Hacker News Reader

Comment by dehrmann | Hacker News Reader

My fear is that 2-3 months of lockdown isn't a cure, it turns into on-and-off lockdown, herd immunity is never established because immunity wears off in 2 years, and a vaccine is 2-5 years out.

Ignoring the economics, preserving life takes on new meaning if you count a every locked down day as taking away an hour of life from someone. Take the Bay Area. At 7.7M people, every day, there are 11.7 lifespans wasted by lockdown. There have been 3.2 covid-19 deaths per day.

View on HN

There's no basis for your fear that immunity would wear off in two years. Unlike the cold and the flu, these coronavirus strains do not mutate quickly enough to cause quick loss of immunity. It seems more akin to chickenpox, which you can only catch once (and shingles doesn't count).

So, take heart in this at least?

common cold = caused by coronaviruses, COVID-19 = an uncommonly deadly coronavirus

RNA viruses have a faster mutation rate than DNA viruses.

Chickenpox = DNA virus, Coronavirus = RNA virus.

That Chickenpox is a DNA virus is why, like HIV, it can survive in the body for the long term and re-emerge decades later as shingles. DNA has a double helix which has error-correction and is more stable. However that makes it also physically larger and more complicated. RNA is small, sloppy, and cheap.

Source of all this: Spillover, David Quammen: https://www.amazon.com/Spillover-Animal-Infections-Human-Pan..., it's a good & topical book, a little bleak but good. There's a discussion of exactly this about halfway through the book.

So I do not believe your comment is factually correct. Sadly, the COVID-19 causing virus should have a high potential mutation rate similarly to all RNA viruses.

Nope. The common cold is a catch-all term for over 200 different mild upper respiratory viruses, the clear majority of which are not coronaviruses. The most common strain of virus causing the common cold is a rhinovirus, which does have the property of mutating well and thus being hard to develop a resistance to. It is true that some of the common cold strains are coronavirus, but not most of them, and regardless, they aren't COVID-19 (which is of recent zoonotic origin). Preliminary analysis of COVID-19 indicates that catching it once is likely to confer life-long immunity.

https://en.wikipedia.org/wiki/Common_cold https://en.wikipedia.org/wiki/Coronavirus

It seems like you know more than I do -- that's good news, thank you for correcting me! I was wrong about coronavirus causing all forms of the common cold. They only cause 15%, whereas rhinoviruses as you say, cause 30–80%.

Still, "the Coronavirus" COVID-19 causing virus is an RNA virus correct? Those mutate rapidly & in fact, evading immune systems via rapid evolution, is part of what has allowed RNA viruses to exist & thrive.

This fact of being an RNA virus, might be one reason that making a vaccine is difficult & that long term immunity is in question: https://en.wikipedia.org/wiki/RNA_virus#Mutation_rates

> Preliminary analysis of COVID-19 indicates that catching it once is likely to confer life-long immunity.

I wasn't able to find this in your links. Regardless, I hope that is the case.

There's a lot, lot, lot more to it than simply saying that it's a DNA vs an RNA virus and that one categorically mutates faster than the other. The most relevant factor here is that COVID-19 only has a single strand of RNA, whereas e.g. influenza has 8. This allows a lot more mutation from pieces of RNA swapping around between different strands, which just can't happen on COVID-19. You can sort of think of it as analogous to sexual vs asexual reproduction; the former has a lot more potential for variation. Plus there's factors relating to the specific mechanism that coronaviruses use to attach to animal cells that make them less capable of mutating into any sort of a different shape that's still effective at all.

And I'm nothing close to an expert on any of this. But refer to sources, e.g.:

https://www.businessinsider.com/new-coronavirus-mutates-slow...

https://www.washingtonpost.com/health/the-coronavirus-isnt-m...

https://www.businessinsider.com/new-coronavirus-mutates-slow...

Thanks for sharing -- great link, I learned something, thank you.

> My fear is that 2-3 months of lockdown isn't a cure, it turns into on-and-off lockdown, herd immunity is never established because immunity wears off in 2 years, and a vaccine is 2-5 years out.

I wonder if any models take into account the availability of drugs. I wonder because (perhaps because I studied pharmacology back in the days) while not effective as a vaccine, proper clinical management of this disease with drugs would help a lot in helping hospitals.

Instead the media seems only to focus on a vaccine (which is putting all eggs in one basket, if it fails).

Are there specific drugs you think would be helpful in treating COVID?

Most of the drugs being trialed are repurposed drugs, so we can't expect miracles. Scant evidence (at least until the trials end) say that giving them early on may lead to better response.

Currently, there are a number being tested by WHO and other trials, I list the ones that come to mind:

- remedisivir (repurposed anti-Ebola drug): several trials to end by May-June

- lopinavir/ritonavir (anti-HIV drugs): those delivered bad results in a recent study, but those so far were (a limitation noted by the study authors) on patients with rather severe sympthoms, so it's still undecided whether they're effective or not

- Chloroquine family (chloroquine/hydroxychloroquine, with or without azithromycin): some preliminary studies may have shown interesting effects, but there were small sample sizes (also in another study which apparently was not very successful). U of Minnesota started a largish (3000 people) trial to see if it's prophylactic for immediate post-exposure to the virus. Another one started a couple of days ago to test the combination with the antibiotic (whose reported purpose is to fight off secondary infections)

There are others with less spotlight such as favipiravir, which provided a (modest) improvement in a small trial in China, and it's now part of a Phase 3 trial in Japan, or whole classes of drugs to combat the secondary but clinically important sympthoms like overinflammation (which occurs in some patients) like tocilizumab.

A lot of eyes are pointed on the chloroquines because they are already available (although they do present significant side-effects).

Neither of these drugs (or many others, see for example https://biocentury.com/coronavirus for some lists) will likely provide miracles. What the trials will do (hopefully!) is to help understanding how early they must be taken, and how effective they are in clinical management. An advantage, however, is that they will be available faster than a vaccine (modulo some non trivial issues like mass production).

Reply on news.ycombinator.com