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Discussion thread V - COVID-19 (new coronavirus)

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Population immunity is slowing down the pandemic in parts of the US
...
by Antonio Regaladoarchive page
August 11, 2020
...
“I believe the substantial epidemics in Arizona, Florida and Texas will leave enough immunity to assist in keeping COVID-19 controlled,” Trevor Bedford, a pandemic analyst at the University of Washington, said on Friday, in a series of tweets. “However, this level of immunity is not compatible with a full return to societal behavior as existed before the pandemic.”
...
What is known is that after rising at an alarming pace starting in May, new cases of covid-19 in Sun Belt states like Florida have started to fall. Some of that may be due to social distancing behavior, but rising rates of immunity are also a factor, according to Youyang Gu, a computer scientist whose Covid-19 Projections is among 34 pandemic models tracked by the US Centers for Disease Control and Prevention.

“Immunity may play a significant part in the regions that are declining,” says Gu. At least until the fall, which is how far his models look forward, he says, “I don’t think there is going to be another spike” of infections in southern states.
...

https://www.technologyreview.com/2020/08/11/1006366/immunity-slowing-down-coronavirus-parts-us/
 
Potential linkage between pathogenesis of COVID-19 and ADE[edit]


The pathophysiology of SARS and COVID-19 diseases may be associated with ADE. The authors of the study[SUP][15][/SUP] believe that ADE is a key step in the progression of disease from its mild to severe form. Onset of ADE, due to antigenic drift, can explain the observed sudden immune dysregulation, including apoptosis of immune cells, which promotes the development of T-cell lymphopenia and an inflammatory cascade with the lung accumulation of macrophages and neutrophils, as well as a cytokine storm. ADE goes along with reduction of Th1 cytokines IL2, TNF-α and IFN-γ and increase of Th2 cytokines IL-10, IL-6, PGE-2 and INF-α, as well as with inhibition of STAT pathway.[SUP][24][/SUP]

Perhaps ADE is the reason why the course of SARS and COVID-19 is more severe for older people compared to younger people. It is likely that in older people the production of antibodies is slower and by the time the antibodies are developed in the titer that is sufficient to neutralize the virus, the virus changes its antigenic determinants. In this case, immuno-dominant neutralizing antibodies might start forming unstable complexes with the new form of the virus and start to infect monocytes/macrophages causing ADE. This process can trigger generalized infection of immune cells in multiple organs and cytokine storm.[SUP][25][/SUP][SUP][26][/SUP]

It is interesting that in mice similar phenomenon of developing more severe disease in old compared to young animals exists. In contrast to old mice, in young mice, despite detectable viral replication оf SARS-CoV-1 in the lungs upon infection, clinical signs of the disease do not develop.[SUP][27][/SUP]

Also, an ongoing question in the COVID-19 pandemic is whether—and if so, to what extent—COVID-19 receives ADE from prior infection with other coronaviruses
https://en.wikipedia.org/wiki/Antibo...nt_enhancement
 
and then, does this immunity wane after ._3-5 months since we often see another wave after that time
 
Vaccine research being done on retired Seattle policewoman with MS and asthma.
I've followed this channel for awhile. This is a genuine person. I was surprised that they are already testing on vulnerable people. She also just had surgery with general anesthesia to remove a foot tumor. She can't talk about the research itself, so we don't know which vaccine is being tested, but she is allowed to describe side effects. None are mentioned but she was driving herself home after the first injection and hasn't posted since then. (And she might have gotten whatever they consider to be a placebo.


https://www.youtube.com/watch?v=OKHm5J07v3Y
 
Emily said:
Vaccine research being done on retired Seattle policewoman with MS and asthma.
I've followed this channel for awhile. This is a genuine person. I was surprised that they are already testing on vulnerable people. She also just had surgery with general anesthesia to remove a foot tumor. She can't talk about the research itself, so we don't know which vaccine is being tested, but she is allowed to describe side effects. None are mentioned but she was driving herself home after the first injection and hasn't posted since then. (And she might have gotten whatever they consider to be a placebo.


https://www.youtube.com/watch?v=OKHm5J07v3Y
Click to expand...

That's really odd - I have read a couple of posts - including these from Tetano - https://flutrackers.com/forum/forum/...ty-of-covid-19

https://flutrackers.com/forum/forum/...-with-covid-19 that tended to show that people with Asthma fared rather better than others.
 
I am also concerned about what happens when someone with Covid antibodies contracts a subsequent coronavirus infection. As far as I can tell there are no investigations in animals or otherwise in this regard. What is nagging at me is simply this - that coronaviruses in general have evolved NOT to generate a long term antibody response in their hosts. There will be a reason for this. As far as I can tell the only situation where this is not the case is in felines where an ADE type response gives rise to Feline Infectious Peritonitis. Therefore, I am greatly concerned that vaccines that are using RNA fragments only to generate antibody responses may not result in these limitations (secondary effects that limit long term antibody immunity), but then could (theoretically) generate an ADE type response, not only to Covid challenge, but to any coronavirus challenge. I wish I could find some evidence for ongoing research that covers additionally safety checks before widespread human testing roll out of candidate vaccines. I fear that at least one will produce some severe adverse events, and if this happens, public confidence in vaccines as a whole will be demolished. I sincerely hope that these concerns are unfounded and if anyone has any research to hand that suggests otherwise I would be very happy to hear it.
 
I think that based on observations and the uptick in cases in the Southern Hemisphere, that there is some degree of seasonality or enhanced transmission in conditions of higher humidity and lower UV intensity. As it is now fairly conclusive that there is at least some degree of airborne very small droplet spread, perhaps spread is more limited outside in conditions of higher UV intensity and/or lower levels of humidity... much like the common cold. If this premise is correct there will be an uptick when the N hemisphere enters our autumn and winter. What I am trying to say is that there is perhaps a 'sweet spot' for maximal transmission that produces a small degree of seasonality. The answer to this will become self evident in a few weeks, but would not surprise me if it happens. Re: the 20% herd immunity theory, the study that looked at seroprevalence in a slum in India showed 59% odd seroprevalence would tend to argue against this idea... however, it may apply to the numbers of people who can catch this virus severely. i.e T cell immunity may ameliorate disease severity, but not susceptibility to Covid 19.
 
Completely agree. Test before going to work daily = safe working, or going to school. It is sensitive enough for that. You could also use these tests before travelling at airports and (potentially) on arrival, to open up international travel. Life has to be a balance between health and the economy so that the cure is not worse than the disease itself, and we do most likely have to learn to live with this virus. We have to not let perfect become the enemy of 'good enough'. combined with mask wearing and hand hygiene such measures could go a long way to keep infection levels within acceptable bounds.
 
Covid Spread Can’t Only Be Explained by Who’s Being ‘Bad’

Seeing disease in moral terms seems to be the American way. But scientists still have a lot of questions.

By Faye Flam
August 13, 2020, 9:00 AM CDT
...
A few scientists are examining the possibility that previously hard-hit areas are now being affected by a buildup of immunity, even if it flies in the face of the widespread understanding that the disease has to run through at least 60% of the population to achieve so-called herd immunity. (So far, antibody tests show only some 10-20% of the U.S. population has had the disease.)

The term herd immunity is a little vague in this context. It was created to characterize the impact of immunization. It refers to the percentage of the population that must get immunized in order for a pathogen to die out — a quantity that depends on the nature of the virus, the efficacy of the vaccine and the behavior of the hosts. If natural immunity is starting to help in some places, that would suggest herd immunity is a reasonable and worthy goal of an immunization program.

But scientists have little experience applying herd immunity to a natural infection, and what understanding they have is changing. Scientists have started to investigate the possibility that there’s another critical factor here — heterogeneity in the way humans interact, and in our inherent, biological susceptibility to this disease.

...
https://www.bloomberg.com/opinion/a...s-forcing-scientists-to-rethink-herd-immunity
 
Links to the studies mentioned in this article:

Thread

Youyang Gu
@youyanggu

https://twitter.com/youyanggu/status/1292898685173534722
-----------------------------------
Estimating True Infections: A Simple Heuristic to Measure Implied Infection Fatality Rate

By: Youyang Gu
July 29, 2020 (Last Updated: August 10, 2020)

https://covid19-projections.com/estimating-true-infections/
-------------------------------------
A mathematical model reveals the influence of population heterogeneity on herd immunity to SARS-CoV-2

View ORCID ProfileTom Britton1,*Frank Ball2, Pieter Trapman1
See all authors and affiliations

Science 14 Aug 2020:
Vol. 369, Issue 6505, pp. 846-849
DOI: 10.1126/science.abc6810

https://science.sciencemag.org/content/369/6505/846
-------------------------------------------
Selective and cross-reactive SARS-CoV-2 T cell epitopes in unexposed humans

View ORCID ProfileJose Mateus1, View ORCID ProfileAlba Grifoni1, View ORCID ProfileAlison Tarke1, View ORCID ProfileJohn Sidney1, View ORCID ProfileSydney I. Ramirez1,3, View ORCID ProfileJennifer M. Dan1,3, View ORCID ProfileZoe C. Burger3, View ORCID ProfileStephen A. Rawlings3, View ORCID ProfileDavey M. Smith3, View ORCID ProfileElizabeth Phillips2, View ORCID ProfileSimon Mallal2, View ORCID ProfileMarshall Lammers1, View ORCID ProfilePaul Rubiro1, View ORCID ProfileLorenzo Quiambao1, View ORCID ProfileAaron Sutherland1, View ORCID ProfileEsther Dawen Yu1, View ORCID ProfileRicardo da Silva Antunes1, View ORCID ProfileJason Greenbaum1, April Frazier1, View ORCID ProfileAlena J. Markmann4, View ORCID ProfileLakshmanane Premkumar5, View ORCID ProfileAravinda de Silva5, View ORCID ProfileBjoern Peters1,3, View ORCID ProfileShane Crotty1,3, View ORCID ProfileAlessandro Sette1,3,*,†, View ORCID ProfileDaniela Weiskopf1,*,†
See all authors and affiliations

Science 04 Aug 2020:
eabd3871
DOI: 10.1126/science.abd3871

https://science.sciencemag.org/content/early/2020/08/04/science.abd3871

----------------------------------------------
Individual variation in susceptibility or exposure to SARS-CoV-2 lowers the herd immunity threshold

View ORCID ProfileM. Gabriela M. Gomes, Rodrigo M. Corder, Jessica G. King, Kate E. Langwig, Caetano Souto-Maior, Jorge Carneiro, Guilherme Goncalves, Carlos Penha-Goncalves, Marcelo U. Ferreira, Ricardo Aguas
doi: https://doi.org/10.1101/2020.04.27.20081893

This article is a preprint and has not been peer-reviewed [what does this mean?]. It reports new medical research that has yet to be evaluated and so should not be used to guide clinical practice.

https://www.medrxiv.org/content/10.1101/2020.04.27.20081893v3
 
Herd immunity is 1-1/R0 so if R0=2 it = 1/2 or 50%. It is the point when enough host are removed from the susceptible population to drive the Rt below 1 causing any outbreak to die out. How these host are removed from the susceptible population, prior infection or vaccine derived sterilizing immunity is irrelevant.
For each host who becomes immune the Rt is reduced slightly so the pathogen's spread is slowed in much the same way as physical distancing measures.
 
"Seeing disease in moral terms seems to be the American way."
Maybe in this case politics is more in play than morals.
 
Herd immunity thresholds for SARS-CoV-2 estimated from unfolding epidemics

Ricardo Aguas, Rodrigo M. Corder, Jessica G. King, Guilherme Goncalves, Marcelo U. Ferreira, M. Gabriela M. Gomes
doi: https://doi.org/10.1101/2020.07.23.20160762

This article is a preprint and has not been peer-reviewed [what does this mean?]. It reports new medical research that has yet to be evaluated and so should not be used to guide clinical practice.
Abstract


As severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spreads, the susceptible subpopulation declines causing the rate at which new infections occur to slow down. Variation in individual susceptibility or exposure to infection exacerbates this effect. Individuals that are more susceptible or more exposed tend to be infected and removed from the susceptible subpopulation earlier. This selective depletion of susceptibles intensifies the deceleration in incidence. Eventually, susceptible numbers become low enough to prevent epidemic growth or, in other words, the herd immunity threshold is reached. Here we fit epidemiological models with inbuilt distributions of susceptibility or exposure to SARS-CoV-2 outbreaks to estimate basic reproduction numbers (R_0) alongside coefficients of individual variation (CV) and the effects of containment strategies. Herd immunity thresholds are then calculated as 1-(1⁄R_0 )^(1⁄((1+〖CV〗^2 ) )) or 1-(1⁄R_0 )^(1⁄((1+〖2CV〗^2 ) )), depending on whether variation is on susceptibility or exposure. Our inferences result in herd immunity thresholds around 10-20%, considerably lower than the minimum coverage needed to interrupt transmission by random vaccination, which for R_0 higher than 2.5 is estimated above 60%. We emphasize that the classical formula, 1-1⁄R_0 , remains applicable to describe herd immunity thresholds for random vaccination, but not for immunity induced by infection which is naturally selective. These findings have profound consequences for the governance of the current pandemic given that some populations may be close to achieving herd immunity despite being under more or less strict social distancing measures.

...

https://www.medrxiv.org/content/10.1....23.20160762v1
 
not all hosts are equally likely to spread it. Some habits,groups, professions are superspreading.
Get them immunity.
 
in Germany we have only 1% infected, still it went down everywhere as in a normal
epidemic curve. In many countries of Eastern Europe they probably had even less in wave 1.
otoh in Bergamo >50% were infected despite strict measures, 20% in NYC.
That was >4 months ago, now we have wave2, but science rarely discusses
-let alone understands- this
 
HEALTH NEWSAUGUST 17, 2020 / 9:47 PM / UPDATED 11 HOURS AGO

More infectious coronavirus mutation may be 'a good thing', says disease expert

SINGAPORE (Reuters) -
...
Paul Tambyah, senior consultant at the National University of Singapore and president-elect of the International Society of Infectious Diseases, said evidence suggests the proliferation of the D614G mutation in some parts of the world has coincided with a drop in death rates, suggesting it is less lethal.

“Maybe that’s a good thing to have a virus that is more infectious but less deadly,” Tambyah told Reuters.

Tambyah said most viruses tend to become less virulent as they mutate.

“It is in the virus’ interest to infect more people but not to kill them because a virus depends on the host for food and for shelter,” he said.
...
https://www.reuters.com/article/us-...-good-thing-says-disease-expert-idUSKCN25E08Y
 
I do not believe S D614G is of any great importance.
There are much more plausible explanations.
We have a much better idea now, having learnt from our mistakes, how, when, and in what dosage to use the treatments we have. The same NY hospitals are now getting much better survival rates compared to when they first started getting COVID patients - with the same strain.
The hospitalised patients are also changing as care homes have figured out how to keep SARS out and the average age has dropped 20 years.
There are many factors at play host adaption being the least amongst them.
 
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