While obviously decreases in severe disease and mortality is significant and a great accomplishment it is still frustrating to have those be the metrics everyone always discusses. Long haul covid19 and damage to multiple systems is a serious issue as well (and in the long run will majorly impact our health care systems). It seems even the mild and asymptomatic cases among vaccinated can result in long covid. I am really worried about this for myself and my unvaccinated kids.
Same! Long COVID (plus unknown long-term damage that may come back to bite us years from now) has been my biggest fear for myself since we first started hearing about it. It makes me so mad that it almost never gets mentioned in mainstream coverage! In case you're a new subscriber (or anyone else reading this thread is), Dr. Jetelina did an update on long COVID in breakthrough cases a couple weeks ago: https://yourlocalepidemiologist.substack.com/p/long-covid-among-breakthrough-cases I really appreciate that even if Dr. Jetelina doesn't bring it up in every post, she does give it regular attention, which again is more than mainstream news.
💯 agree! Long Covid is being mostly ignored. We need this information and it needs to be talked about as much as severity of disease. I don’t know if it’s rare or just rarely discussed. I have illnesses that mimic long haul & am disabled.
Yes! As a sufferer of chronic Lyme (many of the same symptoms), I don’t wish chronic disease on anyone. People think death is the worst outcome, but being physically and/or mentally debilitated should not be an acceptable outcome. I’m finally feeling a little better from Lyme and would be devastated to get another set of chronic issues. My life was turned upside down for several years during a peak time of my life. I missed out on so many things and will never get that time back. Now, I’m terrified of what the long term issues could be if my young son were to get it, even if he seemingly recovers. Things like this stay in your system and pop out at random times, even many years later in life.
Should we be concerned that unvaccinated individuals are infectious for 16 days? That is much longer than the recommended 10 day quarantine. Thank you for all you do!!!
Thank you. Can you help me understand this statement: “Vaccinated seem to not be infectious after 9 days (Ct=30) compared to unvaccinated at 16 days.” ? Are you aware of any reference that explains how the CDC quarantine and isolation lengths were/are determined? I’m also curious how/why the CDC determined asymptomatic vaccinated exposed people should be tested 3-5 days after exposure. Thank you for any insight or references.
I do know that with the pre-delta version of the virus, there were a number of studies done where they tried to infect cells with virus extracted from human samples at various timepoints after infection. And those studies showed that people can shed virus fragments for a long time after the virus has cleared, but the virus fragments aren't able to replicate. So the CDC and many other agencies switched guidance from a PCR-based test to a time-based criteria for release from isolation after infection. I think they picked 10 days. Others have done work and determined that very high cycle counts in PCR means that the viral load is so low regardless, it's hard to transmit at Ct values above 30. Low Ct values mean there was a lot of virus present, high Ct values mean there is little present. Every 3 Ct units is a factor of 10 less in viral concentration, give or take. If I got any of that wrong, someone can chime in.
Here's a reference to the CDC guidance on isolation. They state with references that replication-competent virus hasn't been isolated after 10 days except in rare circumstances like severe disease or immunocompromised. https://www.cdc.gov/coronavirus/2019-ncov/hcp/duration-isolation.html
Oh yeah, on the 3-5 day wait after exposure, I believe the logic was to prevent false negatives they want the person to wait long enough to develop enough virus in the system to detect with the RT-PCR. Sampling too soon could yield a negative just because there wasn't enough virus present.
Thank you. Has it been documented that the incubation period of Delta is shorter than the “original strain?” Unvaccinated, exposed, asymptomatic people are supposed to wait until day 5 to test and return after day 7 if the test is negative.
I watched a talk from Micheal Osterholm that said the incubation period wasn't shorter, but there were more offspring. I wonder if they'll decide to decrease the wait until test with delta, since the viral load seems to be much higher? Good question.
I contracted COVID in November 2020 and was vaccinated in December/January with Pfizer. Is there data out regarding infection rates with Delta amongst those who have had natural infection plus are fully vaccinated? I am being told colleagues are seeing it, but I have not read anything concrete addressing it.
To piggyback off this comment, do you know what the current data is regarding infection only protection?
I read somewhere recently (over a week ago) that vaccine + infection = best protection, vaccine = good protection, and infection only = ok protection. I won't bother with the alleged percentages because the data is constantly changing.
Doesn't the fact that breakthroughs appear to be starting off with higher viral loads suggest some sort of detection bias? Is there something special about the kinds of people having the breakthrough cases that would cause them to have higher viral loads?
Overall, the people who suffered breakthrough infections did have more comorbidities but that's not true for all of them. Most likely, the combination of a tighter bond to the ACE2 receptor by the receptor binding domain AND the fact that more viable viral replicates are produced with each intracellular replication process are the reason we're seeing more breakthrough infections than we expected.
Thank you. 4 of my family members have had breakthrough cases here in Mississippi and many of my friends and family are vaccine hesitant or resistant. I came across an article from the UK that I found helpful even with its limitations. One finding I find particularly interesting is that vaccine resistant participants relied significantly more on social media than any other information source while vaccine accepting participants consumed significantly more information from newspapers, television, radio, doctors, other health professionals, and government agencies.
Resistance has been so strong on social media, but this encourages me to continue sharing reputable information on these platforms. Just wanted to share to encourage others as well.
Are false negative rapid tests less of a problem for Delta than for the original strain because of the increased viral load? It seems reasonable to suspect this would be the case.
Two things: Your surmise is correct in that Delta being so speedy means antigen will trip faster, but also, accuracy is a kind of weird conversation, because antigen is really answering "is this person a problem for everybody else" rather than "what is wrong with this person" and the numbers are extremely good for them first question.
If vaccine-resistant strains start spreading, can the vaccines quickly be tweaked to cover the new variants and go straight into arms? Or do Pfizer, Moderna etc need to go through another round of trials before offering the public a shot that protects against new variants?
Great post. I had a question about how the viral load measured really connects to the ability for the vaccinated to infect. Since Rt PCR only measures viral fragments, how do we know it equates to ability to infect? Last year it was shown that people can shed viral RNA for months after they are no longer infectious. Also, the Singapore data is for breakthrough cases, but does the same relationship exist for subclinical and asymptomatic cases? I assume breakthroughs happen because the immune response post-vaccination is sub-optimal to begin with. The reason I ask is that many of us, and the media and scientific sources have been saying that the unvaccinated not only carry the burden of disease but are also responsible for spread. If both groups spread similarly, even in asymptomatic and subclinical cases like they do with breakthroughs, maybe we need to lay off the focus on vaccinations protecting others argument. And what does that mean for herd immunity in general long-term?
You have a number of questions. I'll see what I can do.
1) rt-PCR shouldn't be used for perhaps 90 days after symptoms clear because remnant fragments do persist. Antigen testing, however, performed serially, will provide some better information on ongoing infection as it's less focused on the subfragments identified by PCR. In addition, for breakthrough diagnosis, a diagnosis of exclusion can be employed if influenza testing is negative, but the spectrum of ILI symptoms is present.
1a) In patients who were PCR-positive for COVID-19, one may assume intact infection-conferred immunity, and thus something approaching sterilizing immunity during the 90 day interval. These people are unlikely to transmit replicatable virus.
2) There has been hypothesized a correlation between intensity of symptoms and disease severity and immune response but this is not always valid. anecdotally, my immune response, with very mild symptoms, was much more robust than my wife's who experienced moderate disease symptoms, but is immune-compromised. In other words, it's not uniform across the population.
3) Breakthrough cases happen when someone is overwhelmed with infective, reproductive viral particles that can attach to the receptors on viable cells, infect the cells and reproduce. In the case of delta, the number of particles produced with each reproductive cycle is higher than with earlier variants, and the modifications to the S1 protein, spike conformation and receptor binding domain region make it a better competitor for cellular access than existing antibodies are for competition to prevent disease. In some cases, prior to delta, peoples' various immune responses may not be available in sufficient numbers to overwhelm the attacker, which is why we're now talking boosters. The cellular immune system can take some period of time to ramp back up to circulating antibodies once it's turned on to the presence of a known agent. This interval may make someone susceptible. I'm aware of at least one person who was infected with 3 different strains of SARS-CoV-2 as determined by a university lab's genotyping efforts.
It's currently thought that most vaccinated persons, and virtually all who were previously infected and subsequently vaccinated, will have a muted reproductive response, and are less, or unlikely to spread actively. This includes especially the asymptomatic persons who were previously vaccinated.
I can give a real life example and then I have a question. Colleague of mine , 28 yo male, got delta at a party 2 weeks ago. 10 vaccinated people there and all indoors. J&J person ended up having symptoms. 4 people total infected. Colleague was most symptomatic and it took 4 days from exposure to show up. Loss of taste, smell, cough and shortness of breath. Symptomatic for 3 days and on the mend on day 4 short of taste and smell. My question is now on mandates. Sounds like tons of companies have them with a target of October 1. How much can we disrupt this wave? Challenge to the mandate is demographic it is targeting and also if you don't get it, you are just subject to mandatory testing , so it doesn't solve the vaccine issue.
Are these studies showing viral load just using Ct values of PCR tests. Wouldn’t it be better to be using PCR test with antigen testing? Ct values of PCR just tell us that “pieces” of virus are present, that doesn’t necessarily mean it’s infectious virus that is being found… specifically in the vaccinated.
Read this study and their methodology (cited above), this is how they tested for infectiousness, and they didn't just test for presence, they also took into account the threshold. This makes more sense to me than rapid antigen pairing.
I understand how they are using Ct threshold to estimate viral load and infectiousness. We do the same where I work. But, I have seen patients that test PCR positive months out from their initial infection. I’m just wondering if there is a better way than just assuming lower Ct values (more genetic material) means higher infectious viral load. Especially in the vaccinated individual.
There is a threshold they use to determine presence and infectiousness, so it's not just that there are "pieces" there, it's a certain number that has to exceed the threshold. If it's below the threshold it's considered not detected, I believe. Rapid antigen tests only test for the presence of the protein, not the actual mRNA, and are notorious for having widely varying sensitivity and thus increase likelihood of false negatives (ie not detecting a positive case). PCR is more accurate detection method.
I’m not saying use antigen instead of PCR, what I am saying is that just because there is a person PCR positive does not mean they are infectious. PCR is looking for genetic material and is not live virus specific. Using antigen in conjunction with PCR might offer more information on whether a person that is PCR positive and has actual live virus present.
Got it--in the study above it looked like they were also documenting signs and sx as a sign of infectiousness. Why the paired rapid antigen testing, then? Because it offers evidence of live virus? Have you seen this suggestion in literature? I'm curious.
Thank you so much for this newsletter. Subscribed today.
I have several questions about this.
1) If the effectiveness against asymtopmatic to mild disease is 49-59%, and the effectiveness against severe disease is much higher, what is the overall effectiveness against being able to transmit COVID-19 to others?
2) With these lower effectiveness rates against positive cases, what does it say about the ability to vaccinate our way out of COVID (assuming high uptake of vaccinations)? Is that enough? If not, then what?
3) I remember reading a month or two ago now that one of the vaccine makers, I think Pfizer, was developing a variation of the mRNA vaccine targeted at the COVID variants circulating now. I have seen little about that since. Is that still ongoing? Would it help with Delta?
4) I'm seeing some preliminary news stories about vaccine resistance of lambda or other new variants, based solely on lab studies. Is there anything we can learn about that - perhaps contextualizing it with what the same lab studies said about Delta?
Do you have any other information or know of any data sets that have been collected about vaccine efficacy in pregnant women against the Delta variant? I had COVID in Nov 2020, got fully vaxxed in March/April, but now I'm pregnant and I just feel like none of these data sets really apply to me and I would just love to know how protected I am.
Thank you as always.
While obviously decreases in severe disease and mortality is significant and a great accomplishment it is still frustrating to have those be the metrics everyone always discusses. Long haul covid19 and damage to multiple systems is a serious issue as well (and in the long run will majorly impact our health care systems). It seems even the mild and asymptomatic cases among vaccinated can result in long covid. I am really worried about this for myself and my unvaccinated kids.
Same! Long COVID (plus unknown long-term damage that may come back to bite us years from now) has been my biggest fear for myself since we first started hearing about it. It makes me so mad that it almost never gets mentioned in mainstream coverage! In case you're a new subscriber (or anyone else reading this thread is), Dr. Jetelina did an update on long COVID in breakthrough cases a couple weeks ago: https://yourlocalepidemiologist.substack.com/p/long-covid-among-breakthrough-cases I really appreciate that even if Dr. Jetelina doesn't bring it up in every post, she does give it regular attention, which again is more than mainstream news.
💯 agree! Long Covid is being mostly ignored. We need this information and it needs to be talked about as much as severity of disease. I don’t know if it’s rare or just rarely discussed. I have illnesses that mimic long haul & am disabled.
Yes! As a sufferer of chronic Lyme (many of the same symptoms), I don’t wish chronic disease on anyone. People think death is the worst outcome, but being physically and/or mentally debilitated should not be an acceptable outcome. I’m finally feeling a little better from Lyme and would be devastated to get another set of chronic issues. My life was turned upside down for several years during a peak time of my life. I missed out on so many things and will never get that time back. Now, I’m terrified of what the long term issues could be if my young son were to get it, even if he seemingly recovers. Things like this stay in your system and pop out at random times, even many years later in life.
Should we be concerned that unvaccinated individuals are infectious for 16 days? That is much longer than the recommended 10 day quarantine. Thank you for all you do!!!
We only saw a plot of viral load, not ability to infect. I think somebody would need to measure viral titer to really determine that.
Thank you. Can you help me understand this statement: “Vaccinated seem to not be infectious after 9 days (Ct=30) compared to unvaccinated at 16 days.” ? Are you aware of any reference that explains how the CDC quarantine and isolation lengths were/are determined? I’m also curious how/why the CDC determined asymptomatic vaccinated exposed people should be tested 3-5 days after exposure. Thank you for any insight or references.
Here's a starting reference for the Ct stuff... https://www.sciencemag.org/news/2020/09/one-number-could-help-reveal-how-infectious-covid-19-patient-should-test-results
I do know that with the pre-delta version of the virus, there were a number of studies done where they tried to infect cells with virus extracted from human samples at various timepoints after infection. And those studies showed that people can shed virus fragments for a long time after the virus has cleared, but the virus fragments aren't able to replicate. So the CDC and many other agencies switched guidance from a PCR-based test to a time-based criteria for release from isolation after infection. I think they picked 10 days. Others have done work and determined that very high cycle counts in PCR means that the viral load is so low regardless, it's hard to transmit at Ct values above 30. Low Ct values mean there was a lot of virus present, high Ct values mean there is little present. Every 3 Ct units is a factor of 10 less in viral concentration, give or take. If I got any of that wrong, someone can chime in.
Here's a reference to the CDC guidance on isolation. They state with references that replication-competent virus hasn't been isolated after 10 days except in rare circumstances like severe disease or immunocompromised. https://www.cdc.gov/coronavirus/2019-ncov/hcp/duration-isolation.html
Oh yeah, on the 3-5 day wait after exposure, I believe the logic was to prevent false negatives they want the person to wait long enough to develop enough virus in the system to detect with the RT-PCR. Sampling too soon could yield a negative just because there wasn't enough virus present.
Thank you. Has it been documented that the incubation period of Delta is shorter than the “original strain?” Unvaccinated, exposed, asymptomatic people are supposed to wait until day 5 to test and return after day 7 if the test is negative.
I watched a talk from Micheal Osterholm that said the incubation period wasn't shorter, but there were more offspring. I wonder if they'll decide to decrease the wait until test with delta, since the viral load seems to be much higher? Good question.
I wonder if Delta could be more detectable, and if so whether that could be its Achilles heel.
Is there any data yet about whether vaccinated individuals are having asymptomatic transmission with Delta or only when symptomatic?
I contracted COVID in November 2020 and was vaccinated in December/January with Pfizer. Is there data out regarding infection rates with Delta amongst those who have had natural infection plus are fully vaccinated? I am being told colleagues are seeing it, but I have not read anything concrete addressing it.
To piggyback off this comment, do you know what the current data is regarding infection only protection?
I read somewhere recently (over a week ago) that vaccine + infection = best protection, vaccine = good protection, and infection only = ok protection. I won't bother with the alleged percentages because the data is constantly changing.
i would agree with that assessment. the risk of reinfection is higher for Delta. I’m happy to throw a post together on this
Doesn't the fact that breakthroughs appear to be starting off with higher viral loads suggest some sort of detection bias? Is there something special about the kinds of people having the breakthrough cases that would cause them to have higher viral loads?
Overall, the people who suffered breakthrough infections did have more comorbidities but that's not true for all of them. Most likely, the combination of a tighter bond to the ACE2 receptor by the receptor binding domain AND the fact that more viable viral replicates are produced with each intracellular replication process are the reason we're seeing more breakthrough infections than we expected.
Thank you. 4 of my family members have had breakthrough cases here in Mississippi and many of my friends and family are vaccine hesitant or resistant. I came across an article from the UK that I found helpful even with its limitations. One finding I find particularly interesting is that vaccine resistant participants relied significantly more on social media than any other information source while vaccine accepting participants consumed significantly more information from newspapers, television, radio, doctors, other health professionals, and government agencies.
Resistance has been so strong on social media, but this encourages me to continue sharing reputable information on these platforms. Just wanted to share to encourage others as well.
URL: https://www.nature.com/articles/s41467-020-20226-9
Are false negative rapid tests less of a problem for Delta than for the original strain because of the increased viral load? It seems reasonable to suspect this would be the case.
Two things: Your surmise is correct in that Delta being so speedy means antigen will trip faster, but also, accuracy is a kind of weird conversation, because antigen is really answering "is this person a problem for everybody else" rather than "what is wrong with this person" and the numbers are extremely good for them first question.
Here's a conversation about that very question: https://mobile.twitter.com/MCSlab_uiuc/status/1436535100590723077
And here's more about rapid antigen vs PCR on the "is this person my problem" question. https://mobile.twitter.com/michaelmina_lab/status/1433969213773914115
Also, I love Michael Mina's crusade, I've been following him on Twtter for a while
So if better detectability is Delta's Achilles heel why aren't we going all in with rapid home tests???
If vaccine-resistant strains start spreading, can the vaccines quickly be tweaked to cover the new variants and go straight into arms? Or do Pfizer, Moderna etc need to go through another round of trials before offering the public a shot that protects against new variants?
Can you clarify the role of AZ vaccine (not an mRNA vaccine) in the REACT-UK study in your conclusions?
Great post. I had a question about how the viral load measured really connects to the ability for the vaccinated to infect. Since Rt PCR only measures viral fragments, how do we know it equates to ability to infect? Last year it was shown that people can shed viral RNA for months after they are no longer infectious. Also, the Singapore data is for breakthrough cases, but does the same relationship exist for subclinical and asymptomatic cases? I assume breakthroughs happen because the immune response post-vaccination is sub-optimal to begin with. The reason I ask is that many of us, and the media and scientific sources have been saying that the unvaccinated not only carry the burden of disease but are also responsible for spread. If both groups spread similarly, even in asymptomatic and subclinical cases like they do with breakthroughs, maybe we need to lay off the focus on vaccinations protecting others argument. And what does that mean for herd immunity in general long-term?
You have a number of questions. I'll see what I can do.
1) rt-PCR shouldn't be used for perhaps 90 days after symptoms clear because remnant fragments do persist. Antigen testing, however, performed serially, will provide some better information on ongoing infection as it's less focused on the subfragments identified by PCR. In addition, for breakthrough diagnosis, a diagnosis of exclusion can be employed if influenza testing is negative, but the spectrum of ILI symptoms is present.
1a) In patients who were PCR-positive for COVID-19, one may assume intact infection-conferred immunity, and thus something approaching sterilizing immunity during the 90 day interval. These people are unlikely to transmit replicatable virus.
2) There has been hypothesized a correlation between intensity of symptoms and disease severity and immune response but this is not always valid. anecdotally, my immune response, with very mild symptoms, was much more robust than my wife's who experienced moderate disease symptoms, but is immune-compromised. In other words, it's not uniform across the population.
3) Breakthrough cases happen when someone is overwhelmed with infective, reproductive viral particles that can attach to the receptors on viable cells, infect the cells and reproduce. In the case of delta, the number of particles produced with each reproductive cycle is higher than with earlier variants, and the modifications to the S1 protein, spike conformation and receptor binding domain region make it a better competitor for cellular access than existing antibodies are for competition to prevent disease. In some cases, prior to delta, peoples' various immune responses may not be available in sufficient numbers to overwhelm the attacker, which is why we're now talking boosters. The cellular immune system can take some period of time to ramp back up to circulating antibodies once it's turned on to the presence of a known agent. This interval may make someone susceptible. I'm aware of at least one person who was infected with 3 different strains of SARS-CoV-2 as determined by a university lab's genotyping efforts.
It's currently thought that most vaccinated persons, and virtually all who were previously infected and subsequently vaccinated, will have a muted reproductive response, and are less, or unlikely to spread actively. This includes especially the asymptomatic persons who were previously vaccinated.
I can give a real life example and then I have a question. Colleague of mine , 28 yo male, got delta at a party 2 weeks ago. 10 vaccinated people there and all indoors. J&J person ended up having symptoms. 4 people total infected. Colleague was most symptomatic and it took 4 days from exposure to show up. Loss of taste, smell, cough and shortness of breath. Symptomatic for 3 days and on the mend on day 4 short of taste and smell. My question is now on mandates. Sounds like tons of companies have them with a target of October 1. How much can we disrupt this wave? Challenge to the mandate is demographic it is targeting and also if you don't get it, you are just subject to mandatory testing , so it doesn't solve the vaccine issue.
Are these studies showing viral load just using Ct values of PCR tests. Wouldn’t it be better to be using PCR test with antigen testing? Ct values of PCR just tell us that “pieces” of virus are present, that doesn’t necessarily mean it’s infectious virus that is being found… specifically in the vaccinated.
Read this study and their methodology (cited above), this is how they tested for infectiousness, and they didn't just test for presence, they also took into account the threshold. This makes more sense to me than rapid antigen pairing.
https://spiral.imperial.ac.uk/bitstream/10044/1/90800/2/react1_r13_final_preprint_final.pdf
"We analysed Ct values associated with positive results among vaccinated and unvaccinated
individuals as a measure of viral load and as a proxy for infectiousness. For all positives in
round 13, at ages 18 to 64 years, median Ct value was higher for vaccinated participants at
27.6 (25.5, 29.7) compared with unvaccinated at 23.1 (20.3, 25.8) (positive defined as N
gene Ct <37 or both N gene and E gene positive, Methods) (Table 7, Figure 3). The higher
Ct values among vaccinated people indicate lower infectiousness, consistent with
transmission studies conducted when the Alpha variant was dominant, in which vaccinated
individuals were at substantially lower risk of passing on infection [15]. However, as a
secondary analysis, we reduced the Ct threshold for positivity, representing strong positives
with greater infectiousness. As the Ct threshold for positivity was reduced, the difference
between medians for vaccinated and unvaccinated individuals became smaller. However, at
the same time our estimate of vaccine effectiveness increased to 54% (29%, 71%) at a Ct
threshold of 35, plateauing between 57% (32%, 72%) at a Ct threshold of 33 and 58% (33%,
73%) at a Ct threshold of 27 (Table 7, Figure 3)."
I understand how they are using Ct threshold to estimate viral load and infectiousness. We do the same where I work. But, I have seen patients that test PCR positive months out from their initial infection. I’m just wondering if there is a better way than just assuming lower Ct values (more genetic material) means higher infectious viral load. Especially in the vaccinated individual.
Btw, I just subscribed today and I really appreciate your newsletter. Thank you for all you do.
There is a threshold they use to determine presence and infectiousness, so it's not just that there are "pieces" there, it's a certain number that has to exceed the threshold. If it's below the threshold it's considered not detected, I believe. Rapid antigen tests only test for the presence of the protein, not the actual mRNA, and are notorious for having widely varying sensitivity and thus increase likelihood of false negatives (ie not detecting a positive case). PCR is more accurate detection method.
I’m not saying use antigen instead of PCR, what I am saying is that just because there is a person PCR positive does not mean they are infectious. PCR is looking for genetic material and is not live virus specific. Using antigen in conjunction with PCR might offer more information on whether a person that is PCR positive and has actual live virus present.
Got it--in the study above it looked like they were also documenting signs and sx as a sign of infectiousness. Why the paired rapid antigen testing, then? Because it offers evidence of live virus? Have you seen this suggestion in literature? I'm curious.
I listen to TWIV and they have had discussions related to this.
Oh, interesting! I have to check that out. Is it more recent podcasts that's been brought up? I notice they go back aways...
Thank you so much for this newsletter. Subscribed today.
I have several questions about this.
1) If the effectiveness against asymtopmatic to mild disease is 49-59%, and the effectiveness against severe disease is much higher, what is the overall effectiveness against being able to transmit COVID-19 to others?
2) With these lower effectiveness rates against positive cases, what does it say about the ability to vaccinate our way out of COVID (assuming high uptake of vaccinations)? Is that enough? If not, then what?
3) I remember reading a month or two ago now that one of the vaccine makers, I think Pfizer, was developing a variation of the mRNA vaccine targeted at the COVID variants circulating now. I have seen little about that since. Is that still ongoing? Would it help with Delta?
4) I'm seeing some preliminary news stories about vaccine resistance of lambda or other new variants, based solely on lab studies. Is there anything we can learn about that - perhaps contextualizing it with what the same lab studies said about Delta?
Thank you!
A great source of data for Israel's cases is at https://github.com/dancarmoz/israel_moh_covid_dashboard_data
Definitely high viral loads in vaccinated and unvaccinated, but can we really call those Ct values the same? I thought the Ct values are logarithmic not linear, so the Ct values of 22.77 (unvaccinated) and 21.54 (vaccinated) appear close, but they represent viral loads in the unvaccinated group that are more than double that of the vaccinated group. (Each Ct increase of 3.3 typically represents an order of magnitude in scale. See https://www.thermofisher.com/us/en/home/life-science/pcr/real-time-pcr/real-time-pcr-learning-center/real-time-pcr-basics/real-time-pcr-understanding-ct.html).
Looking for your info on this. Thanks
So I've been following info on pregnant women here: https://covid.cdc.gov/covid-data-tracker/#pregnant-population
Do you have any other information or know of any data sets that have been collected about vaccine efficacy in pregnant women against the Delta variant? I had COVID in Nov 2020, got fully vaxxed in March/April, but now I'm pregnant and I just feel like none of these data sets really apply to me and I would just love to know how protected I am.