05-15-2020, 07:23 PM
T cells found in COVID-19 patients ‘bode well’ for long-term immunity: https://www.sciencemag.org/news/2020/05/...m-immunity
Would be great news.
Would be great news.
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T cells found in COVID-19 patients ‘bode well’ for long-term immunity
T cells found in COVID-19 patients ‘bode well’ for long-term immunity
T cells found in COVID-19 patients ‘bode well’ for long-term immunity: https://www.sciencemag.org/news/2020/05/...m-immunity
Would be great news.
Would be great news.
The Cell paper is a very interesting one. It shows that Covid19 triggers a normal cellular immune response. This is a good sign for the feasibility of a vaccine, and that there is likely some durable immunity in survivors.
Even more tantalizing to me were their findings that even people who had never been exposed to SARS-COV2 had helper T-cells which could recognize it (50% of their sample actually!). They theorize this could be related to prior non-covid19 coronavirus exposure. If so could explain some of the patients who have a mild or asymptomatic course. This is speculative at this stage but definitely an area for future study. Identifying serology negative people with helper T cells that can still recognize SARS-COV2, and then studying this cohort over time to see if they catch covid19 and what their clinical course is like would be very interesting.
Will need to read more closely and take a look at the other preprint paper which I hadn't seen before.
Even more tantalizing to me were their findings that even people who had never been exposed to SARS-COV2 had helper T-cells which could recognize it (50% of their sample actually!). They theorize this could be related to prior non-covid19 coronavirus exposure. If so could explain some of the patients who have a mild or asymptomatic course. This is speculative at this stage but definitely an area for future study. Identifying serology negative people with helper T cells that can still recognize SARS-COV2, and then studying this cohort over time to see if they catch covid19 and what their clinical course is like would be very interesting.
Will need to read more closely and take a look at the other preprint paper which I hadn't seen before.
The Cell paper is a very interesting one. It shows that Covid19 triggers a normal cellular immune response. This is a good sign for the feasibility of a vaccine, and that there is likely some durable immunity in survivors.
Even more tantalizing to me were their findings that even people who had never been exposed to SARS-COV2 had helper T-cells which could recognize it (50% of their sample actually!). They theorize this could be related to prior non-covid19 coronavirus exposure. If so could explain some of the patients who have a mild or asymptomatic course. This is speculative at this stage but definitely an area for future study. Identifying serology negative people with helper T cells that can still recognize SARS-COV2, and then studying this cohort over time to see if they catch covid19 and what their clinical course is like would be very interesting.
Will need to read more closely and take a look at the other preprint paper which I hadn't seen before.
Even more tantalizing to me were their findings that even people who had never been exposed to SARS-COV2 had helper T-cells which could recognize it (50% of their sample actually!). They theorize this could be related to prior non-covid19 coronavirus exposure. If so could explain some of the patients who have a mild or asymptomatic course. This is speculative at this stage but definitely an area for future study. Identifying serology negative people with helper T cells that can still recognize SARS-COV2, and then studying this cohort over time to see if they catch covid19 and what their clinical course is like would be very interesting.
Will need to read more closely and take a look at the other preprint paper which I hadn't seen before.
(05-16-2020, 09:34 AM)dabigv13 Wrote: The Cell paper is a very interesting one. It shows that Covid19 triggers a normal cellular immune response. This is a good sign for the feasibility of a vaccine, and that there is likely some durable immunity in survivors.
Even more tantalizing to me were their findings that even people who had never been exposed to SARS-COV2 had helper T-cells which could recognize it (50% of their sample actually!). They theorize this could be related to prior non-covid19 coronavirus exposure. If so could explain some of the patients who have a mild or asymptomatic course. This is speculative at this stage but definitely an area for future study. Identifying serology negative people with helper T cells that can still recognize SARS-COV2, and then studying this cohort over time to see if they catch covid19 and what their clinical course is like would be very interesting.
Will need to read more closely and take a look at the other preprint paper which I hadn't seen before.
So, a possible implication is that we should all get colds from coronaviruses besides sars-cov2 to reduce the severity of covid-19. I'd volunteer for that study. Hopefully someone is doing this.
The problem with the tracking study of people with possible immunity is that you'd need a truly enormous sample size to catch enough sars-cov2 infections to do any legit analysis. Regardless, it's an interesting idea.
(05-16-2020, 09:34 AM)dabigv13 Wrote: The Cell paper is a very interesting one. It shows that Covid19 triggers a normal cellular immune response. This is a good sign for the feasibility of a vaccine, and that there is likely some durable immunity in survivors.
Even more tantalizing to me were their findings that even people who had never been exposed to SARS-COV2 had helper T-cells which could recognize it (50% of their sample actually!). They theorize this could be related to prior non-covid19 coronavirus exposure. If so could explain some of the patients who have a mild or asymptomatic course. This is speculative at this stage but definitely an area for future study. Identifying serology negative people with helper T cells that can still recognize SARS-COV2, and then studying this cohort over time to see if they catch covid19 and what their clinical course is like would be very interesting.
Will need to read more closely and take a look at the other preprint paper which I hadn't seen before.
So, a possible implication is that we should all get colds from coronaviruses besides sars-cov2 to reduce the severity of covid-19. I'd volunteer for that study. Hopefully someone is doing this.
The problem with the tracking study of people with possible immunity is that you'd need a truly enormous sample size to catch enough sars-cov2 infections to do any legit analysis. Regardless, it's an interesting idea.
So, you need to take two big jumps from concrete data to get to that point. One big jump is assuming the people infected with the endemic coronaviruses will generate these CD4 cells that recognize SARS-COV2. What if it's due to a completely unrelated antigenic protein that is similar, or if it is from an endemic coronavirus, are all equally effective at inducing these cells or is it only some.
And then the second jump you need to make is whether the presence of these cells is at all clinically relevant. Perhaps humoral immunity (antibody mediated) is more important, and even a competent cellular immune response is not sufficiently protective.
Now that other preprint article goes some ways to answering the first question I posed. They showed 34% of serology negative patients had CD4 cells that could recognize SARS-COV2 peptides, but they recognized only portions of the spike protein that were most similar to the portions conserved in other endemic coronaviruses, as opposed to the CD4 cells of covid+ patients, which recognize several different areas of the SARS-COV2 spike protein.
These two papers do have me feeling good though. I think with some defensible assumptions, infection in the past few years with an endemic coronavirus may give some degree of immunity. Those folks may still be at risk of forward transmission. And probably there are patients in whom prior endemic coronavirus exposure does not confer any immunity, probably due to some intrinsic quality of their immune system. In the preprint paper they found 100% of tested samples had antibodies to endemic coronavirus, but not all of them had helper T cells that recognized the SARS-COV2 peptides. I couldn't find the supplemental figure for this though.
And yeah, a cohort study would need to be big and long term, unless you could do it in a hot spot area. I imagine there is some good cell culture and animal research that could fill in gaps and be done in a relatively quick timeframe as well.
And then the second jump you need to make is whether the presence of these cells is at all clinically relevant. Perhaps humoral immunity (antibody mediated) is more important, and even a competent cellular immune response is not sufficiently protective.
Now that other preprint article goes some ways to answering the first question I posed. They showed 34% of serology negative patients had CD4 cells that could recognize SARS-COV2 peptides, but they recognized only portions of the spike protein that were most similar to the portions conserved in other endemic coronaviruses, as opposed to the CD4 cells of covid+ patients, which recognize several different areas of the SARS-COV2 spike protein.
These two papers do have me feeling good though. I think with some defensible assumptions, infection in the past few years with an endemic coronavirus may give some degree of immunity. Those folks may still be at risk of forward transmission. And probably there are patients in whom prior endemic coronavirus exposure does not confer any immunity, probably due to some intrinsic quality of their immune system. In the preprint paper they found 100% of tested samples had antibodies to endemic coronavirus, but not all of them had helper T cells that recognized the SARS-COV2 peptides. I couldn't find the supplemental figure for this though.
And yeah, a cohort study would need to be big and long term, unless you could do it in a hot spot area. I imagine there is some good cell culture and animal research that could fill in gaps and be done in a relatively quick timeframe as well.
So, you need to take two big jumps from concrete data to get to that point. One big jump is assuming the people infected with the endemic coronaviruses will generate these CD4 cells that recognize SARS-COV2. What if it's due to a completely unrelated antigenic protein that is similar, or if it is from an endemic coronavirus, are all equally effective at inducing these cells or is it only some.
And then the second jump you need to make is whether the presence of these cells is at all clinically relevant. Perhaps humoral immunity (antibody mediated) is more important, and even a competent cellular immune response is not sufficiently protective.
Now that other preprint article goes some ways to answering the first question I posed. They showed 34% of serology negative patients had CD4 cells that could recognize SARS-COV2 peptides, but they recognized only portions of the spike protein that were most similar to the portions conserved in other endemic coronaviruses, as opposed to the CD4 cells of covid+ patients, which recognize several different areas of the SARS-COV2 spike protein.
These two papers do have me feeling good though. I think with some defensible assumptions, infection in the past few years with an endemic coronavirus may give some degree of immunity. Those folks may still be at risk of forward transmission. And probably there are patients in whom prior endemic coronavirus exposure does not confer any immunity, probably due to some intrinsic quality of their immune system. In the preprint paper they found 100% of tested samples had antibodies to endemic coronavirus, but not all of them had helper T cells that recognized the SARS-COV2 peptides. I couldn't find the supplemental figure for this though.
And yeah, a cohort study would need to be big and long term, unless you could do it in a hot spot area. I imagine there is some good cell culture and animal research that could fill in gaps and be done in a relatively quick timeframe as well.
And then the second jump you need to make is whether the presence of these cells is at all clinically relevant. Perhaps humoral immunity (antibody mediated) is more important, and even a competent cellular immune response is not sufficiently protective.
Now that other preprint article goes some ways to answering the first question I posed. They showed 34% of serology negative patients had CD4 cells that could recognize SARS-COV2 peptides, but they recognized only portions of the spike protein that were most similar to the portions conserved in other endemic coronaviruses, as opposed to the CD4 cells of covid+ patients, which recognize several different areas of the SARS-COV2 spike protein.
These two papers do have me feeling good though. I think with some defensible assumptions, infection in the past few years with an endemic coronavirus may give some degree of immunity. Those folks may still be at risk of forward transmission. And probably there are patients in whom prior endemic coronavirus exposure does not confer any immunity, probably due to some intrinsic quality of their immune system. In the preprint paper they found 100% of tested samples had antibodies to endemic coronavirus, but not all of them had helper T cells that recognized the SARS-COV2 peptides. I couldn't find the supplemental figure for this though.
And yeah, a cohort study would need to be big and long term, unless you could do it in a hot spot area. I imagine there is some good cell culture and animal research that could fill in gaps and be done in a relatively quick timeframe as well.
05-16-2020, 02:46 PM
It seems like you could do some sort of analysis to see if "parents of young children" have less severe disease than a matched cohort who aren't parents. Lord knows it feels like I've seen every cold virus known to man over the past 4 years. It wouldn't be iron-clad by any means, but it would be suggestive.
It seems like you could do some sort of analysis to see if "parents of young children" have less severe disease than a matched cohort who aren't parents. Lord knows it feels like I've seen every cold virus known to man over the past 4 years. It wouldn't be iron-clad by any means, but it would be suggestive.
05-16-2020, 06:24 PM
Another possibility is that previous exposure to other coronaviruses could increase the likelihood of a cytokine storm or a post-inflammatory state like the Kawasaki-like syndrome seen in children. No one knows yet.
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