[__blockcipher__]

There is no credible evidence of re-infection. The isolated cases can be explained away in a bayesian sense by PCR false positives or false negatives. It’s the usual base rate neglect fallacy.

The idea of reinfection contradicts decades of well established immunological principles. It also ignores the fact that we have a close relative of SARS-2 to study. That relative is SARS-1 and we have detected strong t cell activation after 17+ years. Therefore immunity is enduring and long lasting.

SARS-2 is substantially structurally similar to SARS-1.

Alternatively, take a statistical argument. There have been millions of cases around the world. SARS-2 is highly infectious for those who are susceptible. Therefore we would have thousands if not more well-documented, inarguable cases of reinfection. We don’t have those. All we have is a bunch of articles from heavily biased sources like Vox that have a vested interest in pushing the “doomer” narrative.

Why haven’t we seen widespread reinfection if it is truly possible?

[claudeganon]

As I pointed out downthread, there's a Kings College study under review that says antibodies seems to wane rapidly:

https://www.sfchronicle.com/health/article/With-coronavirus-...

https://www.medrxiv.org/content/10.1101/2020.07.09.20148429v....

Likewise, asymptomatic cases appear to have limited immune duration and development:

https://www.jci.org/articles/view/138759#ABS

And meaningful immunity might depend on how much of the virus one is exposed to:

https://www.nature.com/articles/s41591-020-0965-6

If this research holds up, we'll have your well documented cases in probably 3-6 months. Frontline doctors, outside the one cited in the Vox article, are already insisting its true.

[__blockcipher__]

Antibodies do wane, and they are supposed to. They generally don't last longer than a few months with SARS-[1,2].

Even though they wane, memory b cells persist, meaning subsequent infection is milder and theoretically less transmissible.

Additionally that reinfection potential only exists if you ignore t-cells. When you factor in t-cells, it simply does not happen.

We're in July 2020. SARS-2 existed since some point in 2019, probably midway through. Granted we couldn't detect reinfection until the whole globe had been freaking out about it, so let's start our clock from January 2020.

It's been 6 months and we don't have dozens of well-documented, credible reinfections?

No, such one-off supposed reinfections are much more explainable from a bayesian perspective of either false positives or false negatives of PCR.

Find me someone who is not immunocompromised, who is PCR-positive for SARS-2 and from whom viable SARS-2 is successfully cultured, then show them fighting off the infection and being PCR-negative and symptom-free for weeks, then show me them being PCR-positive again with viable SARS-2 cultured from their body. That's the standard.

20 examples of that and reinfection definitely happens. Until then, our priors are that we should assume it does not.

Such fears are just used to argue against herd immunity, which has been made into a "dirty word" (phrase). Herd immunity is a natural phenomenom, arguing "against" it is like arguing against natural selection in my book. (The analogy is not perfect but I hope you see the point. I'm tired of being called callous for saying "hey let's not fuck with the normal population immunity dynamics that we've used for every other highly infectious virus in existence")

---

BTW, I can't find the study but they have tested reinfection in primates and showed them unable to get reinfected

[claudeganon]

This is addressed in the Nature article I linked. They compare SARS/MERS immunity to COVID-19 and find different results:

>Sustained IgG levels were maintained for more than 2 years after SARS-CoV infection. Antibody responses in individuals with laboratory-confirmed MERS-CoV infection lasted for at least 34 months after the outbreak. Recently, several studies characterizing adaptive immune responses to SARS-CoV-2 infection have reported that most COVID-19 convalescent individuals have detectable neutralizing antibodies, which correlate with the numbers of virus-specific T cells. In this study, we observed that IgG levels and neutralizing antibodies in a high proportion of individuals who recovered from SARS-CoV-2 infection start to decrease within 2–3 months after infection. In another analysis of the dynamics of neutralizing antibody titers in eight convalescent patients with COVID-19, four patients showed decreased neutralizing antibodies approximately 6–7 weeks after illness onset. One mathematical model also suggests a short duration of immunity after SARS-CoV-2 infection. Together, these data might indicate the risks of using COVID-19 ‘immunity passports’ and support the prolongation of public health interventions, including social distancing, hygiene, isolation of high-risk groups and widespread testing.

So the rate of decrease is already greater than SARS and MERS under this initial investigation. I agree that we don't know the rate or duration of immunity, but nothing so far seems to point in the direction you keep emphasizing or justifies your confidence. I actually do hope immunity ends up being longer lasting, but what I "hope" is irrelevant.

I don't know that herd immunity is a dirty word, but might, for COVID, be being deployed dangerously and pseudo-scientifically. The "natural phenomenon" you refer to does not occur in all cases for all diseases. It's not callousness unless you're explicitly denying that reality and justifying excess death and illness on a dynamic which may not even be in play.

[__blockcipher__]

> The "natural phenomenon" you refer to does not occur in all cases for all diseases.

What's an example of an infectious disease that the body can fight off that does not result in herd immunity? (so, herpes and aids don't count because the body doesn't fight them off whereas we KNOW that the body fights off SARS-like diseases)

As far as reinfection is concerned, T-cells are more relevant. I am aware that antibody response fades sooner for SARS-CoV-2.

("SARS-CoV-2-specific T cell immunity in cases of COVID-19 and SARS, and uninfected controls")[https://www.nature.com/articles/s41586-020-2550-z] - Published: 15 July 2020

* Here, we first studied T cell responses to structural (nucleocapsid protein, NP) and non-structural (NSP-7 and NSP13 of ORF1) regions of SARS-CoV-2 in COVID-19 convalescents (n=36). In all of them we demonstrated the presence of CD4 and CD8 T cells recognizing multiple regions of the NP protein. We then showed that SARS-recovered patients (n=23) still possess long-lasting memory T cells reactive to SARS-NP 17 years after the 2003 outbreak, which displayed robust cross-reactivity to SARS-CoV-2 NP.

* Surprisingly, we also frequently detected SARS-CoV-2 specific T cells in individuals with no history of SARS, COVID-19 or contact with SARS/COVID-19 patients (n=37)

> It's not callousness unless you're explicitly denying that reality and justifying excess death and illness on a dynamic which may not even be in play.

Again, the excess death is the deaths caused by lockdown, not the deaths caused by a highly infectious respiratory virus. All highly infectious respiratory viruses are dealt with the same way: acquiring population immunity. Vaccines are just a way to achieve that more cheaply, but because we do not currently have a vaccine it does not make sense to try to "stop, drop and roll" until we have one. Especially because, speaking for the US, we are on track to hit population immunity before we ever get one.

[claudeganon]

>Again, the excess death is the deaths caused by lockdown, not the deaths caused by a highly infectious respiratory virus.

At the point that you're making blatantly counterfactual statements like this, it's hard to take anything else you say seriously. Some estimates put excess deaths from things besides COVID during lockdowns at about 35% to the total, but they in no way exceed the excess COVID deaths themselves, especially given the likelihood of COVID death undercounts.

You also obviously don't understand how the thresholds for herd immunity work are dependent on duration of immunity and social dynamics of populations. All of humanity doesn't just get together and say "let's get together, right now, and see which of us dies," as much as you would seemingly like to argue that they should. We don't have herd immunity to any number of diseases (e.g. cholera) because we quash their spread through other means, like sanitation, quarantines, using masks. I don’t know why you cite SARS over and over again without acknowledging that we don’t have herd immunity or a vaccine for it.

[__blockcipher__]

(1) You misunderstand my use of the term excess death. I was using it in the same sense of the comment I was replying to.

I wasn’t talking about “excess deaths” ie the extra deaths not explainable by known covid deaths. Sorry for the confusion. (Although I think more of those deaths are non-covid, likely cardiac disease etc due to fear of hospital)

(2) I talk about sars-1 because covid is caused by sars-2. You understand that right?

We don’t have herd immunity to sars-1 because it burned itself out. Sars-2 will not do that because it is not nearly as lethal and exhibits presymptomatic spread. It is here to stay.

Also by pointing out we don’t have a vaccine for sars-1 that only strengthens my argument that banking on a vaccine for sars-2 is foolish

[js2]

Meta: your comments on this thread imply a degree of certainty that isn't justified by the evidence as I understand it. I am just a lay person here, but that's my impression as someone who has done a lot of reading.

As far as coronaviruses go, there are four mild human coronaviruses that are responsible for about 15% of common colds and for which humans do not develop any long lasting immunity.

There are also the three severe human coronaviruses: MERS, SARS-CoV, and SARS-CoV-2. AFAIU, long-lasting immunity to these is not well understood.

I do not understand how you can make such an authoritative statement about re-infection risk based on the limited data we have about SARS-CoV-2. Here's what immunologists have to say:

> In summary, progress since January 2020 has been impressive, but there is still so much more to learn. Are T cells protective and if so which are the key antigens and and cytokine effector programs to focus on? Are all T cell responses beneficial, or are some contributory to immunopathology and to be avoided? If it is indeed the case that antibodies are transient and T cell memory is more durable (though, how durable?), what can we learn about anomalies of T follicular helper-B cell interactions in germinal centers? In the short to medium term, we need to ensure that all of this T cell toolkit and knowledge is brought to bear on robust, comparative evaluation of the different vaccine platforms, their immunogenicity, efficacy and safety. Entering the next part of the battle, there are many thousands of people suffering the chronic aftermath of infection posed by chronic, so-called ‘long-COVID’ cases, characterized by diverse symptoms including fatigue, joint pain and dyspnea (19). A more detailed understanding of the T cell immunology will be valuable in deciphering this pathogenesis.

https://immunology.sciencemag.org/content/5/49/eabd6160.full

What I read there is a lot of "we're not sure yet."

[__blockcipher__]

Of course there's uncertainty, but the idea of re-infection contradicts decades of established immunological principles.

At a minimum, we can agree that in the event of re-infection, the subsequent infection will hit a lower peak viral load and therefore theoretically a much milder outcome with reduced transmissibility, right? This is called immunological memory and arises due to memory b cells and memory t cells which persist across decades.

Anyway, please see https://www.nature.com/articles/s41586-020-2550-z

It establishes that those exposed to SARS-1, which structurally and functionally is incredibly similar to SARS-2 and thus is our best model of how to think about SARS-2, have long-lasting immunity. Their t-cells not only react to SARS-1 after 17 years, they also have immunity to SARS-2, which is a testament to how similar they are structurally speaking.

Additionally exposure to those common cold human coronaviruses you mentioned almost certainly confers immunity to SARS-2 based off that same paper. We're still hashing out the details, of course.

Immunology is incredibly complex and there is still plenty to learn about as far as the exact specifics of what unfolds here, yes. But we should assume reinfection isn't possible, because:

- It doesn't happen in SARS-1 which is by far the best model we have

- If it did happen, given the MILLIONS of cases of COVID-19 worldwide, we would have seen THOUSANDS of rigorously documented examples of the phenomenom happening

- Those arguing for reinfection tend to not make any mention of immunological memory

- Those arguing for reinfection do so to in an attempt to scare us into staying locked down until "the vaccine", which I am opposed to because I am opposed to any public health policy that banks on a future technological innovation that does not yet exist, particularly when I fear that the environment of irrational fear and anxiety and outright hysteria is going to be used to mandate vaccines, which is highly unethical under my moral framework

--

As far as me sounding over-certain, frankly it's cognitive draining to be arguing against a horde of people whose priors have been completely screwed up by programming from a media that takes delight in knowingly lying to citizens, and even our trusted public health officials like Fauci don't have the courage or perhaps the desire to break out of the collective mass delusion we are all trapped in.

So yes, if I had infinite time and energy I agree, I could do a way better job of capturing uncertainty. I've written an 8000+ word writeup on COVID that does a much better job capturing the uncertainty, but it's very difficult to do without...writing 8000 words.

Also this doesn't justify it but I do feel the need to point out that those arguing for the "doom" scenario are even more egregiously overstating certainty, and tend to not be called out on their ridiculous statements. So that's why I tend to come into these threads guns blazing, with the predictable result of getting hammered by downvotes. C'est la vie.