Neverending Covid-19 Coronavirus

debianlinux said:
While in Boston I used the YMCA on Huntington. It's an amazing old building but it's terrible as a gym for all the reasons you just listed. I can imagine how many buildings are in exactly the same state.
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It's not just the beautiful old buildings. It's new schools as well.

The high school I went too was brand new. Built in 1999.

Air Conditioning is not considered essential for schools here. 3 seasons out of the year you don't need it, and schools are not open in the summer. Around here, if we happen to get a heat wave while schools are open, school is canceled like a snow day. It happens, but school is still more likely to be canceled because of snow than heat.

When they designed my high school, they did layout one option that had HVAC and good air circulation. It was not chosen because the added expense was considered prohibitory. The town did not have the money, and the amount of money the state approved to aid the project was not enough.

Schools are generally built with the bare minimum of heating system they can get away with. As that's all that they have in their budgets.

School systems don't have the money to update older buildings. And the cost of building a new building are so high and the amount of funding they have available is less that what it used to be. State aid has been way down since the "Big Dig". Cuts to the education budget are in place for 50 years to help payoff the big dig project. Towns have been attacking property taxes and lowering them instead of increasing them.

Even if they had the budget, I would not expect most to include it. For example, university and college dorms do not have AC around here. If new construction of a dorm includes it it's an exception to the rule.
 
Turbo said:
It's not incorrect to refer to them as different strains. Technically any genetic variant can be considered to be a different "strain" - but you have to be careful because it doesn't necessarily mean that the new "strain" is functionally different from the original one. It's a bit of a wishy washy term. With influenza, when you talk about different strains, you usually mean there were significant antigenic changes to the surface proteins (which means different antibodies/vaccines may be needed to combat it).

In this case, I wanted to be sure that it was understood that the 2nd "strain" didn't infect because antibodies from the 1st infection didn't work - scientists seem to think that coronavirus neutralising antibodies don't stay around for very long, and that seems to be the case for SARS-CoV-2 as well (the length of time probably varies between individuals and depending on how severe the 1st infection is).

Basically, the 2nd infection for this case is not because of genetic changes that circumvented antibodies from the 1st infection but because there were no neutralising antibodies remaining from the first infection. The immune system did do something though because the second infection was asymptomatic. It will be interesting to find out what happened.
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What about T-cell memory. I'm trying to wrap my head around this one because I've read that the T-cells remember covid19 and can create antibodies for it.

These donors exhibited robust memory T cell responses months after infection, even in the absence of detectable circulating antibodies specific for SARS-CoV-2, indicating a previously unanticipated degree of population-level immunity against COVID-19. We found that T cell activation, characterized by the expression of CD38, was a hallmark of acute COVID-19. Similar findings have been reported previously in the absence of specificity data (Huang et al., 2020; Thevarajan et al., 2020; Wilk et al., 2020). Many of these T cells also expressed HLA-DR, Ki-67, and PD-1, indicating a combined activation/cycling phenotype correlates with an early strong immune response, including an early SARS-CoV-2-specific IgG response, and to a lesser extent with plasma levels of various inflammatory markers. Our data also showed that many activated/cycling T cells in the acute phase were functionally replete and specific for SARS-CoV-2. Equivalent functional profiles have been observed early after immunization with successful vaccines (Blom et al., 2013; Miller et al., 2008; Precopio et al., 2007). Accordingly, the expression of multiple inhibitory receptors, including PD-1, likely indicates early activation rather than exhaustion (Zheng et al., 2020a; Zheng et al., 2020b).

www.sciencedirect.com

Robust T Cell Immunity in Convalescent Individuals with Asymptomatic or Mild COVID-19

SARS-CoV-2-specific memory T cells will likely prove critical for long-term immune protection against COVID-19. Here, we systematically mapped the fun…
www.sciencedirect.com www.sciencedirect.com

I'm really interested in how this works because I'm not 100% on it. Why would T-cells not work on genetically different strain that wasn't significant enough of a difference to change the antibodies? Is it because they didn't get the disease severely enough in the first round? But that wouldn't matter if it produced the same antibodies, right? This is the piece I'm having trouble with right now.
 
nolalady said:
What about T-cell memory. I'm trying to wrap my head around this one because I've read that the T-cells remember covid19 and can create antibodies for it.

These donors exhibited robust memory T cell responses months after infection, even in the absence of detectable circulating antibodies specific for SARS-CoV-2, indicating a previously unanticipated degree of population-level immunity against COVID-19. We found that T cell activation, characterized by the expression of CD38, was a hallmark of acute COVID-19. Similar findings have been reported previously in the absence of specificity data (Huang et al., 2020; Thevarajan et al., 2020; Wilk et al., 2020). Many of these T cells also expressed HLA-DR, Ki-67, and PD-1, indicating a combined activation/cycling phenotype correlates with an early strong immune response, including an early SARS-CoV-2-specific IgG response, and to a lesser extent with plasma levels of various inflammatory markers. Our data also showed that many activated/cycling T cells in the acute phase were functionally replete and specific for SARS-CoV-2. Equivalent functional profiles have been observed early after immunization with successful vaccines (Blom et al., 2013; Miller et al., 2008; Precopio et al., 2007). Accordingly, the expression of multiple inhibitory receptors, including PD-1, likely indicates early activation rather than exhaustion (Zheng et al., 2020a; Zheng et al., 2020b).

www.sciencedirect.com

Robust T Cell Immunity in Convalescent Individuals with Asymptomatic or Mild COVID-19

SARS-CoV-2-specific memory T cells will likely prove critical for long-term immune protection against COVID-19. Here, we systematically mapped the fun…
www.sciencedirect.com www.sciencedirect.com

I'm really interested in how this works because I'm not 100% on it. Why would T-cells not work on genetically different strain that wasn't significant enough of a difference to change the antibodies? Is it because they didn't get the disease severely enough in the first round? But that wouldn't matter if it produced the same antibodies, right? This is the piece I'm having trouble with right now.
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Antibodies and T-cells are 2 different strategies used by the immune system.

Antibodies are made by B cells following infection once the body recognizes a foreign pathogen. It takes a little while to make them but those antibodies (and B cells) can stick around for a while to quickly prevent re-infection. Neutralizing antibodies act quickly if present. How long they stick around varies from disease to disease and I'm not sure we know exactly why. It does seem that when you get severe disease with COVID, they stick around longer (but we're too early in this to know how long exactly).

T-cells are also made once the body recognises a foreign pathogen. As far as I understand, they act slower so there might still be infection but I guess with COVID that reinfection may be milder.

WRT to your genetic question, the spike and envelope proteins were probably not genetically different in their epitopes - the part recognized by the antibodies and T cells. So both antibodies from the 1st infection and the T cells could have recognized it. But researchers are saying that the neutralising antibodies (and I suppose the specific B cells) didn't stick around after the first COVID, so the idea is that the 2nd infection was dealt with using non-antibody based immunity - so probably T cells that stuck around (the T cell memory you referred to).

1598450486047.png

As an aside, one example where neutralizing antibodies are crucial is with tetanus and the vaccine against it. Tetanus bacteria releases a toxin immediately after infection - so fast that the body actually has zero time to make antibodies and T cells and mount an immune defense. Vaccination allows the body to make neutralizing antibodies in advance, so if you get infected, your body has an immune defense ready to go. It's one of these cases where you can't count on a prior infection because the disease is fast acting and severe. The antibodies last about 10 years with tetanus vaccination so everyone should renew that periodically.
 
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Turbo said:
Antibodies and T-cells are 2 different strategies used by the immune system.

Antibodies are made by B cells following infection once the body recognizes a foreign pathogen. It takes a little while to make them but those antibodies (and B cells) can stick around for a while to quickly prevent re-infection. Neutralizing antibodies act quickly if present. How long they stick around varies from disease to disease and I'm not sure we know exactly why. It does seem that when you get severe disease with COVID, they stick around longer (but we're too early in this to know how long exactly).

T-cells are also made once the body recognises a foreign pathogen. As far as I understand, they act slower so there might still be infection but I guess with COVID that reinfection may be milder.

WRT to your genetic question, the spike and envelope proteins were probably not genetically different in their epitopes - the part recognized by the antibodies and T cells. So both antibodies from the 1st infection and the T cells could have recognized it. But researchers are saying that the neutralising antibodies (and I suppose the specific B cells) didn't stick around after the first COVID, so the idea is that the 2nd infection was dealt with using non-antibody based immunity - so probably T cells that stuck around (the T cell memory you referred to).

View attachment 63100

As an aside, one example where neutralizing antibodies are crucial is with tetanus and the vaccine against it. Tetanus bacteria releases a toxin immediately after infection - so fast that the body actually has zero time to make antibodies and T cells and mount an immune defense. Vaccination allows the body to make neutralizing antibodies in advance, so if you get infected, your body has an immune defense ready to go. It's one of these cases where you can't count on a prior infection because the disease is fast acting and severe. The antibodies last about 10 years with tetanus vaccination so everyone should renew that periodically.
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Okay, so B-cells are in charge of making antibodies and T-cells are what trigger B-cells to make antibodies and they also mount the attack on foreign invaders. And in this case, we saw that B-cells and antibodies didn't stick around for long--which, from what I understand, is one of those coronavirus traits--this means that T-cells were likely mounting a defense but it took a while to generate everything even with the T-cell memory.

This seems like some good-ish news. It looks like our problem with a vaccine is that we don't really have anything that insights mucosal IgA antibody production which is the antibody that is produced on mucus membranes--apical surfaces of epithelial cells. So we are really looking for this since it has the ability to prevent the disease:

Infection with poliovirus causes IgM and IgG responses in the blood, but mucosal IgA is vital for blocking infection.

The vast majority of influenza vaccines are administered by injection and stimulate the production of IgG antibodies; they are poor inducers of mucosal IgA antibodies. The efficacy of influenza vaccines would likely be markedly improved if they could be designed to stimulate mucosal immunity.

Virus neutralization by antibodies

The antibody response is crucial for preventing many viral infections and may also contribute to resolution of infection. When a vertebrate is infected with a virus, antibodies are produced against many epitopes on multiple virus proteins. A subset of these antibodies can block virus infection...
www.virology.ws www.virology.ws

Okay, so there is evidence that the body's T-cells remember the virus but it doesn't have time to mount a defense prior to getting infected. A vaccine would (hopefully) spark the production of mucosal IgA antibodies which would actually prevent disease. Neat. I learned something today.
 
nolalady said:
Okay, so B-cells are in charge of making antibodies and T-cells are what trigger B-cells to make antibodies and they also mount the attack on foreign invaders. And in this case, we saw that B-cells and antibodies didn't stick around for long--which, from what I understand, is one of those coronavirus traits--this means that T-cells were likely mounting a defense but it took a while to generate everything even with the T-cell memory.

This seems like some good-ish news. It looks like our problem with a vaccine is that we don't really have anything that insights mucosal IgA antibody production which is the antibody that is produced on mucus membranes--apical surfaces of epithelial cells. So we are really looking for this since it has the ability to prevent the disease:

Infection with poliovirus causes IgM and IgG responses in the blood, but mucosal IgA is vital for blocking infection.

The vast majority of influenza vaccines are administered by injection and stimulate the production of IgG antibodies; they are poor inducers of mucosal IgA antibodies. The efficacy of influenza vaccines would likely be markedly improved if they could be designed to stimulate mucosal immunity.

Virus neutralization by antibodies

The antibody response is crucial for preventing many viral infections and may also contribute to resolution of infection. When a vertebrate is infected with a virus, antibodies are produced against many epitopes on multiple virus proteins. A subset of these antibodies can block virus infection...
www.virology.ws www.virology.ws

Okay, so there is evidence that the body's T-cells remember the virus but it doesn't have time to mount a defense prior to getting infected. A vaccine would (hopefully) spark the production of mucosal IgA antibodies which would actually prevent disease. Neat. I learned something today.
Click to expand...

You got it - just to add complexity - there are different types of T cells: helper T cells and cytotoxic (or killer) T cells. Those that help trigger the B cells to produce antibodies are the helper T cells, those that recognize infected cells and kill them are cytotoxic T cells (the helper T cells also activate the cytotoxic T cells). If you notice from the diagram I posted, antibodies neutralize the pathogen before it gets a chance to infect while the role of the cytotoxic T cells is to kill infected cells.
 
www.cnn.com

Don't argue with anti-maskers, CDC warns stores

When in doubt, don't argue with anti-maskers.
www.cnn.com www.cnn.com

The CDC's guidance is now for stores to not argue, prevent entry or kick out Anti Maskers for their own safety. They are trying to protect employees from violence in the workplace. They are telling service workers and stores for their own safety don't engage a anti-masker to enforce their mask policies.
 
RenegadeMonster said:
www.cnn.com

Don't argue with anti-maskers, CDC warns stores

When in doubt, don't argue with anti-maskers.
www.cnn.com www.cnn.com

The CDC's guidance is now for stores to not argue, prevent entry or kick out Anti Maskers for their own safety. They are trying to protect employees from violence in the workplace. They are telling service workers and stores for their own safety don't engage a anti-masker to enforce their mask policies.
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Haha, it’s literal disease control. The disease of fucking insanity can get you maimed or killed. It’s like they’re zombies.
 
So people who still have SARS-CoV-2 neutralising antibodies from a prior infection do appear to be completely immune. So this is good news if we can get a vaccine that produces antibodies for a reasonable period of time.

jcm.asm.org

Neutralizing Antibodies Correlate with Protection from SARS-CoV-2 in Humans during a Fishery Vessel Outbreak with a High Attack Rate

The development of vaccines against SARS-CoV-2 would be greatly facilitated by the identification of immunological correlates of protection in humans. However, to date, studies on protective immunity have been performed only in animal models and correlates of protection have not been established...
jcm.asm.org jcm.asm.org
 
debianlinux said:
Something bad happened, medical attention was needed, a gofundme came into play to assist. Tell me again why MFA is the boogie man?
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Besides the racist argument that peoples tax dollars will be going to providing medicare for minorities on welfare (my father's objection against MFA), the largest issue is MFA is a big unknown. How will peoples coverage be impacted. How much will it cost? Will their taxes go up?

People have successfully been sold fear that universal healthcare means long waits and subpar medical care. People who have good insurance fear they will get worse coverage with MFA. What the cover MFA provides is unknown, because the GOP will try to Erode as much as they can form it, and if it is not done correct it will be broken, cost a lot more and not solve the expenses a single payer system set out to solve. And lastly, taxes will go. People don't see the savings they would get if they didn't have their healthcare premiums deducted out of their paychecks. They only see how much their taxes will go up. Plus, you have the people who want the option to not have healthcare if they are young and healthy because it simply costs too much, and their willing to take the risk of not having healthcare to be able to get by on low wages.
 
RenegadeMonster said:
Besides the racist argument that peoples tax dollars will be going to providing medicare for minorities on welfare (my father's objection against MFA), the largest issue is MFA is a big unknown. How will peoples coverage be impacted. How much will it cost? Will their taxes go up?

People have successfully been sold fear that universal healthcare means long waits and subpar medical care. People who have good insurance fear they will get worse coverage with MFA. What the cover MFA provides is unknown, because the GOP will try to Erode as much as they can form it, and if it is not done correct it will be broken, cost a lot more and not solve the expenses a single payer system set out to solve. And lastly, taxes will go. People don't see the savings they would get if they didn't have their healthcare premiums deducted out of their paychecks. They only see how much their taxes will go up. Plus, you have the people who want the option to not have healthcare if they are young and healthy because it simply costs too much, and their willing to take the risk of not having healthcare to be able to get by on low wages.
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Sometimes the question is rhetorical.
 
www.lgnewsroom.com

LG REVOLUTIONIZES PERSONAL CLEAN AIR WITH PURICARE™ WEARABLE AIR PURIFIER | LG NEWSROOM

LG Unveils the Future of Healthy Respiration at IFA Berlin SEOUL, Aug. 27, 2020 — LG Electronics (LG) will give new meaning to clean, personal air with the introduction PuriCare™ Wearable Air Purifier
www.lgnewsroom.com www.lgnewsroom.com

www.cnn.com

LG has designed a wearable air purifier for your face

That cloth face mask covering your face could soon be a thing of the past. LG has unveiled a wearable air purifier mask that could soon replace your face covering.
www.cnn.com www.cnn.com
 
RenegadeMonster said:
www.lgnewsroom.com

LG REVOLUTIONIZES PERSONAL CLEAN AIR WITH PURICARE™ WEARABLE AIR PURIFIER | LG NEWSROOM

LG Unveils the Future of Healthy Respiration at IFA Berlin SEOUL, Aug. 27, 2020 — LG Electronics (LG) will give new meaning to clean, personal air with the introduction PuriCare™ Wearable Air Purifier
www.lgnewsroom.com www.lgnewsroom.com

www.cnn.com

LG has designed a wearable air purifier for your face

That cloth face mask covering your face could soon be a thing of the past. LG has unveiled a wearable air purifier mask that could soon replace your face covering.
www.cnn.com www.cnn.com
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I feel like this should be made available in Darth Vader design.
 
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RenegadeMonster said:
Central Valley Foster Farms plant shut down amid uncontrolled COVID-19 outbreak, 8 deaths


What is really interesting about this case is this plant is in California. Has ignored the social distancing and other guidance of of health officials to prevent an outbreak and once the outbreak occurred, health officials had to force them to close.
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Wow - this is a complete contrast from the results at plants where proper precautions were taken:

More recently, an Oregon seafood processing plant where workers were required to wear face masks reported an outbreak of 124 cases, 95 percent of which were asymptomatic. Similarly, in a Tyson chicken processing plant outbreak in Arkansas where workers were provided mandatory masks, 455 out of 481, or nearly 95 percent were asymptomatic.
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www.ucsf.edu

One More Reason to Wear a Mask: You’ll Get Less Sick From COVID-19

It’s likely that face masks, by blocking even some of the coronavirus-carrying droplets you inhale, can reduce your risk of falling seriously ill from COVID-19, according to Monica Gandhi, an infectious disease specialist at UCSF.
www.ucsf.edu www.ucsf.edu
 
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