Coronavirus 14: Boosted Waves or Merely a Ripple?

Is it over?

  • YES

    Votes: 9 17.3%
  • NO

    Votes: 14 26.9%
  • It will never be over

    Votes: 13 25.0%
  • I'm over it

    Votes: 14 26.9%
  • I'm more worried about Monkey Pox

    Votes: 2 3.8%

  • Total voters
    52
I am not sure how to interpret this, but it definitely does not mean that it is good to get covid to protect against the flu.

The omicron coronavirus variant may protect against flu

Being infected with the omicron variant of the coronavirus may give some protection against flu.​
In a laboratory study, the bronchial cells were infected with the delta variant of the coronavirus, the BA.1 omicron subvariant – the original omicron variant – or the BA.5 omicron subvariant, which is currently dominant.​
As a control, the researchers treated some cells with a saline solution that didn’t contain any coronavirus variant.​
After two days, the team exposed the SARS-CoV-2-infected cells and the control cells to the H1N1 strain of influenza virus. H1N1 was responsible for the global swine flu outbreak in 2009-10. It is now one of the seasonal flu viruses that circulate every winter.​
One day later, the researchers measured the H1N1 levels in all the cells. In the control cells and those infected with the delta variant, H1N1 levels increased by roughly 10,000-fold. This is compared with no increase in the cells containing either omicron subvariant.​
The findings may be reflective of SARS-CoV-2 and flu infection rates over the pandemic.​
“Following the lifting of restrictions in July 2021 in England, we saw a delta wave accompanied by an increase in influenza-like illnesses, those diagnosed as the flu and those which seemed to be the flu,” says Michaelis. “But then, since omicron BA.1 became dominant, influenza-like illnesses dropped and have stayed low.”​

Paper (not peer reviewed) Writeup (paywalled, content in spoiler)

Spoiler Article :
Being infected with the omicron variant of the coronavirus may give some protection against flu.

Martin Michaelis at the University of Kent in the UK and his colleagues collected bronchial cells from a person with emphysema, a condition where the lungs’ air sacs are damaged, but the bronchi airways are unaffected.

The cells were extracted as part of a standard diagnostic or treatment procedure. With the bronchi being unaffected by emphysema, the results are expected to apply to people without the condition, according to Michaelis.

In a laboratory study, the bronchial cells were infected with the delta variant of the coronavirus, the BA.1 omicron subvariant – the original omicron variant – or the BA.5 omicron subvariant, which is currently dominant.

As a control, the researchers treated some cells with a saline solution that didn’t contain any coronavirus variant.

After two days, the team exposed the SARS-CoV-2-infected cells and the control cells to the H1N1 strain of influenza virus. H1N1 was responsible for the global swine flu outbreak in 2009-10. It is now one of the seasonal flu viruses that circulate every winter.

One day later, the researchers measured the H1N1 levels in all the cells. In the control cells and those infected with the delta variant, H1N1 levels increased by roughly 10,000-fold. This is compared with no increase in the cells containing either omicron subvariant.

The team also found that the cells containing the omicron subvariants produced a protective immune response called the interferon response, which is known to reduce the replication of flu viruses. Among the control cells and those infected with the delta variant, this response was much lower and insufficient to suppress H1N1 replication.

The findings may be reflective of SARS-CoV-2 and flu infection rates over the pandemic.

“Following the lifting of restrictions in July 2021 in England, we saw a delta wave accompanied by an increase in influenza-like illnesses, those diagnosed as the flu and those which seemed to be the flu,” says Michaelis. “But then, since omicron BA.1 became dominant, influenza-like illnesses dropped and have stayed low.”

However, these patterns could be due to other factors, such as people being more careful to avoid infections during winter, he says.

Understanding how different covid-19 variants trigger varying immune responses may help researchers more quickly understand the potential impact of new variants.

“Apart from out of curiousity, such findings can help to reveal how covid variants differ and could help us to understand and predict how any new variants that appear might behave,” says Michaelis.

The work doesn’t suggest people should purposely catch covid-19 to avoid flu, the researchers have stressed.

“We, of course, don’t advise people to purposely get infected with covid-19 to protect against influenza. With SARS-CoV-2 infection, there’s always a chance you could die,” says Michaelis.

If you are admitted to hospital with both covid-19 and flu, you are more likely to become critically ill and die, says Kenneth Baillie at the University of Edinburgh, UK.

What’s more, the results are based on a laboratory model, which may not translate well to people, says Michaelis.

Nevertheless, such work is of interest to virologists and supports decades of research that has found infecting cells with one virus makes it harder to infect them with another, says Baillie.
 
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Interesting. It's been noticeable that Covid variants have seemed remarkably good at outcompeting their older cousin variants. Delta pretty much extinguished Alpha, and Omicron in turn seems to be wiping out Delta. Perhaps rather more than can be accounted for simply by having a higher R number and epidemiological pressure. It also seems to be very rare to see Covid superinfections - I've only seen a few reported cases, mostly involving the older strains in immunocompromised patients.

I'm wondering if Covid has evolved a way of actively deterring competition by other viruses - both older Covid variants, and unrelated viruses such as influenza. It could also be an alternative explanation for the near non-existence of the 2020/21 flu season. We've been chalking that one up to a side effect of the various anti-Covid social changes, but this would be another possibility. Or at least a contributing factor.

I could imagine a few ways such a deterrent might work. We know that it triggers an interferon response - the interferon system is supposed to steer the immune system to produce the most appropriate antibodies for a given virus. But viruses have evolved their own ways of hiding from it, and throwing spanners into its workings. If it triggered an inappropriate interferon response - one directed towards the wrong types of virus, that might produce an effect like this. Or it could simply be that Covid is hidden, and unaffected by resulting the interferon response. That would still give a passive effect deterring viruses that are affected and exposed to the response. Certainly it would be an evolutionary advantage not to have other viruses competing for the same host cells.
 
It could also be an alternative explanation for the near non-existence of the 2020/21 flu season. We've been chalking that one up to a side effect of the various anti-Covid social changes, but this would be another possibility. Or at least a contributing factor.
That would only be likely, if this somehow granted long-lasting immunity. At any given time, only a small fraction of the population was infected. So if the protection lasted only as long as the person was infected, the effective R for the flu would also be reduced by a small fraction. Any half-decent anti-Covid measure should have had much larger effect than that. Only if the effect was cumulative, you would get a big enough immunity against he flu to have a significant impact.

The interferon response should not last much longer than the infection, right?
 
That would only be likely, if this somehow granted long-lasting immunity. At any given time, only a small fraction of the population was infected. So if the protection lasted only as long as the person was infected, the effective R for the flu would also be reduced by a small fraction. Any half-decent anti-Covid measure should have had much larger effect than that. Only if the effect was cumulative, you would get a big enough immunity against he flu to have a significant impact.

The interferon response should not last much longer than the infection, right?
This is the way I interpreted it, the interferon would only be there during the active infection. This is in cell culture, who knows how it related to in vivo.
 
That would only be likely, if this somehow granted long-lasting immunity. At any given time, only a small fraction of the population was infected. So if the protection lasted only as long as the person was infected, the effective R for the flu would also be reduced by a small fraction. Any half-decent anti-Covid measure should have had much larger effect than that. Only if the effect was cumulative, you would get a big enough immunity against he flu to have a significant impact.

The interferon response should not last much longer than the infection, right?

Yes, fair point. File under "possible contributing factor" rather than alternative explanation. Also, thinking about it, there was an upsurge in flu cases back when measures were relaxed, which wouldn't really fit with that explanation given how prevalent Omicron already was becoming at that stage.
 
I’m a superdodger by action if not genetics. Hopefully I am also from the superior gene pool.
tl;dr hikikomori desu ka?
 
Now I'm working again at an university hospital, made it easier to be a part of a trial ^^.
I'll get the bivalent Pfizer vaccine (I think) in December. They're testing differences of this booster between a first Jansen vaccination versus a first mRNA vaccination. Not tremendously thrilling, but getting the vaccine at work saves me the trip to a vaccination center here.
Apparently they're a bit in a rush, needed to recruit 400 people in less than a month.
 
My test came back with 2 pink lines.

After 2.5 years I finally caught COVID. :cry:

Dumb Riotfest music festival!
Coolio had a fun 30 minute performance at Riotfest on the 18th, and now he's dead 10 days later! :cry:

 
How a COVID lockdown changed bird behaviour

To see how a COVID-19 lockdown affected birds in the United Kingdom, Warrington and her colleagues tallied sightings of the 25 most common birds between March and July 2020 — during the country’s first lockdown — and compared their data set with data from previous years. In total, the study included around 870,000 observations.​
The team then compared this information to data showing how people split their time between home, essential shops and parks: three places people in the United Kingdom were allowed to be during the lockdown.​
Because people spent more time at home and in parks than before March 2020, the analysis found that 20 of the 25 bird species examined behaved differently during lockdown. Parks — which were flooded with visitors — saw an an uptick in the numbers of corvids and gulls, whereas smaller birds, such as Eurasian blue tits (Cyanistes caeruleus) and house sparrows (Passer domesticus), were spotted less frequently than in previous years. And because people spent more time at home, the number of avian species that visited domestic gardens also dropped, by around one-quarter, compared with previous years.​
Other species, including rock pigeons (Columba livia), didn’t react to the lockdown at all. Warrington found this surprising, because pigeons are city dwellers, so she thought they would be affected by the changes in people’s behaviour. “But they don’t give a crap about what we do,” she says.​

Writeup UK Birds (hard paywall) US Birds



Spoiler US Birds in detail :
 
The bivalent vaccine we now have available in Alberta for boosting is a 50/50 combo of Original Strain (wtf?) and Omicron BA.1
 
Is the reason for keeping Classic Coronavirus as part of the formula primarily scientific or legal? I wonder if they change it too much if they can’t use the existing license on it, or if they need it to preserve some intellectual property, or is it that the protein strains or whatever (no clue what I’m talking about) bind to something and they don’t want to reinvent the wheel?
 
I think it's more of a "never change a winning team" thing, and not necessarily well reasoned.
IP-wise, there are so many relevant patents not related to this, that it certainly doesn't matter. From the science side, I'd say it's pointless. Just keeping what's working, I'd say :dunno:.
 
The bivalent vaccine we now have available in Alberta for boosting is a 50/50 combo of Original Strain (wtf?) and Omicron BA.1

I've no boosters, and not getting that one. I'd get the Pfizer BA.4/5 bivalent if it were available. (Both preference for BA.4/5 targetting, and for lower dosage after Moderna initial course.)

That should be the one distributed in most places in the west. I'm participating in a trial with that one too. I think it'll need to be shown if the original strain in there is of any relevance, but I have my doubts too.

Why not the BA.4/5 bivalents?
 
I think your guess is as good as mine.
Might be just the necessary turnover time. The development of the situation is just faster than the development in the lab/factory. And while you can in theory just plug in a new sequence, I would guess that they certainly still need to a) make some tests and b) manufacture everything afterwards.
 
I don't let go of bones where spurious "news" are involved. Given time attention recedes and the flaws (or outright lies) emerge and get exposed. That can in fact be quite fast, but be "drown out" for a while by a lot of noise supportin the flawed claims.

Past year one guy with a blog made the rounds in attempting to discredit studies positive towards ivermectin use as a treatment for covid. This one. It was argued about on a previous thread here. @The_J you should remember that one, you just took it at face value.

It has been a long time since, rationality unfortunately is always slower to reassert itself than I expect, but this blogger has been forced to walk back publicly on a number of false accusations which were nothing more than petty attempts at character assassination. Will likely lose a lawsuit by at least one of the persons he defamed (more on that if it happens and I notice the news). And has had his methods thoroughly demolished by this other blogger (and other people, follow the links and controversy...) who has been willing to put in months for looking into the whole thing. I'm linking to the current easiest to follow reply, there are others.

The original blog piece was "popular" because it was preaching to the choir. Not because it was in any way a rigorous assessment of the data it claimed to assess. This should be a warning about how easily claims about "the science" are cover for which hunts, when issues are political, or are materially very relevant ($ billions), or simply involve pride (and prejudice). The history of this one has not yet been finished.
 
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