Comment by giantrobot | Hacker News Reader

Comment by giantrobot | Hacker News Reader

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Even with tens of millions vaccinated COVID is too contagious and deadly to avoid social mitigation like restricting businesses, large gathering, mandating masks, and even lockdowns.

The long incubation period and asymptomatic carriers makes for easy spread of the virus. It's hospitalization rate means a wide spread will literally shut down hospitals in whole regions. At current infection rates we're seeing hospitals being overwhelmed at regional levels.

Even if vaccines had been delivered after a Phase 1 trial of "no one died immediately" in the trial group, we wouldn't have enough vaccinated people to avoid social mitigation. We'd be in a similar situation as we're in right now.

It will take something like 75% of the population to be immune (by vaccine or previous infection) to have effective herd immunity. Even if vaccines had started distributing months ago it would still be a long time before we hit that 75%. Distributing vaccines after the phase 1 trials might ultimately get an immune population to that 75% sooner but it wouldn't stop any of the damage happening until that number is reached.

Even if no one died from COVID the "long hauler" after effects can be crippling. Some 10-20% of COVID patients end up "long haulers". If the virus were to spread to significant portions of the population because no one practiced social spread mitigation because they assumed the vaccine would fix everything you're still in a terrible situation.

> The long incubation period and asymptomatic carriers makes for easy spread of the virus

Long? The median is between 4 and 6 days. The 14 days often quoted is the 99th percentile. Can we stop perpetuating this myth?

> asymptomatic carriers makes for easy spread of the virus

Actually, most of the spread comes from superspreading events. Most people with the virus don't spread the virus at all, or spread it very little. True asymptomatic people are far less contagious than symptomatic people (up to 10 fold or so less). Severity of the symptoms is also associated with higher chance of spread.

> It will take something like 75% of the population to be immune (by vaccine or previous infection) to have effective herd immunity.

This is often calculated considering an equally susceptible population (which is not the case) with uniform mixing (same), so it's a very pessimistic estimate. The actual figure might be lower (though not as low as 20% as some "skeptics" say).

I am looking for 14 days quoted in the parent comment and not finding it.

> Actually, most of the spread comes from superspreading events.

I don't know if we can say this for certain at this point. I was very firmly on the "superspreader" train some time ago but I find it hard to believe given the spread we are seeing in places like Canada where most of what we thought were superspreader circumstances are now illegal. I am sympathetic to the idea but being overconfident about this stuff is also not helpful.

> I am looking for 14 days quoted in the parent comment and not finding it.

2 to 6 days incubation time is not "long".

> I am sympathetic to the idea but being overconfident

It's not being overconfident: it's what the currently available data says. The largest contact tracing study I am aware of, in India, reported that the largest cause of spread were superspreading events.

Saying that you are not being overconfident with that level of confidence seems like a red flag.

If COVID-19 is primarily driven by superspreader events that are largely not happening anymore in the 2nd wave that is causing case increases across nearly every jurisdiction in the world I have doubts.

> Saying that you are not being overconfident with that level of confidence seems like a red flag.

Were it just me, I'd agree with you, however it is the data that we must look at:

https://science.sciencemag.org/content/early/2020/09/29/scie...

In the spirit of open discussion I would like to raise to you some salient facts.

The article in question does not address the fact that I raised, and also you shouldn't make claims the authors are not making:

"Our findings, based on comprehensive surveillance and contact-tracing data from the Indian states of Tamil Nadu and Andhra Pradesh, provide insight into the epidemiology of COVID-19 in resource-limited populations."

Specifically: "Whereas incidence declined steadily at ages older than 30 to 39 years in the two Indian states, incidence increased at ages of ≥65 years in the United States."

So their finding might be applicable if the general trends matched but the study specifically says they don't, in the way that I generally pointed towards.

Also the study in question points to "superspreading individuals" but not "superspreading events" and that difference is significant. A "superspreader" who attends an event that can cause superspreading event, but a superspreader that goes to many places and meets just a few people at those places can super-spread! It's different! The study does NOT support your implied claim that asymptomatic spreaders can't be superspreaders.

A six day incubation period is a long time. Even four days is a long time considering how infectious the virus is. That's a work week being unknowingly infectious.

Considering we're in the middle of a huge spike in cases that started two weeks after Thanksgiving, suggesting superspreader events are the primary source of infections is ludicrous. Canada had the same problem after their Thanksgiving holiday.

You're also seeming to dismiss asymptomatic carriers because individually they are less infectious than symptomatic carriers. This completely ignores the behavioral component of infection. An asymptomatic carrier will have no reason to seek out testing or participate in contact tracing programs. Someone that becomes symptomatic will know to at least inform recent contacts so they can get tested and attempt to isolate themselves to limit the spread.

Not all vaccines are going to be compatible with one another. If millions of people take your early-release vaccine and it's ineffective they may not be able to get a second one or not get it for a while. This apparently is an issue with the Russian vaccine because of the way it's introduced to the immune system.

This is why vaccines are tested in multiple phases. It's not just to make sure people don't have immediate adverse reactions but to find the edge cases and boundary conditions.

True asymptomatics are rare in the infected population. Most of people are presymptomatic (=they will develop symptoms), and their peak infectiousness is one or two days before symptom onset, according to published data.

> If millions of people take your early-release vaccine and it's ineffective

Phase 3 studies on Moderna, Pfizer, and AstraZeneca vaccines have shown that they are effective (and nowhere close to an "early release"). Statistics don't lie in that regard.

> This apparently is an issue with the Russian vaccine because of the way it's introduced to the immune system.

I'm not aware of any of such issues. Do you have a primary source I can look up?

This paper is the specific issue I was talking about [0]. Individuals who were Ad5 seropositive had an immune response to subsequent Ad5-based treatments. They developed an immunity to Ad5 which is just a delivery vector for the viral protein you're trying to introduce.

The CanSino vaccine also uses Ad5 as it's viral vector. An immunity to Ad5 from say Sputnik V would apparently prevent you from being able to get the CanSino one should Sputnik V prove ineffective for you. You'd also not be able to get a booster of Sputnik V later.

There's lots of adenovirus strains and a few other vaccines are using them for their delivery vectors. Ad5 is an edited adenovirus that has it's replication system retarded/removed. There's other articles I've seen but can't find now lamenting the use of Ad5 specifically. There was also the STEP study that showed increased HIV susceptibility in people that had received Ad5 vaccines.

I am not a medical professional but I do understand immunology is extremely complex. Effective vaccines in vitro aren't necessarily effective in vivo. There's also complex issues around dosing which is part of human trials. Even if a vaccine is "effective" it's not necessarily obvious or known what sort of dosing is appropriate for wide deployment in the general population. A completely "effective" vaccine at the wrong dose can end up being ineffective.

[0] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756115/

Sputnik is two vectors: Ad26 and Ad5. That looks like the reason why they kept having a high efficacy (today's press release from Gamaleya says 92%).

Dosing is done in Phase 1 trials, which also included antibody level testing. This has been already taken into account in the current trials.

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