Omicron variant more resistant to vaccine but causes less severe Covid: study

I won't deny that this is good news, but considering Omicron is much more transmissible than other variants (I've seen numbers saying 4x more transmissible, though I don't have a source right now), wouldn't that still mean higher hospitalizations and healthcare overwhelm?

Drug assessment goes through three stages of human testing, after other models, to assess safety, efficacy, and finally, dosing.

If possible, basic efficacy testing is done on non-human models, either in vitro or animal models. For species-specific viruses, this is difficult and may be impossible. I'm not sure what if any such testing was done with the SARS-COV-2 vaccine candidates.

A basic safety test with dosages thought to be low enough not to present any risks. The goal here is simply to see what if any side effects occur. Any comorbidities, no matter how unrelated, are reported. Note that these may occur in a control / nontreated population, so the key isn't "individual was treated, had condition", but "there is a statistically robust difference in rates of co-morbidities between treatment and control populations" In normal circumstances, such safety testing may take a year or more, and data reporting are ongoing through drug development and use.

Efficacy is determined, where groups treated are assessed for whether or not the drug provides any measureable effect. Note that this can range anywhere from "provides 100% immunity from infection" to "cancer patient dies a horrible painful death 2 weeks after control group". (If you're familiar with cancer research, it is rife with very marginal "positive responses" to therapy. Yes, with some spectacularly better instances.)

Finally, dosing is dialed in to find out how much and how often to deliver the drug. That's how we're ending up with single vs. double innoculation recommendations, and/or boosters, and wait times between dosing. Again, multiple groups followed over time.

All of this takes time. Since COVID-19 has a course of about 1--2 months from exposure to resolution (you get better or you die), and vaccinations have a lead time of about 2 weeks after second dose to full efficacy, that's about four momths just to get baseline measurements.

A typical drug study might have as few as 30--60 patients, though many have more. In the case of the SARS-COV-2 vaccines, trials were much larger as I understand (I don't have data or reports in front of me, so don't take my comments here as significant.)

If there's earlier research to build off of (e.g., mRNA base models of solutions and methods) then some of this process can be based on earlier research, which helps.

But you're still looking at 6--9 months before a vaccine can be recommended with strong assurances even under highly expedited conditions. Given circumstances, health authorities might be willing to operate more quickly and with less data, but those decisions would have to be considered preliminary and subject to revision. Revised understanding around COVID-19 has been highly problematic around the world, leading to trust issues and opportunists spreading disinformation.

And once you have a candidate treatment, you've still got to produce and supply that, with manufacturing and logistics considerations, all of which were evident in the rollout of existing SARS-COV-2 vaccines (e.g., production issues, patent licensing, quality control, storage and refrigeration, cold-chain management, patient contact, scheduling, and follow-up, etc.).

It's complicated.

Source: Some ancillary PHARMA related work in the past, eccelctic interests.

Which begs the question of the long term utility and effect of symptom suppressing vaccines (that don't prevent transmission).

If a virus that would make make you very sick is contracted by someone who's vaccinated - They will now be in the 2nd category you describe ~'Sick, but not sick enough to stop them going out' -- They're now giving mobility to that virus that it would have otherwise not had (If they weren't vaccinated and were feeling too sick to go out and about)

So by usage of vaccines that only prevent severe symptoms, we pervert that normal negative feedback loop of virus spread and instead set the parameters to be more likely to propagate severe virus' that would usually keep you sick at home.

Viral evolution can go down that path, provided there are selection pressures that select for weaker viruses. Viral evolution can also not follow that path at all. Evolution doesn't have a chosen path, and it doesn't have an end-goal. Evolution is the name that we give to the effect that chance has on genetics.

The selection pressure that can select for weaker viral variants is the rapid and widespread deaths of viral hosts. The stronger viral variants literally die off in the hosts they kill, and can't keep spreading, whereas the viral variants that didn't kill their hosts before spreading their genes can keep replicating.

The majority of people with COVID do not die before spreading it to other people. That selection pressure isn't there for COVID, therefore there is nothing really stopping it from mutating into stronger variants. If it starts killing people like Ebola does, then the selection pressure for weaker variants might exist because a lot of hosts will die. Even in that case, it isn't a given that a highly fatal virus would mutate to become weaker. It could very well wipe out entire species and die off itself like the majority of species in the history of the Earth, or it could become endemic in a different species afterwards and live on.

All of this selection happens over evolutionary timelines, which span over many human lifetimes. If the virus becomes weaker, it could take many human lifetimes to reach that point.

From the AP's "Viruses can evolve to be more deadly" article[1]:

> “Becoming more transmissible and less lethal are absolutely what’s best for the pathogen,” said Day. “But the problem is that it’s not always possible, and in many instances is never possible, to be more transmissible and also less lethal.”

> Day said there are documented cases of animal viruses that evolved over time to become more lethal, including myxoma virus in rabbits and Marek’s disease in chicken.

> Some viruses provoke severe symptoms in their hosts that make it easier to transmit the virus to others. But those same symptoms can wind up killing the hosts.

> Adalja said one example is Ebola, a deadly virus that spreads through the blood and body fluids of infected people. Another example is norovirus, which causes diarrhea and vomiting, and leads to hundreds of deaths each year in the U.S.

> “The virus, speaking anthropomorphically, just wants to spread and have its genes replicated,” said Adalja. “If the best way for it is to spread by causing severe symptoms it will continue to do that.”

[1] https://apnews.com/article/fact-checking-011488089270

> I would imagine all viral contagions would eventually go that route.

There is no intelligence making this decisions, its just some random mutations, so we cannot predict what path the virus will take.