I've mostly been staying silent about all the Omicron news. The data is still very preliminary and even experts widely disagree about what it all means. Why would I get in the middle of all that? Especially since nothing much has changed on a practical level: the best advice is still to get vaxed and wear a mask indoors.
However, the CDC finally got me curious about something. According to their surveillance data, Omicron has gone from 0% of all COVID cases three weeks ago to 73% of all cases last week. Given the current number of new daily cases, this means that Omicron has gone from 0 to 91,000 cases within 14 days. At the same time, Delta went from 107,000 to 35,000 cases.
I don't get this. Why would Delta infections fall off a cliff like that? Shouldn't Delta continue to spread independent of Omicron, at least for a while? Or is Omicron spreading so thoroughly that every time a Delta virus tries to spread it finds that Omicron has already been there? That would stop Delta in its tracks, but it seems unlikely since it implies that virtually all Omicron cases are among people who coincidentally get Delta infections a few days later.
Something about the math doesn't seem to add up here. What am I missing?
I suspect there might be some sampling bias here. Omicron has a distinctive signature on a PCR test called the S-gene dropout which flags the sample as a possible omicron case, although the signature is not unique to omicron.
I was just talking to the spouse about this. It seems weird to have omicron be much more infectious than Delta, but instead of spreading independently and massively increasing cases, it is displacing Delta and cases are rising slowly, if at all.
My state had one of the very first identified omicron cases, yet our overall case rate is going down. Omicron should be infecting tons of people who would otherwise not be infected. But that isn't what the current data shows.
My only guess is that omicron is producing a ton of
nearly asymptomatic infections among the vaccinated. Real cases are many times higher than they were a week or two ago, but people don't recognize the infection, and are not getting tested. That would potentially explain why a much more infectious strain is displacing Delta, but without a ton of measured case increases.
Perhaps as people test ahead of travel this week we'll see massive spikes in reported cases among the asymptomatic.
I've reada significant number of positive tests (~40%) now are asymptomatic. Not sure how that has changed since earlier waves. Since more testing = more cases, less testing = less Covid! That accounts for the NFL's change of protocol to test symptomatic players only. Fewer games to reschedule. Brilliant.
My unscientific wild ass guess about the decline of Delta: it's about the ease of transmission. Omicron (apparently) is contagious with with a smaller number of particles and/or a less invasive penetration of the respiratory system. A person exposed to the Covid virus is more likely to be infected if exposed to the Omicron variant. Omicron at first had less prevalence than Delta, but because it is so contagious it has quickly become more prevalent than Delta. It's possible that whatever variant first infects a person replicates quickly enough to preclude the infection of another variant. In any case, it appears that once a variant becomes dominant, other variants decline in prevalence.
An actual scientific explanation here regarding spread of Delta, from July:
Why Do Variants Such as Delta Become Dominant?
Mutations that make a virus more transmissible are only part of the equation
https://www.scientificamerican.com/article/why-do-variants-such-as-delta-become-dominant1/
One advantage Omicron has over Delta is greater ability to evade vaccine immunity.
The problem is, it doesn't evade it. It just shows up as a asymptomatic case.
I know lots of 20-30 somethings in Brooklyn all vaccinated & most boosted who've gotten covid in last week. Some asymptomatic, many with mild symptoms (headache, low fever, cough, fatigue). All testing positive. They all know each other and felt fairly invincible up to now.
Right. But nope. Most have not. 40% of all cases are asymptomatic.
Joseph,
Respectfully think you are missing the point.
Your post and the scientific American article, which I did read, explains omicron outcompeting delta by evolutionary relative advantage. But that cannot really explain why delta goes down so fast. Initially that would not cause delta to decline at all. Omicron would just grow faster. But then the natural immunity caused by all the omicron infections would reduce delta spread. But that takes a longer period and is more gradual. And not enough time to see that yet. Omicron has not been here long enough to develop much natural immunity I those recovered.
That article is from July and I did notice it said that the virus cannot really mutate much on spike protein and still work. That was theory why vaccine immunity would be better than natural for mutations. The scientists had focused on the spike because no way the virus can mutate much there to avoid vaccine antibodies and still be effective.
Well omicron says hi and demolishes that scientific conceit .
There's a lot we don't know. We don't know how long Omicron has been around. Waste water tests have shown it's more prevalent than individual Covid testing shows, and likely here longer than we knew as well. Symptomatic people getting tested are a lagging indicator. We also don't know long before an infection provides immunity to other variants.
Omicron:
a) much more contagious than Delta (higher R0)
b) much larger target population than Delta (probably over 80% for O, under 30% for D)
That accounts for the rapid rise and higher incidence of Omicron. But my guess is it also explains the decline in Delta. Delta spreads more slowly but almost entirely among the smaller group with no immunity (from prior infection or vax) who practice risky behavior (no masks, distancing, etc.). People in that group are now much more likely to have already been exposed to Omicron before Delta arrives. The population of people ripe for a Delta infection is diminishing quickly. Any assumptions about how long that process should take is conjecture. The data supports the idea that it's happening rapidly.
The lineage goes back to October 7 so not before then right?
"... What am I missing?"
A couple of possibilities. The 95% PI interval is huge. Also as usual the Thanksgiving holiday has messed up the reported data.
A very good question, that is not answered just by noting that omicron is more contagious than delta. The proportion of active cases in the population at any one time is relatively small, and the proportion of susceptible hosts is relatively much larger, so the new-case rates for each variant should be almost completely independent.
There has been a significant uptick in vaccination rates in the last few weeks. It seems likely that other transmission-inhibiting behaviors have increased as well: more mask-wearing, more distancing, fewer interactions, more cancellations of events, etc. That is what has reduced cases - absent the behavioral response, both delta and omicron case numbers would be higher.
I believe behavior changes underlie at least part of the waves that we have seen in case numbers - when cases rise dramatically, people become more cautious, and cases fall again, leading to complacency….
The susceptible population has dropped from a combination of previous exposure to Delta, a surge of booster vaccinations, and then exposure to Omicron. Delta was all set to decline rapidly before Omicron got here, and then Omicron drained the susceptible pool even further.
Semi-OT: A question that had been nagging me was, why do viruses often become less severe as they become more contagious? This post by Kevin got me thinking a bit more about it. I had also been thinking that it would be useful to model the pandemic from the virus’ ‘point of view’, so to speak. The virus has the problem that, once it infects a host, the clock starts ticking: either the host’s immune system will destroy it, or it will destroy the host and with that, itself. It must absolutely find a new host before either of those outcomes occurs. So just now, I realized that it is to the virus’ advantage to allow its host to be up and walking around, the better to come into contact with a new host. What makes the common cold common is that the cold sufferer is generally able to continue most normal activity, and thereby pass the virus along. Negligible lethality is adaptive, if you happen to be a virus.
"Negligible lethality is adaptive, if you happen to be a virus."
That is precisely true, and probably the reason that "Sweating Sickness" disappeared and H5N1 Influenza only gets a shot at human populations once every two or three generations. If you're lethal virus, people avoid you --- like the Plague.....
It's called tradeoff theory (between infectiousness and virulence).
Ken, I think you've identified an attribute at the microscopic level that some religious zealots have always thought of only at the highest level--intelligent design. 😉
Maybe, to put that last sentence slightly differently, transmissibility is the trait that most favors continued/expanded reproduction in a mobile host population? A virus or pathogen that was both highly transmissible and 100% lethal would be self-limiting at some point, where one that was highly transmissible, negligibly lethal, and capable of reinfecting would bounce around in perpetuity. Everything else is somewhere between those extremes.
Smallpox, iirc, was about 30% lethal at its worst, extremely transmissible, but not able to reinfect the same individuals. It left enough carriers alive to recur in periodic outbreaks in different places. But like chicken pox it didn't mutate.
The common cold and flu viruses do, so they can reinfect the same individuals. In those cases, the mutations that favor transmissibility would tend toward dominating, and those that favor lethality would tend toward not dominating, wouldn't they? But I don't think that's a guarantee against a set of mutations that combine both extreme transmissibility and high lethality. More like a preponderance of pressures toward transmissibility and away from lethality.
Anyway, it's a theory.
Googling around a bit, the picture is (of course) more complicated - a virus that is highly infectious in early stages can kill its host and still survive in the population. There are multiple trade-offs among virulence, lethality, ‘immune escape’ and the time courses of each that play into the evolution of a disease.
https://www.politifact.com/factchecks/2021/dec/08/facebook-posts/viruses-and-other-pathogens-can-evolve-become-more/
A very learned friend of mine used to say "it's more complex than that" to just about any hypothesis, and invariably was right. Thanks for the link--
Apparently where Omicron invades...the bronchial lining (rather than the aveoli, as the original and Delta versions of the virus) gives your body a better chance of fighting it off. In London (a week or two ahead of us in infection) it seems the reported symptoms of Omicron are runny nose, headache, fatigue, sneezing and sore throat. It will be interesting to see if that's what is reported here in a week or so.
Here's where I got that info...
https://www.youtube.com/watch?v=84XMFVcLScw
" reported symptoms of Omicron are runny nose, headache, fatigue, sneezing and sore throat."
I've had allergies for years, and have those symptoms almost all the time.
you are forgetting another possibility.
what if the stronger of the variants to date caused damage to the immune system itself?
Then it would be HIV, not SARS CoV 2.
isn't it possible that they dont?
We all know the 4th (or 5th) wave of the Spanish flu killed more people than the first 3 or 4 waves did.
Of course we didn't have the technology we have today, that would allow us to know, back then just what the difference was between the waves.
Same with the flu - some strains are worse than others.
lawn
I read an article today that said researchers in Israel's Ben Gurion University are studying this closely.
I saw this story after I read the Ben-Gurion
https://www.nbcsandiego.com/news/local/i-had-been-convinced-that-i-was-super-immune-california-man-tests-positive-for-second-breakthrough-case/2821606/
If one assumes that all variants of the virus especially Delta have been here way longer than we know, and you believe strongly in post infection immunity, then we also have to assume PII is much less effective than we are lead to believe. We KNEW we would have to tweak the vaccines to meet the challenge of a highly mutated virus. But you can't tweak the bodies immune system UNLESS you get sick.
that poor guy had been vaccinated and got covid twice. His immune system has got to be a mess right about now.
They don't. It's random.
It’s not random; it depends on the particular characteristics of the infectious ages t, the host organism(s) and the environment, which exert selection pressure on the agent. Many, but by no means all, evolve to be less lethal, some become more so, some remain about the same for long periods.
Viruses often don't become les lethal. Small Pox didn't. Polio and spanish flu became more lethal. Don't believe AIDS or Ebola became les lethal.
In a head to head exposure contest, Omicron wins by virtue of viral load.
Three people in a room:
Person A = Delta
Person B = Omicron
Person C = Unvaccinated dumbass
After an hour, Person C is infected with Omicron, not Delta, because Omicron's viral load is vastly higher (2x or more) than Delta. Some experts think Omicron's infectiousness is on par (or higher) than Measles. I think the fast rise of Omicron as a percentage of infections makes it pretty clear that Omicron is more infectious than Measles.
The latest data I've seen puts the R naught for omicron at 3-5. Measles R naught is 12-18.
Delra is 5-6, omicron is 8-12. Chicken pox is 9-10. Measeles is 12-18.
I was hoping that someone would leave a really satisfying explanation to Kevin's quandary, which is what I have been trying to understand for a long time now. And not just with omicron . Same sort of thing happened with delta pushing put alpha and alpha original ( although that was not as quick) . The old virus just declined quicker than would seem likely in all these events, and in all sorts of different places .
But no comment here really makes me say " oh now I understand ".
So a few things mentioned
1) rattus. Have not heard that on sampling bias. Where did you see it? So really some of the " omicron cases " are still delta?
Problem is that issue, if only with omicron, does not help explain the " too fast " decline of alpha and original when delta hit . This was not as noticeable in usa as prior covid versions were going down and low anyway before delta hit. But was seen other places where delta hit when other variants still strong.
2) Cephalopod,
That is something I have been considering for months. But, if you model it, the number of true infections in a short time has to be such a huge percentage of people to account for it being in someone frequently enough to " force out" the other virus that it cannot be correct , at least for our concept of " infection ".
If delta would have been plateuing with flat R of 1.0 now without omicron, and omicron makes it go down in a short period by 30%, then 30% of those who would have been infected by delta must have already had omicron. That is a huge number .
But a key here is the overlap rate of populations. If you think of being infected as a random event, then if 30% of those who would have been delta infected have omicron to block it, then 30% of entire population are infected with omicron . Of that is true, this will be over real quick. But, if those infected with delta were inevitably going to be infected ( it was " their time") , then that 30% of the small pool who would have been delta infected implies nowhere near that rate among general public.
But that changes our whole concept of the pandemic and what works. That is more like living in a sea of virus all the time and warding off " infection ". Until some sort of internal thing makes you vulnerable and then you are getting infected pretty much no matter what. Just depends which virus gets you .
But I have a slightly different variant below
3) micro infections. What is an infection? We seem to conceive of that as having any virus invade your body but not how we define it in reality. The idea that ANYBODY has manages to avoid ever breathing in any covid virus is fanciful . Read on how many individual viruses there are in someone with an active infection. If you are 10 feet away from someone with an active infection breathing, you will breathe in more than one single virus.
If you define infected as having any virus enter your body , we likely have all " been infected " HUNDREDS of times. Just that vast majority go nowhere fast. They have to get by innate immune system first ( this is not adaptive and not antibodies) . That stops most viruses. And if through that the virus has to manage to beat the adaptive immune system before it can knock it out. In order to really become what we think of as a true " infection " , the virus has to get established enough to make enough copies to overwhelm defenses at least temporarily. And it fails the large majority of the time.
So consider that we really have numerous " micro infections " where some virus enters our body. And some of them become " invading infections " ( my made up term) which get by the innate immune system. And only a small fraction of those become " established infections " where it gets established. But only those " established infections " are what we commonly actually call an infection, and only some of those are confirmed by testing.
But what if omicron is competing with delta at all stages . So knocking out delta when both would be trying to just get by innate immune system, at a stage we would not even notice ( would only get picked up by pcr test if done at exactly right time) .
Hard to believe that 30% of those who would have had an established delta infection would have an established omoicron to knock it out . But could 30% of those who would have had an established delta infection have had an omicron micro infection to knock it out at an earlier stage ( but mostly not manage to become established itself) ? I think that could be.
And micro infections might also answer another quandary. Before omicron, look at fla and their delta wave. Went down real fast and then the decline slowed and plateued. That should happen eventually but not that soon. Hard to explain the rapid rate of initial decline if the R jumps up to 1.0 again in a month. Natural immunity does not decline that fast.
But maybe again issue is microinfections . And maybe they , if they get by innate immune system but do not become established, still can stimulate the immune system . Say you were vaccinated or had natural immunity from winter 2020. In summer 2021 delta wave, plenty of virus out there. You get micro infected often, which prompts the prior immune system to not wane and you keep making antibodies. But once the wave dissipates and micro infections tail off, immunity starts to wane .
Basically waning of natural or vaccine immunity is not constant . It depends on the extent of little microinfections you get warning the immune system the virus is still out there. So the speed of any person's waning of immunity is negatively correlated with how much virus in community.
What is an infection?
Answer, from physics viewpoint biologists really suck at science. They have absolutely no idea how to properly formulate theory and love to use terms without ever properly defining them. So infection means whatever you want it to mean when you look at borderline cases.
Here's an explanation from an expert (Trevor Bedford):
https://twitter.com/trvrb/status/1470420195567030274
Delta displacement is consistent with this scenario: "And with higher intrinsic transmissibility and lower immune escape (Omicron R0 = 8, immune escape = 33%), Omicron's wave really knocks down Delta."
FWIW, he views displacement as good news from a public health standpoint:
"If Omicron and Delta co-circulate then annual vaccines would be best formulated as multiple valencies (just like flu vaccine has both B/Victoria and B/Yamagata) and we can expect generally higher levels of viral circulation than in the displacement scenario.
I'm very much hoping we'll see displacement, but we should have first hint at outcome in the next few weeks as we see to what degree the Omicron wave reduces Delta circulation in the US and Europe."
I believe that perhaps our models are wrong on this. We are pathetic on testing and especially on sequencing
We also have a MUCH larger pool of available victims with Omicron than any previous variant. If you haven't been vaccinated RECENTLY (including boosters) or haven't contracted DELTA recently you are available for Omicron
Here's the Atlantic with another thought. How about an incubation period of 3 days? THAT would be astonishing.
https://www.theatlantic.com/science/archive/2021/12/omicron-incubation-period-testing/621066/
{snip}
It certainly might not seem like it given the pandemic mayhem we’ve had, but the original form of SARS-CoV-2 was a bit of a slowpoke. After infiltrating our bodies, the virus would typically brew for about five or six days before symptoms kicked in. In the many months since that now-defunct version of the virus emerged, new variants have arrived to speed the timeline up. Estimates for this exposure-to-symptom gap, called the incubation period, clocked in at about five days for Alpha and four days for Delta. Now word has it that the newest kid on the pandemic block, Omicron, may have ratcheted it down to as little as three.
{snip}
And this
{snip}
If Omicron’s incubation period turns out to be conclusively shorter, we would still have to figure out how it got winnowed down. Some of it could be inherent to the virus itself. Omicron’s spike protein is freckled with more than 30 mutations, some of which, based on previous variants, could help it grip more tightly onto cells and wriggle more efficiently into their interiors. Two recent laboratory studies, neither yet published in scientific journals, may be hinting at these trends. One, from a team at Harvard University, showed that a harmless virus, engineered to display Omicron’s spike on its surface, more easily penetrated human cells in a dish; another, out of Hong Kong University, found that Omicron multiplied dozens of times faster than Delta in tissue extracted from the upper airway. The findings won’t necessarily translate into what goes on in actual bodies, but they support the idea that Omicron is turbocharging the rate at which it accumulates to contagiousness. The faster that happens, the more quickly the virus can spill out of one person and into the next. If the data pan out, “this could go a long way in explaining the rapid transmission,” Lisa Gralinski, a virologist at the University of North Carolina at Chapel Hill, told me.
The unvaccinated remain most at risk, but this trend would have troubling consequences for the vaccinated and previously infected too, especially if they’re unboosted. Many of the antibodies we marshaled against previous versions of the coronavirus don’t recognize Omicron very well, and won’t be able to sequester it before it foists itself into cells. Eventually, a vaccine- or infection-trained immune system will “catch up,” Ryan McNamara, a virologist at Harvard Medical School, told me, churning out more antibodies and launching an army of T cells that can quell the virus before it begets serious disease. But those defenses take a few days to kick in and might not arrive in time to forestall the early, and often most potent, stages of transmission. The faster Omicron sprints, the more of a head start it gets against the body’s defenses.
{snip}
This would explain earlier studies indicating that vaccines were only 20% effective at affecting Omicron and 19% for post infection immunity protection.
Symptoms start before help arrives.
Mild or not you are spreading this if you are carrying it.
We're in for a long winter because of the sheer size of our population and the uneven-ness of the spread.
For some reason, “can,” “may,” and “should” not being synonymous comes to mind…
But doesn't a longer period before symptoms appear favor greater transmission? An infected person who is unaware of the infection and is going about his normal routine would be likely to pass the virus on than someone who is sick in bed. One of Covid's hallmarks from the first has been the fact that it becomes communicable before it becomes symptomatic.
Two likely contributing factors:
1) Delta was already declining from its Thanksgiving-induced peak.
2) Testing capacity is limited. Some people aren't going to wait in line for a test, driving down the absolute number of detected Delta cases.
Vog, that's a lot of good info and reasonable speculation. In particular, I wish we could convince everybody of the importance of your last two short paragraphs.
For a distressingly large number of people, it's impossible to get them to protect themselves with masks. Trying to get them to protect other folks by masking to reduce their aerosol exhalations? Sadly, that's a bridge too far.
Here's what I don't understand. If an Omicron infection can keep out a Delta infection, that's because the immune system is producing antibodies in the fight against Omicron that keep out Delta, right? Yet Omicron "evades" the antibodies vaccinated people already have? Does that suggest we NEED an Omicron-specific vaccine because it sparks a wider immune system response than the existing vaccines?
Or it’s just that omicron has bound to so many ACE-2 receptors that there are fewer available for delta to bind to.
Pieces of data that I'd want:
1. Is dual infection possible? That is, can someone be infected with both Delta and Omicron at the same time, for example.
2. If dual infection is possible, when someone is infected with both Delta and Omicron and their version of the virus is tested for type, what is the result?
A lot of things could be going on if this is the right tree to be sniffing at: a "dual Delta-Omicron" infection could become just an Omicron infection because Omicron legitimately outcompetes Delta in the body of the infected; or testing for Omicron is easier (or maybe more emphasized), and when they find Omicron they don't bother testing for Delta. Many other possibilities.
Very likely dual infections are possible. As for what a test would detect, that depends on what the test is. If it's just a PCR test looking for spike gene target failure, then it would detect Delta. If the sample is sequenced, the consensus genome would be whichever had a higher viral load in the sample, but the second genome could be detectable if someone is looking. Tests designed specifically to distinguish between the two would probably detect both, depending the details of the test.
Okay, from the pit of ignorance... How do they know? Is every positive case of COVID gene-sequenced? Or are the symptoms different enough between variants to tell? If a person dutifully calls their state health department to say they think they have COVID, are they tested and sequenced?
In short, where are these variant numbers coming from? (Along with all the sampling issues etc noted by rational thought et al.
Salamander
One of the reason I go to data from other countries is because of this long standing fear I have that Governors of red states would adjust numbers. They have by delaying reports etc.
But in going back to the South African study dated 3 Dec this struck me
https://www.science.org/content/article/covid-19-reinfection-study-south-africa-yields-ominous-data-about-omicron
***********An analysis of 35,670 reinfections among nearly 2.8 million positive tests carried out through late last week******** suggests their fears are warranted. The study does not indicate whether Omicron makes people sicker, nor was it able to look at the vaccination status of infected people. An earlier infection or vaccination might still offer some protection from severe disease.
Juliet Pulliam, an infectious disease epidemiologist at the South African Centre of Excellence in Epidemiological Modelling and Analysis, and her colleagues started investigating the rate of reinfections in January, after Beta had emerged. Beta seemed to evade immune responses from previously infected people in lab experiments, but the researchers wanted to better understand its real-world behavior.
Taking advantage of South Africa’s extensive records of tests for SARS-CoV-2, they analyzed the number of reinfections, defined as a positive test more than 90 days after the same person had an initial infection. They found that a prior bout reduced people’s risk of another one by about the same amount during both the Beta and Delta waves.
After Delta subsided, the researchers wrote a paper, which they posted as a preprint last month. But they continued to update their database. In October, Pulliam says, while overall rates of infection were quite low, they noticed something odd: The risk of first infections was decreasing—possibly due to a pickup in vaccinations—whereas the risk of reinfections seemed to increase sharply. “I thought something was wrong” with the data or the programming, she says. “Then about 2 weeks ago, we started seeing other signals” that SARS-CoV-2 was gaining ground again. “Wastewater sampling started showing increases, labs started showing significant increases in positive cases, and other bells started going off.”
****************************************************
They analyzed 36750 cases?
That is a large study.
But I wonder about the waves that South AFrican had. They had Alpha, then Beta (which they thought evaded immunity protection - then Delta
Now, SA is a poorly vaccinated country - I believe that they are still below 50% vaccinated.
They have a population of 59 Million. Roughly half or about 30 Million are vaccinated. They had 3.9M cases or just over 10%. Some of those cases are probably included in the vaccination group now.
But after 3 waves - unknown number of asymptomatic cases - their post infection immunity systems let them down! Why? Have the previous 3 waves caused cytokine storms within their bodies that have damage their immune systems? Vaccines don't do this.
Did Beta and Delta take a much bigger toll on the immune systems than we are aware of? Or is it a combination of excessive mutations and the sheer number of previous waves? Remember that our immune systems generate a number of things to attack the virus and this results in inflammation within the body. This inflammation can cause damage to tissue and organs which MAY cause a lowered response to future infection.
But to study over 36K tests? They put us to shame on that one. And they did it early on too. We DIDN'T want to hear that our bodies might not respond to the re-infection but there haven;t been many studies this large by many countries.
ADDENDUM
Israel now vaccinating 65+ yer olds with round #4 They are keeping people really amped up with protections. They also severely restricted travel from overseas to Israel. They are really being aggressive with vaccines.
The problems I am seeing with Omicron is the speed. 3 days of incubation? You become contagious before the body's immune system can even respond. The CEO of Moderna said they could have an Omicron specific vaccine by early next year? At the rate Omicron is spreading it might be too late then.
20% decrease in incubation time?
Severely decreased effectiveness of current vaccines
Even more severe decrease in post infection immunity effectiveness.
This disease surprises us at every turn. But we can issue 500M at home tests !!!
Wonderful
While others drink concoctions made with bleach just to own the libs? While TFG admits he got a booster? While people STILL push for post infection immunity?
I think everyone is waiting for Apple to create a watch that tells us when our immune system has kicked in to fight an infection !!!
Good grief
But if the story out of Israel is true that they are looking at long term damage to our immune system after DELTA? That might be telling.
Given that sequencing result takes 1 to 3 weeks after the test result is received, are we sure we are comparing the right time periods? Do we need to lag the positive test period by a week or two?
Sequencing is very uneven across states, some states are sequencing 20% of tests, others 2% of tests. I have no idea if the timeliness of sequencing results is similar across states.
Trying to put these two data sets together is unlikely to give an accurate picture.
I wrote a simplistic simulator, with 4 million people, 100 omicron and 3900 delta infections, people stay infectious for 10 days after getting sick, and after 120-160 days they're vulnerable to infection again. I put the likelihood of getting omicron at 2X the likelihood of getting delta, given the same exposure, and everyone has a small chance of being exposed to whatever a randomly chosen person has, on any given day, with the chance of being exposed to a variant being proportional to the population of that variant on that day. Note that this means that initially, a random person is frequently exposed to someone who's healthy.
Running this simulation shows this same effect -- delta craters pretty soon. First, they both grow pretty quickly, though obviously omicron is growing faster. But once you have enough omicron circulating (in this simulation, once it hits about 25% of infections), someone who's vulnerable has a better chance of ending up with omicron instead of delta. As delta people recover, the fact that new infections are biased towards omicron makes it hard for delta to find a foothold in new infections.
Eventually, delta just vanishes, as delta people keep recovering and the odds that someone new will get omicron instead of delta skyrockets.
Kudos! I’ve thought about doing some Monte Carlo modeling, but life is kinda busy here. Thanks for doing this. Would be great if you could make some results/graphs available - dropbox, Google Sheets, or ?
Estimates of Omicron frequency come from two sources of data, surveillance sequencing and diagnostic PCR tests that target the spike gene. Surveillance sequencing is slow and is done only for a small fraction of positive samples. I don't recall what the current fraction is, but the target was around 5%. As with an opinion poll, that's enough to get a good estimate of prevalence for anything that isn't very rare. PCR tests that target spike give a positive result for the N gene but no result for spike when the sample contains Omicron, thanks to a deletion in the spike sequence, and so this can serve as a proxy for Omicron. An imperfect proxy, since some Delta viruses also carry a spike deletion, but it's a small fraction.
What Kevin was quoting was the Nowcast, which is a model-based estimate of what's currently circulating, based on sequencing results from a couple of weeks earlier. It's probably a multinomial logistic regression [poking around .... yup] based on trends seen earlier. Results should be taken with a grain of salt, but it's pretty reliable.
You can also do more targeted investigations, as here, from my place of employment: https://www.wgbh.org/news/local-news/2021/12/20/omicron-is-now-the-dominant-covid-19-variant-in-massachusetts
An important question in predicting what's going to be circulating is the extent to which infection with Omicron confers immunity to Delta. Delta doesn't give a lot of immunity to infection with Omicron, and if the reverse is true, then both could circulate together for some time.
I don't get the question. Delta was expected to decrease as vaccination rates went up. Being more infectious, Omicron will decline when a higher percentage of individuals are immune or somewhat immune, and we're not there.
Not an answer to Kevin's question, but an interesting web site:
https://covariants.org/
Graphs on what variants dominate(d) when and where in the world, among other things.
So, you're standing next to an O carrier and a D carrier. The O carrier sheds 10 times as many virus particles as the D carrier. So you are infected with both, and the O virus is reproducing far more rapidly in your throat than D is in your lungs. The immune system starts to notice and starts ramping up. It's not ramping up fast enough to stop the O, but it does ramp up fast enough to halt D in its tracks. D gets halted because O caused the immune system to ramp up two days earlier than if D hadn't been present.
Meanwhile, if you test this person, there will be ten times as much O as D, and you will say this person is infected with O.
The numbers in Keven's post suggest 1 billion people will be infected with O in 2 weeks, and everyone about 4 days after that. Indoor mask wearing isn't going to be highly effective. And vaccination distribution isn't high enough to have much of an impact.
Meanwhile, conditions are optimal this fortnight for spreading viruses, and the ability of governments to respond is lower as key parts of social communication systems are busy elsewhere for the holidays.
If someone is infected with both Omicron and Delta does the test show up as Omicron and therefore it's Omicron that gets reported?
cld-
I believe the simple answer is yes it would show as Moronicron
This is one weird variant. 7X times faster than Delta while reproducing in the bronchia? Spreading it before you even have symptoms? Need for testing like every day because as little as 12 hours make a huge difference?
I have already told the Mrs the Christmas mass is OUT for us.
As I wrote above, if someone has both Omicron and Delta, what the test shows depends on the test. Estimates of Omicron frequency based on S gene target failure (the failure of the spike gene component of a PCR diagnostic test), which is one of the data sources being used, will biased toward detecting Delta. That's the case for the estimates from Yale-New Haven hospital, for example. Wastewater surveillance (where it's being done) should be unbiased.
US Army Creates Single Vaccine Against All COVID & SARS Variants, Researchers Say,
https://www.defenseone.com/technology/2021/12/us-army-creates-single-vaccine-effective-against-all-covid-sars-variants/360089/
Within weeks, scientists at the Walter Reed Army Institute of Research expect to announce that they have developed a vaccine that is effective against COVID-19 and all its variants, even Omicron, as well as from previous SARS-origin viruses that have killed millions of people worldwide.
The achievement is the result of almost two years of work on the virus. The Army lab received its first DNA sequencing of the COVID-19 virus in early 2020. Very early on, Walter Reed’s infectious diseases branch decided to focus on making a vaccine that would work against not just the existing strain but all of its potential variants as well.
. . .
Unlike existing vaccines, Walter Reed’s SpFN uses a soccer ball-shaped protein with 24 faces for its vaccine, which allows scientists to attach the spikes of multiple coronavirus strains on different faces of the protein.
. . . .
But it's going to be a while before this can be available, probably more than a year.
Tried to blckquote that on my tablet, ths is why we need editing.
Japanese researchers had announced months ago they were looking at doing the same. This is an interesting development. I hope it works
Colorectal cancer vaccine in phase 2 trial,
https://interestingengineering.com/biontechs-mrna-cancer-vaccine-has-started-phase-2-clinical-trial
Hey, antivaxxers . . . check out my cancer-free butt!
"Hey, antivaxxers . . . check out my cancer-free butt!"
You mean everyone's cancer free butt. I really hope this works
But the anti vaxxers have had a tough time of it
They thought they had the answer but then Delta and Omicron showed them that post infection immunity can be evaded
Just like the vaccine protections can be evaded
Vaccines can be tweaked
In order to tweak the human immune response you gotta get sick to do it and we saw what happened with that now didn't we? Millions of deaths.
Unfortunately COVID - at least in my mind - is not over. I suspect Faucci was right that the next big wave is still MONTHs away. We are dealing with a living thing here and the world is very inter-connected
I just realized, when this anti-cancer vaccine finally appears the anti-vaxxers will insist we should all wait for herd immunity.