for 155 days.
3) What happened in Boston with one 45 year old man who was highly infectious for 155 days straight before he died... is exactly what scientists think happened in Kent, England that gave rise to #B117. https://t.co/LBc8eCk3f9
4) Doctors were shocked to find virus has evolved many different forms inside of this one immunocompromised man. 20 new mutations in one virus, akin to the #B117. This is possibly how #B1351 in South Africa 🇿🇦 and #P1 in Brazil 🇧🇷 also evolved. https://t.co/74dr2pFiRg
5) “On its own, the appearance of a new variant in genomic databases doesn’t tell us much. “That’s just one genome amongst thousands every week. It wouldn’t necessarily stick out,” says Oliver Pybus, a professor of evolution and infectious disease at Oxford.
6) “New variants of Sars-CoV-2 are being created all the time but the vast majority of them go absolutely nowhere.
It was only when it became obvious that measures in Kent were failing that Public Health England realised the outbreak was being driven by a new variant.”
7) “#SARSCoV2 isn’t the only virus that can linger for an unusually long time within the human body. Ebola virus RNA has been detected in the semen of men a year after recovery. Some people stay infected with norovirus – a common stomach bug – for more than six months.
8) “One man in the UK has excreted infectious poliovirus for at least 28 years. The man had been shedding mutated virus for so long that researchers writing about his infection said that he, and other chronic excretors, pose an “obvious risk to the [polio] eradication programme”!
9) “But the real problem isn’t chronic infection – it’s a situation where pandemic is so out of control that the virus has endless opportunities to mutate into new variants. That situation is a reality in the UK and in dozens of other countries with dangerously high case rates.
10) ““These are all edge cases, but if you have enough people infected over a long time, you run the risk of hitting those edge cases,” says Hodcroft. It is not surprising that some of the most worrying new variants – from Brazil, South Africa and the UK –
11) ...”emerged from parts of the world with relatively high levels of transmission. “When you have millions of people infected, with millions of viruses replicating in each one, there are lots of chances for the virus to explore new mutations and combinations,” says Lauring.
12) ““If we had control of the virus, we wouldn’t be seeing as many variants pop up, because there wouldn't be as many opportunities for evolution to happen.”
13) Since Sars-CoV-2 infects cells relatively quickly, in most cases it enters a host, replicates and then swiftly infects someone else, leaving little time for the virus to acquire many genetic changes.
14) When the virus enters the body of someone who is already immunocompromised, their body is constantly applying evolutionary pressure on the virus – pushing it to evolve into new and, in some cases, more infectious forms.
15) My take: the moral lesson is that, when given time and opportunity, the virus finds a way. The virus is a cunning mutating beast that will try every way to defeat us if we let it keep proliferating. We must stop it FAST, or else it will evade: https://t.co/Zk46pouYLM
16) And the virus will even evade people who has had prior immunity and prior antibodies to the older common #SARSCoV2. Such as this example — here not even people were protected from severe disease even if with prior immunity. https://t.co/yqgeNJsgzj?
17) Now just look where we are... #B117 is threatening to dominate the US soon next month as well. Florida especially. https://t.co/I7zIjne6nD
18) It’s now growing so fast in Florida, #B117 is already at 10% of all cases. And doubling time in 9 days or maybe even less. https://t.co/DlHtxqaXAr
19) If we go for full suppression, then we can have this too https://t.co/6HkE2IoDTY

More from Eric Feigl-Ding

📍DOUBLE REINFECTIONS—wow, both PM Justin Trudeau and Biden’s HHS Secretary Becerra got *reinfected* with #COVID19–from same conference—➡️when did Becerra last get infected? May 18th 2022—not even a full month ago! Trudeau in Jan 2022. I worry it’s reinfections due to #BA5/#BA4.


2) #BA5 and #BA4 are worrisome. They are surging and they have high reinfection potential. Your past BA1/BA2 doesn’t substantially protect you from #Ba5/4


3) Excess deaths—the new #BA4 & #BA5 variants of the coronavirus are currently the **fastest growing** strains in the US & UK. ➡️They are exponentially replacing all other past strains. Learn from South Africa’s early warning signs and their excess deaths. #CovidIsNotOver #COVID


4) Is it a Paxlovid rebound for Becerra, as some are asking? Unclear—Paxlovid rebound usually only happens at day 10-14 that we know of and have data. The FDA says it’s 1-2% rebound but I counted 12% from this Pfizer graph submitted to FDA.


5) and yes, #ba5 / #BA4 are very problematic. they are 2x more resistant than even BA2 for neutralizing the virus compared to those who had breakthrough reinfections from older Omicron.

More from Science

An interesting thing about carp is that they can go into anoxic hibernation and switch to an anaerobic metabolism based on converting glycogen to ethanol.

The waste ethanol is diffused out the gills

https://t.co/V3D1umHf04

Carp can switch over to an anaerobic metabolism and quietly exhale booze until the situation gets better.

They basically evolved the same metabolic pathway as yeast, independently.

In theory, if you spent a few thousand years breeding carp for it, you could use them to make booze.

They'd be enormous, almost entirely glycogen deposits with a fish added as an afterthought.

The really interesting thing about anaerobic carp, is that they can go 4-5 months without oxygen by relying on liver glycogen.

You, a human, have only about 100 grams of glycogen in your liver, about 400 more grams in your skeletal muscles. Call it 500 grams total.

In humans, glycogen is also burned for energy. This is where the marathon runner's bonk comes from: you only have about 2,000 calories worth, and running a marathon burns those 2,000 calories.
Hugh Everett's birthday! Pioneer of the Many-Worlds Interpretation of quantum mechanics. Let us celebrate by thinking about ontological extravagance. I will do so by way of analogy, because I have found that everyone loves analogies and nobody ever willfully misconstrues them.


We look at the night sky and see photons arriving to us, emitted by distant stars. Let's contrast two different theories about how stars emit photons.

One theory says, we know how stars shine, and our equations predict that they emit photons roughly uniformly in all directions. Call this the "Many-Photons Interpretation" (MPI).

But! Others object. That is *so many photons*. Most of which we don't observe, and can't observe, since they're moving away at the speed of light. It's too ontologically extravagant to posit a huge number of unobservable things!

So they suggest a "Photon Collapse Interpretation." According to this theory, the photons emitted toward us actually exist. But photons that would be emitted in directions we will never observe simply collapse into utter non-existence.
Hard agree. And if this is useful, let me share something that often gets omitted (not by @kakape).

Variants always emerge, & are not good or bad, but expected. The challenge is figuring out which variants are bad, and that can't be done with sequence alone.


You can't just look at a sequence and say, "Aha! A mutation in spike. This must be more transmissible or can evade antibody neutralization." Sure, we can use computational models to try and predict the functional consequence of a given mutation, but models are often wrong.

The virus acquires mutations randomly every time it replicates. Many mutations don't change the virus at all. Others may change it in a way that have no consequences for human transmission or disease. But you can't tell just looking at sequence alone.

In order to determine the functional impact of a mutation, you need to actually do experiments. You can look at some effects in cell culture, but to address questions relating to transmission or disease, you have to use animal models.

The reason people were concerned initially about B.1.1.7 is because of epidemiological evidence showing that it rapidly became dominant in one area. More rapidly that could be explained unless it had some kind of advantage that allowed it to outcompete other circulating variants.

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