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Comment by mrosett | Hacker News Reader

My understanding is that there's little evidence that patients (vaccinated or unvaccinated) have worse outcomes with delta; they're just more likely to spread it.

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Recent Mayo Clinic study estimated Pfizer was 42% effective against Delta, https://www.medrxiv.org/content/10.1101/2021.08.06.21261707v...

> However, in July, the effectiveness against infection was considerably lower for [Moderna] mRNA-1273 (76%, 95% CI: 58-87%) with an even more pronounced reduction in effectiveness for [Pfizer] BNT162b2 (42%, 95% CI: 13-62%). Notably, the Delta variant prevalence in Minnesota increased from 0.7% in May to over 70% in July whereas the Alpha variant prevalence decreased from 85% to 13% over the same time period.

> there's little evidence that patients (vaccinated or unvaccinated) have worse outcomes with delta; they're just more likely to spread it

Entirely possible, as viruses historically evolve to be weaker and more transmissible. That would be good news.

Many other studies disagree with that one. Current consensus is that the Pfizer vaccine is well over 90% effective against severe disease from Delta, and over 80% for infection:

https://nitter.net/mugecevik/status/1430218372348878860?lang...

We also have the study reported in this article.

> Nursing home residents, health care workers lose more than 80% of their COVID-19 immunity six months after Pfizer vaccine.

That sentence is extremely misleading. The study showed people losing more than 80% of their antibody immunity. But they also have T-cell and B-cell immunity which lasts longer.

Here's a third study, from Qatar, based on positive PCR tests in recipients of Pfizer vaccines, which estimated 0% (not a typo) vaccine effectiveness against symptomatic infection after 20 weeks, https://news.ycombinator.com/item?id=28548322

It seems like a broken record but you don't need active antibodies to have protection from the vaccine. Antibodies give you protection in that moment. If you have no antibodies, you are extremely likely to test positive because the virus -- temporarily -- can freely enter your cells and replicate. However, other immune system components quickly identify the invader, re-boost antibodies, and crush the infection.

Expecting the vaccine to produce high antibody counts for life is not how our immune systems work.

>...estimated 0% (not a typo) vaccine effectiveness against symptomatic infection after 20 weeks

That's also extremely misleading. The greatest vaccine benefit is not elimination of merely symptomatic infection, but to reduce serious symptoms (i.e. hospitalization) and death.

Here's what the study says about that:

Meanwhile, BNT162b2-induced protection against hospitalization and death appears to persist with hardly any waning for at least six months following the second dose.

It's good that the CDC updated their definition of vaccine to make it clear to the general population that non-sterilizing Covid vaccines provide "protection" and not "immunity", to reset the expectations of vaccine recipients who may have believed that Covid vaccination provided immunity or stopped transmission.

It’s unfortunate however that public policies in most western countries haven’t adapted to that fact yet (which has been a serious hypothesis since the beginning). they still encourage risk-free patients to get vaccinated in the hope of herd immunity. It’s just sad.

That's interesting. If that bears out, it suggests without antibody immunity people will get infected by COVID. However, that same study also shows that the vaccine still prevents serious illness and death, i.e. those other immunity mechanisms are still there and effective, just not kicking in quickly enough to block infection. So "lose more than 80% of their COVID-19 immunity" is still misleading.

> Qatar

> estimated 0% (not a typo) vaccine effectiveness

yes, that is ridiculous.

pretty certain that study is mostly fit for toilet paper.

Unvaccinated hospitalization and death rates are roughly 2x higher with delta.

https://www.thelancet.com/journals/lancet/article/PIIS0140-6...

Transmissibility and virulence tend to be linked via in-host replication rate (viral load). It isn't quite that simple since if the virus can better evade in-host immune responses then higher viral loads could be better tolerated by the host, but generally transmissibility and virulence are expected to move together. It isn't clear that D614G or B.1.1.7/Alpha involved enhancements in virulence, but delta's advantage in transmission over Alpha does seem to come from increased viral loads, which causes more severe symptoms.

And even the difference seems to be about the same for both groups, which I read as a sign that delta is just better adapted to the upper respiratory tract where immunity from intramuscular vaccines generally doesn't happen. It seems to be a completely separate immune system (this part is not crude layman's speculation but crude layman's rewording of established knowledge I think) which is also consistent with the recorded observation that patients who struggled for their lives typically lost much of their infectivity long before the struggle even started to get serious. In a fully vaccinated environment it might not be so bad to get the "other immune system" to know the virus before the one prepared by intramuscular lowers alert status.

There's no "other immune system" involved. With RNA viruses in particular there's a long phase where infected cells are pumping out viral debris rather than correctly packaged and infectious virions. With severely ill people the cells pumping out viral debris late in the disease cause the same immune response to those proteins just like "live" virus. They aren't infectious though.

This is why a long time ago back in like April 2020 there were reports of "lingering infections" up to 90 days long in South Korea when measured by RT-PCR at high cycle thresholds.

This is probably why Christiano Ronaldo was testing positive for COVID long after he was recovered and (in)famously called PCR testing "bullshit".

With breakthrough infections it is also seen that while the Ct values are comparable between breakthrough infections and unvaccinated infections, the breakthrough infections have less culturable virus and decline faster -- the PCR machine is reading more viral debris.

Also, this is why the whole issue of hospitalized patients being moved back into nursing homes in NYC early in the pandemic is non-issue since they weren't infectious (and the peak in nursing home deaths occurred before the peak in returning patients to nursing homes). Cuomo is still a sexually harassing asshole though.

There's theories that some long COVID cases might be due to lingering viral debris being pumped out by cells, and might be why some vaccine recipients feel relief from symptoms. Although I think its looking more like long-COVID/PASC has more to with autoantibodies.

I think I may be reading/interpreting your comment incorrectly after writing this/digging up these sources -

Whether or not Delta specifically is causing a larger impact on severity of outcomes, we know for a fact that it's more transmissible. And unvaxxed are quite literally dying 99:1 against vaxxed now - mostly from delta. Even if it's less likely to kill/cause severe irreversible organ damage per case, it seems somewhat safe to say the vast majority of unvaxxed are going to get it sooner than later at this point because of increased transmissibility - which will lead to a giant pile of bodies that didn't need to happen.

I would like to think that info alone probably indicates that delta is having a larger affect on the severity of outcomes, but I know there's more to statistical analysis than that. Anyways.

https://www.npr.org/2021/07/16/1017002907/u-s-covid-deaths-a...

https://medicalpartnership.usg.edu/covid-19-staggering-stati...

https://www.cnet.com/health/99-of-covid-deaths-are-now-of-un...

https://www.al.com/news/2021/08/99-of-alabamas-2379-covid-de...

https://www.reuters.com/world/europe/italy-says-99-covid-dea...

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