patrick.net

zzyzzx says

I got the J&J!!
One and done :)

The weird part is....i was supposed to get dementia and now deformations? Even herpes and death is on the agenda!

Weird....not even herpes yet!???? seems to take longer with me. I'll keep you posed. If I dont respond for a few days, you will know I either have dementia or died.

porkchopexpress says

Fine, then pressure "at risk" people to get the vaccine. Over 60 and people with serious underlying conditions. Not me.

The jury is out on it already. No one wants it for the most part. They "estimate" IL is 30% or so vaccinated. I can get ANY of the shots tomorrow. Just roll up and get it.

I don't know, 70% of people in my state don't want it. I'm not a follow a pack guy either, but it's pretty obvious no one wants to take this and thinks it's BS. Everyone getting it is either elderly, essential worker just because it was offered and now anyone that basically wants it. 30% vaccinated.... lol.

Even with such a low vaccination rate, Chicago is planning to "open up," whatever that means. Nothing has changed. We just poked a bunch of people and they were un-brainwashed. It's a miracle. lol.

You know... If this were a real pandemic, we would need to run PR campaigns to encourage people to get a shot.

Just saying.

joshuatrio says

You know... If this were a real pandemic, we would need to run PR campaigns to encourage people to get a shot.

Just saying.

Agreed....its a scamdemic. Still got the shot though.

My cousin posts on FaceBook his bad reaction to both jabs. But FB can't let that go, and interjects a comment:

Zak says

mell says

You don't want to do follow any calculation

You're not doing calculations. You're dismissing broad swaths of society to fudge your numbers.

"This is for 0-21, but the percentage of those with underlying conditions for young adults til age 25 at least if not 30 are probably the same, around 75%. That would cut deaths among "healthy" to 1/4, or 500."

See that. That's bullshit, not math. You just wrote off your argument for 75% of the population. I'm beginning to think you're just fucking insane and its worthless to even talk to you.

It's clear what that means, maybe you're just being obtuse at this point, clinging to your government covid death numbers. It's clear to everyone that if 75% of those dead had underlying health conditions that the risk of dying from covid for the avg. healthy young person is much smaller and not worth the risk of the jab and boosters over time. Whereas the vaccine deaths have no such distribution, they affect otherwise perfectly healthy people the same way. Why is this so hard to understand?

WookieMan says

porkchopexpress says

Fine, then pressure "at risk" people to get the vaccine. Over 60 and people with serious underlying conditions. Not me.

The jury is out on it already. No one wants it for the most part. They "estimate" IL is 30% or so vaccinated. I can get ANY of the shots tomorrow. Just roll up and get it.

I don't know, 70% of people in my state don't want it. I'm not a follow a pack guy either, but it's pretty obvious no one wants to take this and thinks it's BS. Everyone getting it is either elderly, essential worker just because it was offered and now anyone that basically wants it. 30% vaccinated.... lol.

Even with such a low vaccination rate, Chicago is planning to "open up," whatever that means. Nothing has changed. We just poked a bunch of people and they were un-brainwashed. It's a miracle. lol.

That's the thing - it has passed through, the vaccination won't really make a difference as we have approached t cell herd immunity in pretty much all states. Hence your risk of catching covid if you haven't been exposed to it yet (40-81% already have, by now closer to 80%) is so low that the risks of the jab may be quite higher. The antibody test is not perfect unfortunately, since it doesn't tell t cell immunity which is the most important factor, even when antibodies have faded.

mell says

Why is this so hard to understand?

Money or emotion.

Some people are making a lot of money from this scam.

Other people are genuinely terrified and think the only path to safety is EVERYONE conforming to the government's [arbitrary] rules.

Onvacation says

mell says

Why is this so hard to understand?

Money or emotion.

Some people are making a lot of money from this scam.

Other people are genuinely terrified and think the only path to safety is EVERYONE conforming to the government's [arbitrary] rules.

We've had 30 positive pcr tests per day in a county of 1MM even before the mass vaccinations started. It's over and endemic now. And we have therapeutics. The risk profile has completely changed. There is no reason to keep the vaccination push going as it's a losing risk benefit math for 80% of the unvaxxed.

ThreeBays says

Vaccination with current vaccines are shown to elicit higher immune memory than getting the disease, because they deliver a consistent dose. Whereas viral infection has a 100 fold variance in immune memory.

Do you have a link to the study on the experimental biologic agent that shows this? Or did you just pull it out of your ass?

This experimental biologic agent is new. We can speculate, but we have no idea of its long term safety and efficacy.

Even worse, it could just be a placebo to ease us into the new world order.

Thank you Onvacation and Mell for doing all of this heavy lifting. I think Zak may be Bitcoin. They act very similar.

Robert Sproul says

The median age of death has been 83. In other words, folks who were fixing to die anyway.

Given that the media age of a CCP Virus death is greater than the median age at death, one could plausibly argue that the virus extends life.

It's true though. The average age of a CCP Virus death is greater than the median age at death.

Does that not lessen your fear at all?

Onvacation says

Why do you hate children?

Well, somebody hates children.
Infants as young as 6 MONTHS OLD are taking part in vaccine trials by both Pfizer and Moderna.
They don't get it and they don't significantly transmit it, but they need to be vaccinated anyway, apparently.

zzyzzx says

Booger says

Zak says

https://www.cnn.com/videos/world/2021/05/06/india-doctors-hiding-kiley-pkg-lead-vpx.cnn/video/playlists/coronavirus-intl/

ehh.. not that bad really.. just runs the whole ICU out of oxygen... or is this fake news because CNN is the source..??

Fake news / propaganda. That, and if it's true, it says more about one places ability to maintain supplies, or shitty procurement processes.

CNN is Communist propaganda and very very gay.
https://patrick.net/post/1240230/2014-03-25-cnn-comes-out-as-gay?0#com...

Its a fake news an attempt to make it looks real. He is talking about parliament building that was planed more than 2 years ago and linking to virus! Now India's supreme court woke commie judges are on full scale activism and dictating on supplied who should get what and where! These idiots generally take decades to close any legal case if the people are still alive. These judges should be hanged in public.

WineHorror1 says

Thank you Onvacation and Mell for doing all of this heavy lifting. I think Zak may be Bitcoin. They act very similar.

All the NPC's spouts the same propaganda. It's hard to tell them apart.

I think it's a positive thing for them to come here and be subjected to facts and logic.

I used to be so ignorant. I cheered when we bombed Iraq. I bought a house during the bubble. Chemotherapy almost killed my wife.

One day while trying to figure it all out I ran into this site. There are a lot of smart people here that will research "the facts" and argue with logic. I have learned a lot.

If you try to bring lies and emotional arguments you won't get very far.

Onvacation says

WineHorror1 says

Thank you Onvacation and Mell for doing all of this heavy lifting. I think Zak may be Bitcoin. They act very simila

Zak has me on ignore because I made fun of him thinking Bitcoin will crash. He got sooooooooooooooooooo excited when Bitcoin dipped. I told him it will soon hit ATH's and it did......he couldnt take it :)

Patrick says

Robert Sproul says

The median age of death has been 83. In other words, folks who were fixing to die anyway.

Or more likely. all those people who died of old age were classified as being Covid deaths.

You did your research, Right?

Why you still wearing a mask?

PHARMACIST SHOWS BLANK COVID-19 VACCINE INSERT.

ThreeBays says

Here you go: https://science.sciencemag.org/content/371/6529/eabf4063

So you pulled it out of your ass.

ThreeBays says

https://www.youtube.com/watch?v=eK0C5tFHze8

Is there a copy of your vid on a platform that doesn't censor the president?

ThreeBays says

Onvacation says

ThreeBays says

Vaccination with current vaccines are shown to elicit higher immune memory than getting the disease, because they deliver a consistent dose. Whereas viral infection has a 100 fold variance in immune memory.

Do you have a link to the study on the experimental biologic agent that shows this? Or did you just pull it out of your ass?

Here you go: https://science.sciencemag.org/content/371/6529/eabf4063

Looked at antibody, memory B cell, CD4+ T cell, and CD8+ T dynamics over 8 months.

Immunoglobulin G (IgG) to the spike protein was relatively stable over 6+ months. Spike-specific memory B cells were more abundant at 6 months than at 1 month after symptom onset. SARS...

People who have had CV or cold infections have had cross immunity for years if not decades, that's why up to 40% had preexisting immunity. Yet the agent fades after 5-12 months. If you truly believe these claims then you should not return for your "booster" in less than 5 years, maybe you can do one at year two, but generally it's every 5-15 years. Everything else is hogwash. Obviously people with natural infection have vastly superior t cell immunity against various characteristics (protein expression) of the virus, not just the s protein. That's why you usually get influenza every 5-15 years of you had a natural infection. Even the ABs can last years. Anything that "needs" you to come back every year or even more often you should be very skeptical of.

https://www.bmj.com/content/370/bmj.m3563

"
With public health responses around the world predicated on the assumption that the virus entered the human population with no pre-existing immunity before the pandemic,4 serosurvey data are leading many to conclude that the virus has, as Mike Ryan, WHO’s head of emergencies, put it, “a long way to burn.”

Yet a stream of studies that have documented SARS-CoV-2 reactive T cells in people without exposure to the virus are raising questions about just how new the pandemic virus really is, with many implications.

Not so novel coronavirus?
At least six studies have reported T cell reactivity against SARS-CoV-2 in 20% to 50% of people with no known exposure to the virus.5678910

In a study of donor blood specimens obtained in the US between 2015 and 2018, 50% displayed various forms of T cell reactivity to SARS-CoV-2.511 A similar study that used specimens from the Netherlands reported T cell reactivity in two of 10 people who had not been exposed to the virus.7

In Germany reactive T cells were detected in a third of SARS-CoV-2 seronegative healthy donors (23 of 68). In Singapore a team analysed specimens taken from people with no contact or personal history of SARS or covid-19; 12 of 26 specimens taken before July 2019 showed reactivity to SARS-CoV-2, as did seven of 11 from people who were seronegative against the virus.8 Reactivity was also discovered in the UK and Sweden.6910

Though these studies are small and do not yet provide precise estimates of pre-existing immunological responses to SARS-CoV-2, they are hard to dismiss, with several being published in Cell and Nature. Alessandro Sette, an immunologist from La Jolla Institute for Immunology in California and an author of several of the studies (box 1), told The BMJ, “At this point there are a number of studies that are seeing this reactivity in different continents, different labs. As a scientist you know that is a hallmark of something that has a very strong footing.”

Box 1
Swine flu déjà vu
In late 2009, months after the World Health Organization declared the H1N1 “swine flu” virus to be a global pandemic, Alessandro Sette was part of a team working to explain why the so called “novel” virus did not seem to be causing more severe infections than seasonal flu.12

Their answer was pre-existing immunological responses in the adult population: B cells and, in particular, T cells, which “are known to blunt disease severity.”12 Other studies came to the same conclusion: people with pre-existing reactive T cells had less severe H1N1 disease.1314 In addition, a study carried out during the 2009 outbreak by the US Centers for Disease Control and Prevention reported that 33% of people over 60 years old had cross reactive antibodies to the 2009 H1N1 virus, leading the CDC to conclude that “some degree of pre-existing immunity” to the new H1N1 strains existed, especially among adults over age 60.15

The data forced a change in views at WHO and CDC, from an assumption before 2009 that most people “will have no immunity to the pandemic virus”16 to one that acknowledged that “the vulnerability of a population to a pandemic virus is related in part to the level of pre-existing immunity to the virus.”17 But by 2020 it seems that lesson had been forgotten.

RETURN TO TEXT
Researchers are also confident that they have made solid inroads into ascertaining the origins of the immune responses. “Our hypothesis, of course, was that it’s so called ‘common cold’ coronaviruses, because they’re closely related,” said Daniela Weiskopf, senior author of a paper in Science that confirmed this hypothesis.18 “We have really shown that this is a true immune memory and it is derived in part from common cold viruses.” Separately, researchers in Singapore came to similar conclusions about the role of common cold coronaviruses but noted that some of the T cell reactivity may also come from other unknown coronaviruses, even of animal origin.8

Taken together, this growing body of research documenting pre-existing immunological responses to SARS-CoV-2 may force pandemic planners to revisit some of their foundational assumptions about how to measure population susceptibility and monitor the extent of epidemic spread.

Population immunity: underestimated?
Seroprevalence surveys measuring antibodies have been the preferred method for gauging the proportion of people in a given population who have been infected by SARS-CoV-2 (and have some degree of immunity to it), with estimates of herd immunity thresholds providing a sense of where we are in this pandemic. Whether we overcome it through naturally derived immunity or vaccination, the sense is that it won’t be over until we reach a level of herd immunity.

The fact that only a minority of people, even in the hardest hit areas, display antibodies against SARS-CoV-2 has led most planners to assume the pandemic is far from over. In New York City, where just over a fifth of people surveyed had antibodies, the health department concluded that “as this remains below herd immunity thresholds, monitoring, testing, and contact tracing remain essential public health strategies.”19 “Whatever that number is, we’re nowhere near close to it,” said WHO’s Ryan in late July, referring to the herd immunity threshold (box 2).

Box 2
Calculating the herd immunity threshold
In theory, outbreaks of contagious disease follow a certain trajectory. In a population that lacks immunity new infections grow rapidly. At some point an inflection in this growth should occur, and the incidence will begin to fall.

The 1970s gave rise to a theory that defined this inflection point as the herd immunity threshold (HIT) and offered a straightforward formula for estimating its size: HIT=1−1/R0 (where R0 is the disease’s basic reproduction number, or the average number of secondary cases generated by an infectious individual among susceptible people). This simple calculation has guided—and continues to guide—many vaccination campaigns, often used to define target levels of vaccination.20

The formula rests on two assumptions: that, in a given population, immunity is distributed evenly and members mix at random. While vaccines may be deliverable in a near random fashion, from the earliest days questions were raised about the random mixing assumption. Apart from certain small closed populations such as “orphanages, boarding schools, or companies of military recruits,” Fox and colleagues wrote in 1971,21 truly random mixing is the exception, not the rule. “We could hardly assume even a small town to be a single homogeneously mixing unit. Each individual is normally in close contact with only a small number of individuals, perhaps of the order of 10-50.”

Nearly 50 years later, Gabriela Gomes, an infectious disease modeller at the University of Strathclyde, is reviving concerns that the theory’s basic assumptions do not hold. Not only do people not mix randomly, infections (and subsequent immunity) do not happen randomly either, her team says. “More susceptible and more connected individuals have a higher propensity to be infected and thus are likely to become immune earlier. Due to this selective immunization by natural infection, heterogeneous populations require less infections to cross their herd immunity threshold,” they wrote.22 While most experts have taken the R0 for SARS-CoV-2 (generally estimated to be between 2 and 3) and concluded that at least 50% of people need to be immune before herd immunity is reached, Gomes and colleagues calculate the threshold at 10% to 20%.2223

Ulrich Keil, professor emeritus of epidemiology from the University of Münster in Germany, says the notion of randomly distributed immunity is a “very naive assumption” that ignores the large disparities in health in populations and “also ignores completely that social conditions might be more important than the virus itself.” He added, “Tuberculosis here is the best example. We all know that the immune system is very much dependent on the living conditions of a person, and this depends very much on education and social conditions.”

Another group led by Sunetra Gupta at the University of Oxford has arrived at similar conclusions of lower herd immunity thresholds by considering the issue of pre-existing immunity in the population. When a population has people with pre-existing immunity, as the T cell studies may be indicating is the case, the herd immunity threshold based on an R0 of 2.5 can be reduced from 60% of a population getting infected right down to 10%, depending on the quantity and distribution of pre-existing immunity among people, Gupta’s group calculated.24

RETURN TO TEXT
But memory T cells are known for their ability to affect the clinical severity and susceptibility to future infection,25 and the T cell studies documenting pre-existing reactivity to SARS-CoV-2 in 20-50% of people suggest that antibodies are not the full story.

“Maybe we were a little naive to take measurements such as serology testing to look at how many people were infected with the virus,” the Karolinska Institute immunologist Marcus Buggert told The BMJ. “Maybe there is more immunity out there.”

The research offers a powerful reminder that very little in immunology is cut and dried. Physiological responses may have fewer sharp distinctions than in the popular imagination: exposure does not necessarily lead to infection, infection does not necessarily lead to disease, and disease does not necessarily produce detectable antibodies. And within the body, the roles of various immune system components are complex and interconnected. B cells produce antibodies, but B cells are regulated by T cells, and while T cells and antibodies both respond to viruses in the body, T cells do so on infected cells, whereas antibodies help prevent cells from being infected.

An unexpected twist of the curve
Buggert’s home country has been at the forefront of the herd immunity debate, with Sweden’s light touch strategy against the virus resulting in much scrutiny and scepticism.26 The epidemic in Sweden does seem to be declining, Buggert said in August. “We have much fewer cases right now. We have around 50 people hospitalised with covid-19 in a city of two million people.” At the peak of the epidemic there were thousands of cases. Something must have happened, said Buggert, particularly considering that social distancing was “always poorly followed, and it’s only become worse.”

Understanding this “something” is a core question for Sunetra Gupta, an Oxford University epidemiologist who developed a way to calculate herd immunity thresholds that incorporates a variable for pre-existing innate resistance and cross protection.24 Her group argues that herd immunity thresholds “may be greatly reduced if a fraction of the population is unable to transmit the virus.”

“The conventional wisdom is that lockdown occurred as the epidemic curve was rising,” Gupta explained. “So once you remove lockdown that curve should continue to rise.” But that is not happening in places like New York, London, and Stockholm. The question is why.

“If it were the case that in London the disease hadn’t disseminated too widely, and only 15% have experienced the virus [as serology tests indicate] . . . under those circumstances, if you lift lockdown, you should see an immediate and commensurate increase in cases, as we have observed in many other settings,” Gupta told The BMJ, “But that hasn’t happened. That is just a fact. The question is why.”

"
Possible answers are many, she says. One is that social distancing is in place, and people are keeping the spread down. Another possibility is that a lot of people are immune because of T cell responses or something else. “Whatever it is,” Gupta added, “if there is a significant fraction of the population that is not permissive to the infection, then that all makes sense, given how infectious SARS-CoV-2 is.”

Buggert’s study in Sweden seems to support this position. Investigating close family members of patients with confirmed covid-19, he found T cell responses in those who were seronegative or asymptomatic.10 While around 60% of family members produced antibodies, 90% had T cell responses. (Other studies have reported similar results.27) “So many people got infected and didn’t create antibodies,” concludes Buggert.

Deeper discussion
T cell studies have received scant media attention, in contrast to research on antibodies, which seem to dominate the news (probably, says Buggert, because antibodies are easier, faster, and cheaper to study than T cells). Two recent studies reported that naturally acquired antibodies to SARS-CoV-2 begin to wane after just 2-3 months, fuelling speculation in the lay press about repeat infections.282930

But T cell studies allow for a substantially different, more optimistic, interpretation. In the Singapore study, for example, SARS-CoV-1 reactive T cells were found in SARS patients 17 years after infection. “Our findings also raise the possibility that long lasting T cells generated after infection with related viruses may be able to protect against, or modify the pathology caused by, infection with SARS-CoV-2,”8 the investigators wrote.

T cell studies may also help shed light on other mysteries of covid-19, such as why children have been surprisingly spared the brunt of the pandemic, why it affects people differently, and the high rate of asymptomatic infections in children and young adults.

The immunologists I spoke to agreed that T cells could be a key factor that explains why places like New York, London, and Stockholm seem to have experienced a wave of infections and no subsequent resurgence. This would be because protective levels of immunity, not measurable through serology alone but instead the result of a combination of pre-existing and newly formed immune responses, could now exist in the population, preventing an epidemic rise in new infections.

But they were all quick to note that this is speculation. Formally, the clinical implications of the pre-existing T cell reactivity remain an open question. “People say you don’t have proof, and they’re right,” says Buggert, adding that the historical blood donor specimens in his study were all anonymised, precluding longitudinal follow-up.

There is the notion that perhaps T cell responses are detrimental and predispose to more severe disease. “I don’t see that as a likely possibility,” Sette said, while emphasising that we still need to acknowledge the possibility. “It’s also possible that this absolutely makes no difference. The cross reactivity is too small or weak to affect the virus. The other outcome is that this does make a difference, that it makes you respond better.”

Weiskopf added, “Right now, I think everything is a possibility; we just don’t know. The reason we’re optimistic is we have seen with other viruses where [the T cell response] actually helps you.” One example is swine flu, where research has shown that people with pre-existing reactive T cells had clinically milder disease (box 1).121314

Weiskopf and Sette maintain that compelling evidence could come through a properly designed prospective study that follows a cohort of people who were enrolled before exposure to SARS-CoV-2, comparing the clinical course of those with and without pre-existing T cell responses.

Understanding the protective value of pre-existing SARS-CoV-2 T cell reactivity “is identical to the situation on vaccines,” said Antonio Bertoletti, professor of infectious disease at Duke-NUS Medical School in Singapore. “Through vaccination we aim to stimulate antibodies and T cell production, and we hope that such induction of immunity will protect … but we need a phase III clinical study to really demonstrate the effect.”

German investigators came to the same conclusion, arguing that their T cell findings represented a “decisive rationale to initiate worldwide prospective studies” mapping pre-existing reactivity to clinical outcomes.31 Other groups have called for the same thing.6

“At the start of the pandemic, a key mantra was that we needed the game changer of antibody data to understand who had been infected and how many were protected,” two immunologists from Imperial College London wrote in a mid-July commentary in Science Immunology. “As we have learned more about this challenging infection, it is time to admit that we really need the T cell data too.”32

Theoretically, the placebo arm of a covid-19 vaccine trial could provide a straightforward way to carry out such a study, by comparing the clinical outcomes of people with versus those without pre-existing T cell reactivity to SARS-CoV-2. A review by The BMJ of all primary and secondary outcome measures being studied in the two large ongoing, placebo controlled phase III trials, however, suggests that no such analysis is being done.3334

Could pre-existing immunity be more protective than future vaccines? Without studying the question, we won’t know.

Acknowledgments
I thank Juan-Andres Leon and Angela Spelsberg for comments on a draft of this article.

Footnotes
Competing interests: I am a colleague of Ulrich Keil, quoted in this article. A generic statement of competing interests may be found at https://www.bmj.com/about-bmj/editorial-staff/peter-doshi

Provenance and peer review: Commissioned; externally peer reviewed.

This article is made freely available for use in accordance with BMJ's website terms and conditions for the duration of the covid-19 pandemic or until otherwise determined by BMJ. You may use, download and print the article for any lawful, non-commercial purpose (including text and data mining) provided that all copyright notices and trade marks are retained.

https://bmj.com/coronavirus/usage
References
↵Rosenberg ES, Tesoriero JM, Rosenthal EM, et al. Cumulative incidence and diagnosis of SARS-CoV-2 infection in New York. Ann Epidemiol2020;48:23-9.e4. .pmid:32648546PubMedGoogle Scholar
↵Public Health England. Sero-surveillance of COVID-19. 2020. https://www.gov.uk/government/publications/national-covid-19-surveillance-reports/sero-surveillance-of-covid-19
↵Pollán M, Pérez-Gómez B, Pastor-Barriuso R, et al., ENE-COVID Study Group. Prevalence of SARS-CoV-2 in Spain (ENE-COVID): a nationwide, population-based seroepidemiological study. Lancet2020;396:535-44. .pmid:32645347CrossRefPubMedGoogle Scholar
↵CDC. Coronavirus disease 2019 (COVID-19). 2020 https://www.cdc.gov/coronavirus/2019-ncov/hcp/planning-scenarios.html
↵Grifoni A, Weiskopf D, Ramirez SI, et al. Targets of T cell responses to SARS-CoV-2 coronavirus in humans with COVID-19 disease and unexposed individuals. Cell2020;181:1489-1501.e15. .pmid:32473127CrossRefPubMedGoogle Scholar
↵Ng K, Faulkner N, Cornish G, Rosa A, Earl C, Wrobel A, et al. Pre-existing and de novo humoral immunity to SARS-CoV-2 in humans [preprint]. BioRxiv. 2020. doi:10.1101/2020.05.14.095414.Abstract/FREE Full TextGoogle Scholar
↵Weiskopf D, Schmitz KS, Raadsen MP, Grifoni A, Okba NMA, Endeman H, et al. Phenotype of SARS-CoV-2-specific T-cells in COVID-19 patients with acute respiratory distress syndrome [preprint]. MedRxiv 2020. doi:10.1101/2020.04.11.20062349.Abstract/FREE Full TextGoogle Scholar
↵Le Bert N, Tan AT, Kunasegaran K, et al. SARS-CoV-2-specific T cell immunity in cases of COVID-19 and SARS, and uninfected controls. Nature2020;584:457-62. . doi:10.1038/s41586-020-2550-z pmid:32668444CrossRefPubMedGoogle Scholar
↵Meckiff BJ, Ramírez-Suástegui C, Fajardo V, et al. Single-cell transcriptomic analysis of SARS-CoV-2 reactive CD4 + T cells. bioRxiv2020:2020.06.12.148916. doi:10.1101/2020.06.12.148916. pmid:32587963CrossRefPubMedGoogle Scholar
↵Sekine T, Perez-Potti A, Rivera-Ballesteros O, et al. Robust T cell immunity in convalescent individuals with asymptomatic or mild COVID-19 [preprint]. 2020 https://www.biorxiv.org/content/10.1101/2020.06.29.174888v1.abstract.
↵Sette A, Crotty S. Pre-existing immunity to SARS-CoV-2: the knowns and unknowns. Nat Rev Immunol2020;20:457-8. . doi:10.1038/s41577-020-0389-z pmid:32636479CrossRefPubMedGoogle Scholar
↵Greenbaum JA, Kotturi MF, Kim Y, et al. Pre-existing immunity against swine-origin H1N1 influenza viruses in the general human population. Proc Natl Acad Sci U S A2009;106:20365-70. . doi:10.1073/pnas.0911580106 pmid:19918065Abstract/FREE Full TextGoogle Scholar
↵Sridhar S, Begom S, Bermingham A, et al. Cellular immune correlates of protection against symptomatic pandemic influenza. Nat Med2013;19:1305-12. . doi:10.1038/nm.3350 pmid:24056771CrossRefPubMedGoogle Scholar
↵Wilkinson TM, Li CKF, Chui CSC, et al. Preexisting influenza-specific CD4+ T cells correlate with disease protection against influenza challenge in humans. Nat Med2012;18:274-80. . doi:10.1038/nm.2612 pmid:22286307CrossRefPubMedGoogle Scholar
↵Centers for Disease Control and Prevention (CDC). Serum cross-reactive antibody response to a novel influenza A (H1N1) virus after vaccination with seasonal influenza vaccine. MMWR Morb Mortal Wkly Rep2009;58:521-4. https://www.ncbi.nlm.nih.gov/pubmed/19478718.pmid:19478718PubMedGoogle Scholar
↵World Health Organization. Ten things you need to know about pandemic influenza. 2005. http://web.archive.org/web/20081208145210/www.who.int/csr/disease/influenza/pandemic10things/en.
↵Considerations for assessing the severity of an influenza pandemic. Wkly Epidemiol Rec2009;84(22):197-202.PubMedGoogle Scholar
↵Mateus J, Grifoni A, Tarke A, et al. Selective and cross-reactive SARS-CoV-2 T cell epitopes in unexposed humans. Science2020. . doi:10.1126/science.abd3871 pmid:32753554AbstractGoogle Scholar
↵Rosenberg ES, Tesoriero JM, Rosenthal EM, et al. Cumulative incidence and diagnosis of SARS-CoV-2 infection in New York [preprint]. medRxiv. 2020. https://www.medrxiv.org/content/10.1101/2020.05.25.20113050v1.
↵Fine P, Eames K, Heymann DL. “Herd immunity”: a rough guide[Internet]. Clin Infect Dis2011;52:911-6. . doi:10.1093/cid/cir007 pmid:21427399CrossRefPubMedWeb of ScienceGoogle Scholar
↵Fox JP, Elveback L, Scott W, Gatewood L, Ackerman E. Herd immunity: basic concept and relevance to public health immunization practices. Am J Epidemiol1971;94:179-89. . doi:10.1093/oxfordjournals.aje.a121310 pmid:5093648CrossRefPubMedWeb of ScienceGoogle Scholar
↵Aguas R, Corder RM, King JG, Goncalves G, Ferreira MU, Gomes MGM. Herd immunity thresholds for SARS-CoV-2 estimated from unfolding epidemics [preprint]. medRxiv. 2020. https://doi.org/10.1101/2020.07.23.20160762.
↵Gomes MGM, Corder RM, King JG, Langwig KE, Souto-Maior C, Carneiro J, et al. Individual variation in susceptibility or exposure to SARS-CoV-2 lowers the herd immunity threshold [preprint]. MedRxiv. 2 May 2020. https://www.medrxiv.org/content/10.1101/2020.04.27.20081893v3.
↵Lourenco J, Pinotti F, Thompson C, Gupta S. The impact of host resistance on cumulative mortality and the threshold of herd immunity for SARS-CoV-2 [preprint]. medRxiv. 2020. https://www.medrxiv.org/content/10.1101/2020.07.15.20154294v1.
↵Welsh RM, Selin LK. No one is naive: the significance of heterologous T-cell immunity. Nat Rev Immunol2002;2:417-26. . doi:10.1038/nri820 pmid:12093008CrossRefPubMedWeb of ScienceGoogle Scholar
↵Habib H. Has Sweden’s controversial covid-19 strategy been successful?BMJ2020;369:m2376. . doi:10.1136/bmj.m2376 pmid:32532807FREE Full TextGoogle Scholar
↵Gallais F, Velay A, Wendling M-J, et al. Intrafamilial exposure to SARS-CoV-2 induces cellular immune response without seroconversion [preprint]. MedRxiv 2020. https://www.medrxiv.org/content/10.1101/2020.06.21.20132449v1.
↵Long Q-X, Tang X-J, Shi Q-L, et al. Clinical and immunological assessment of asymptomatic SARS-CoV-2 infections. Nat Med2020;26:1200-4. . doi:10.1038/s41591-020-0965-6 pmid:32555424CrossRefPubMedGoogle Scholar
↵Mandavilli A. You may have antibodies after coronavirus infection. But not for long. New York Times. 2020 Jun 18. https://www.nytimes.com/2020/06/18/health/coronavirus-antibodies.html
↵Seow J, Graham C, Merrick B, Acors S, Steel KJA, Hemmings O, et al. Longitudinal evaluation and decline of antibody responses in SARS-CoV-2 infection preprint. MedRxiv. 2020. https://www.medrxiv.org/content/10.1101/2020.07.09.20148429v1.
↵Braun J, Loyal L, Frentsch M, Wendisch D, Georg P, Kurth F, et al. Presence of SARS-CoV-2 reactive T cells in COVID-19 patients and healthy donors [preprint]. MedRxiv 2020. https://www.medrxiv.org/content/10.1101/2020.04.17.20061440v1.
↵Altmann DM, Boyton RJ. SARS-CoV-2 T cell immunity: Specificity, function, durability, and role in protection. Sci Immunol2020;5:eabd6160. doi:10.1126/sciimmunol.abd6160 pmid:32680954Abstract/FREE Full TextGoogle Scholar
↵A study to evaluate efficacy, safety, and immunogenicity of mRNA-1273 vaccine in adults aged 18 years and older to prevent COVID-19. 2020 Aug 19. https://clinicaltrials.gov/ct2/show/NCT04470427.
↵Study to describe the safety, tolerability, immunogenicity, and efficacy of RNA vaccine candidates against COVID-19 in healthy adults. 2020. https://www.clinicaltrials.gov/ct2/show/NCT04368728
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ThreeBays says

Second, regarding your statement, I think to be more accurate, SOME % of people that had CV or cold infections have long term immunity. But it's not 100%, and nobody can predict who has and has not. That's also why Polio requires 3 or 4 shots. It's about having a high degree of certainty of long protection in most people.

Third, it's about keeping immunity activated. We have active systems (antibodies & CD8+ T-cells in the blood) that attack the virus immediately. A high level of antibodies sterilizes viruses - this is how you avoid infection completely. Over time those active systems wane and we lose that "sterilizing" ability so can still get re-infected and be infectious.

If the vaccine were 100% safe, I'd be more inclined to just get it. Keeping the immune system activated artificially? That sounds like a recipe for developing auto-immune disease or hyper-active immune response. No thanks, I'll trust what nature gave me vs a science experiment.

Onvacation says

So you pulled it out of your ass.

John Ioannidis was one of the most published and influential scientists in the world. Then he began to critique the global response to Covid and the media and his profession largely turned against him.
Here is an article from a decade ago that should knock some of the hubris out of the Scientism Worshiping Vaccine Crusaders.
To reiterate the highlight of the quote:
*He charges that as much as 90 percent of the published medical information that doctors rely on is flawed*

“That question has been central to Ioannidis’s career. He’s what’s known as a meta-researcher, and he’s become one of the world’s foremost experts on the credibility of medical research. He and his team have shown, again and again, and in many different ways, that much of what biomedical researchers conclude in published studies—conclusions that doctors keep in mind when they prescribe antibiotics or blood-pressure medication, or when they advise us to consume more fiber or less meat, or when they recommend surgery for heart disease or back pain—is misleading, exaggerated, and often flat-out wrong. He charges that as much as 90 percent of the published medical information that doctors rely on is flawed.”
https://www.theatlantic.com/magazine/archive/2010/11/lies-damned-lies-and-medical-science/308269/

porkchopexpress says

. No thanks, I'll trust what nature gave me vs a science experiment.

EXACTLY!

What the fuck is wrong with these people trying to get every man, woman, and child to take a jab of an experimental biologic agent that at best will make our symptoms "not as bad" if we catch a cold that most "sufferers" don't even know they have " a case" until they take a test?

Personally I have a strong immune system and if I catch a virus there are multiple remedies.

If you want your shot take your shot. Just because you volunteered to be part of this vast experiment does not mean everyone has to go along with you.

ThreeBays says

Then what he did was get ahead of his research to claim COVID was overblown

The Wuhan was overblown. On March 13 2020 we were told that we...

I just realized I have much better things to do than argue with a troll.

Onvacation says

What the fuck is wrong with these people trying to get every man, woman, and child to take a jab of an experimental biologic agent that at best will make our symptoms "not as bad" if we catch a cold that most "sufferers" don't even know they have " a case" until they take a test?

Just a little over a hundred years ago they would have charged you a buck and bled you into a bucket with the same hubristic confidence. And called it science.

Onvacation says

If you want your shot take your shot. Just because you volunteered to be part of this vast experiment does not mean everyone has to go along with you.

If you are afraid of covid and believe that vaccine helps, take a shot. This will (allegedly) protect you from covid and you should not be in danger from unvaxxed masses. By the same logic, you should have no power to force anyone else than you to vaccinate - if vaccine works, it protects you and if someone wants to get covid and die, it is none of your damned business.

ThreeBays says

Vaccination is the route because we're able to conduct the science to estimate how protected people are with N doses, and it's scalable.

I prefer the natural route. Eat right, get exercise, and don’t introduce too many toxins to your system. Also don’t be morbidly obese. If you can’t manage these basics, Mother Nature will weed your ass out one way or another. Maybe you’ll miss Covid but die of a heart attack or the effects of diabetes or cancer or whatever. There are tens of thousands of diseases that will pick off the unhealthy. Covid is just one of those. Why all the concern?

ThreeBays says

People underestimating risk to themselves is also a fact

I don't know, I don't have too much trouble cyphering out what a 1 in 400 fatality rate means to me.
Among the minority of the population that contracts the virus.
And then accounting for my general good health and normal BMI.
I feel like I have a pretty good handle on it.

ThreeBays says

Did you know the hazard ratio for being male is greater than being obese class 2?

True. Being male is a hazard for Covid. Has something to do with the ACE2 receptors and testosterone. Having male pattern baldness increases that risk by another doubling. But it’s all just a risk. I have taken far greater risks for my entire life and nothing has punched my ticket yet. My job is also inherently risky, and driving on the freeway is also risky. Risk management is what is the issue. Are you choosing the proper path via risk management? Or is the risk mitigation you’re pursuing exposing you to greater risk than you’re trying to avoid?
I feel like the vaccine is marginally more risky (with long term effects completely unknown) than the risk of contracting Covid in my risk category. The long term effects being totally unknown is the deciding factor for me.

ThreeBays says

People underestimating risk to themselves is also a fact

It seems to me that humans must have evolved to be able to very accurately evaluate the risks to them. How could it be otherwise?
Maybe they discount risk somewhat, associated with testosterone no doubt, in order to go ahead and get some shit done.
When I look around me, not knowing one person that has had a bad, let alone fatal, time with this bug, I just don’t see much risk. I think our perception of hazard has been created solely by a media that has been shown to be biased 97% to negative Covid coverage.

How the Hell do the Scientism Worshiping Vaccine Crusaders just discount Pfizers criminal history?

Robert Sproul says

How the Hell do the Scientism Worshiping Vaccine Crusaders just discount Pfizers criminal history?

Mainstream media didn't tell them about this.