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Mr._Clark

Audioholic Field Marshall
This article in the NYT has some interesting information about COVID case and death rates for vaccinated vs unvaccinated, but it's based on data from only 14 states and 2 cities.

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>>>Compared with the unvaccinated, fully vaccinated people overall had a much lower chance of testing positive for the virus or dying from it, even through the summer’s Delta surge and the relaxation of pandemic restrictions in many parts of the country. But the data indicates that immunity against infection may be slowly waning for vaccinated people, even as the vaccines continue to be strongly protective against severe illness and death. . . . The C.D.C. data so far runs through early September and captures only the crest of the Delta wave. But data from states like New York and California shows similar patterns through September and October. That suggests that the vaccines, despite some slight differences among the brands, are still working to protect against the most severe outcomes. <<<

It would be interesting to see what the numbers are for unvaccinated but previously infected, and infected then vaccinated, but I'm assuming that data has not been tracked by the states and cities used for this report.

 
mtrycrafts

mtrycrafts

Seriously, I have no life.
I would also like to know the population size this is based on as if it is large enough, it may be a good indicator
 
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Danzilla31

Audioholic Spartan
Quick question I'm going to get my flu vaccine now my covid booster I'd like to do tommorow any problems with just getting them both done back to back like this? Anyone know?
 
davidscott

davidscott

Audioholic Ninja
Supposedly its ok to do but I personally wouldn't and didn't. The reason being I wanted to know which shot was causing any reactions that I was feeling. Just me and I spaced mine 3 weeks apart. But get them. :)
 
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Danzilla31

Audioholic Spartan
Supposedly its ok to do but I personally wouldn't and didn't. The reason being I wanted to know which shot was causing any reactions that I was feeling. Just me and I spaced mine 3 weeks apart. But get them. :)
Ok that's good advice I'll wait a bit for the Covid booster then just got my flu vacc today
 
mtrycrafts

mtrycrafts

Seriously, I have no life.
I waited a week between the two. Wifey did both together. No issues for us.
 
cpp

cpp

Audioholic Samurai
Quick question I'm going to get my flu vaccine now my covid booster I'd like to do tommorow any problems with just getting them both done back to back like this? Anyone know?
I was told by my doctor to wait 14 days from the time of my last vaccine shot and my flu shot. And I did just that, and no issues.
 
panteragstk

panteragstk

Audioholic Warlord
I was told by my doctor to wait 14 days from the time of my last vaccine shot and my flu shot. And I did just that, and no issues.
I feel like that's a good recommendation. Would really suck to have side effects for both at the same time.
 
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Mr._Clark

Audioholic Field Marshall
The usual disclaimers concerning science by press release, relatively small group of study participants, unpublished and unreviewed results, etc. apply, but this certainly sounds like good news so far.

Perhaps @Swerd could comment, but protease inhibitors seem to be fairly well-known (see wiki link below). Somewhat off topic, but wiki says protease inhibitors may have anti cancer activity as well ("Researchers are investigating whether protease inhibitors could possibly be used to treat cancer."). The wiki article does list some potential side effects, but, compared to being dead, they don't seem too bad.

>>>WASHINGTON (AP) — Pfizer Inc. said Friday that its experimental antiviral pill for COVID-19 cut rates of hospitalization and death by nearly 90% in high-risk adults, as the drugmaker joins the race to bring the first easy-to-use medication against the coronavirus to the U.S. market. . . .

Pfizer released preliminary results Friday of its study of 775 adults. Patients who received the company’s drug along with another antiviral shortly after showing COVID-19 symptoms had an 89% reduction in their combined rate of hospitalization or death after a month, compared to patients taking a dummy pill. Fewer than 1% of patients taking the drug needed to be hospitalized and no one died. In the comparison group, 7% were hospitalized and there were seven deaths. . . .

Study participants were unvaccinated, with mild-to-moderate COVID-19, and were considered high risk for hospitalization due to health problems like obesity, diabetes or heart disease. Treatment began within three to five days of initial symptoms, and lasted for five days. Patients who received the drug earlier showed slightly better results, underscoring the need for speedy testing and treatment. . . .

An independent group of medical experts monitoring the trial recommended stopping it early, standard procedure when interim results show such a clear benefit. The data have not yet been published for outside review, the normal process for vetting new medical research. . . .

Pfizer’s drug is part of a decades-old family of antiviral drugs known as protease inhibitors, which revolutionized the treatment of HIV and hepatitis C. The drugs block a key enzyme which viruses need to multiply in the human body. <<< (emphasis added)


 
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Mr._Clark

Audioholic Field Marshall
From the Pfizer press release:

>>>PAXLOVID™ isan [sic*] investigational SARS-CoV-2 protease inhibitor antiviral therapy, specifically designed to be administered orally so that it can be prescribed at the first sign of infection or at first awareness of an exposure, potentially helping patients avoid severe illness which can lead to hospitalization and death. PF-07321332 is designed to block the activity of the SARS-CoV-2-3CL protease, an enzyme that the coronavirus needs to replicate. Co-administration with a low dose of ritonavir helps slow the metabolism, or breakdown, of PF-07321332 in order for it to remain active in the body for longer periods of time at higher concentrations to help combat the virus. PF-07321332 inhibits viral replication at a stage known as proteolysis, which occurs before viral RNA replication. In preclinical studies, PF-07321332 did not demonstrate evidence of mutagenic DNA interactions.<<<

*Editorial comment: C'mon Pfizer, pay a few bucks more and get some real proofreaders!


There is another trial (Phase 3) of the Pfizer drug (PF-07321332) in combination with Ritonavir to see if it prevents COVID in people exposed to the virus. I have not seen any results for this study (the estimated completion date is 12/25/21, so this is probably not surprising)

>>>The purpose of this study is to evaluate the efficacy and safety of PF-07321332/ritonavir as postexposure prophylaxis for adult household contacts of a patient with COVID-19<<<

 
Swerd

Swerd

Audioholic Warlord
Perhaps @Swerd could comment, but protease inhibitors seem to be fairly well-known (see wiki link below).
There are many different protein cutting enzymes (proteases) known in science. And they play many different biological roles in cells and viruses. The proteases in certain viruses, especially the RNA viruses (polio, HIV, other leukemia viruses such as HTLV, hepatitis C, and coronaviruses), play a key role during virus replication. These enzymes recognize unique sequences of amino acids in virus-encoded proteins, that become recognition sites for the protease to make a cut. These recognition sites are unique to the viral proteases, and if inhibitors can be found that mimic these sites, essentially stopping the action of the viral proteases, they can block a necessary step in viral reproduction.

The clinical results of Pfizer's protease inhibitor look very good, and I hope it becomes an approved treatment for Covid-19. It is now November 2021, nearly two years after we learned of SARS-CoV-2 and it's devastating pandemic. (Merck announced the successful trial of it's anti-viral drug, molnupiravir, about two months ago.) Compare that to the less than one year it took to develop several successful vaccines. Many (including me) had predicted it would take longer to develop successful anti-viral drugs than it would take to develop vaccines. And this was with an all-out emergency effort at both drug and vaccine development.
Somewhat off topic, but wiki says protease inhibitors may have anti cancer activity as well ("Researchers are investigating whether protease inhibitors could possibly be used to treat cancer.").
Bortezomib (sold under the name Velcade) is a different protease inhibitor from the RNA virus ones. Discovered in the late 1990s, it works by a quite different mechanism of action. It successfully slows the progress of, but does not cure, multiple myeloma and mantle cell lymphoma.
 
davidscott

davidscott

Audioholic Ninja
Aaron Rogers faking that he got vaccinated. Man I just lost all respect for that guy. Just man up and say you have reservations and follow NFL protocol for the unvaccinated.
 
MaxInValrico

MaxInValrico

Full Audioholic
Aaron Rogers faking that he got vaccinated. Man I just lost all respect for that guy. Just man up and say you have reservations and follow NFL protocol for the unvaccinated.
Yea, now he's a victim. Spare me.
 
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Mr._Clark

Audioholic Field Marshall
This article about so-called hybrid immunity due to infection followed by vaccination is somewhat interesting. I find myself wondering how many of the deaths of unvaccinated people due to a second COVID infection could be avoided.

>>>Not long after countries began rolling out vaccines, researchers started noticing unique properties of the vaccine responses of people who had previously caught and recovered from COVID-19. “We saw that the antibodies come up to these astronomical levels that outpace what you get from two doses of vaccine alone,” says Rishi Goel, an immunologist at the University of Pennsylvania in Philadelphia who is part of a team studying super-immunity — or ‘hybrid immunity’, as most scientists call it.

Initial studies of people with hybrid immunity found that their serum — the antibody-containing portion of blood — was far better able to neutralize immune-evading strains, such as the Beta variant identified in South Africa, and other coronaviruses, compared with ‘naive’ vaccinated individuals who had never encountered SARS-CoV-22. It wasn’t clear whether this was just due to the high levels of neutralizing antibodies, or to other properties. . . .

The most recent studies suggest that hybrid immunity is, at least partly, due to immune players called memory B cells. The bulk of antibodies made after infection or vaccination come from short-lived cells called plasmablasts, and antibody levels fall when these cells inevitably die off. Once plasmablasts are gone, the main source of antibodies becomes much rarer memory B cells that are triggered by either infection or vaccination. . . .

As breakthrough infections caused by the Delta variant stack up, researchers including Nussenzweig are keen to study the immunity in people who were infected after their COVID-19 vaccinations, rather than before. An individual’s first exposure to influenza virus biases their responses to subsequent exposures and vaccinations — a phenomenon called original antigenic sin — and researchers want to know if this occurs with SARS-CoV-2.

Those studying hybrid immunity stress that — whatever the potential benefits — the risks of a SARS-CoV-2 infection mean that it should be avoided. “We are not inviting anybody to get infected and then vaccinated to have a good response,” says Finzi. “Because some of them will not make it through.” <<<

 
Swerd

Swerd

Audioholic Warlord
This article about so-called hybrid immunity due to infection followed by vaccination is somewhat interesting. I find myself wondering how many of the deaths of unvaccinated people due to a second COVID infection could be avoided.

>>>Not long after countries began rolling out vaccines, researchers started noticing unique properties of the vaccine responses of people who had previously caught and recovered from COVID-19. “We saw that the antibodies come up to these astronomical levels that outpace what you get from two doses of vaccine alone,” says Rishi Goel, an immunologist at the University of Pennsylvania in Philadelphia who is part of a team studying super-immunity — or ‘hybrid immunity’, as most scientists call it.

Initial studies of people with hybrid immunity found that their serum — the antibody-containing portion of blood — was far better able to neutralize immune-evading strains, such as the Beta variant identified in South Africa, and other coronaviruses, compared with ‘naive’ vaccinated individuals who had never encountered SARS-CoV-22. It wasn’t clear whether this was just due to the high levels of neutralizing antibodies, or to other properties. . . .

The most recent studies suggest that hybrid immunity is, at least partly, due to immune players called memory B cells. The bulk of antibodies made after infection or vaccination come from short-lived cells called plasmablasts, and antibody levels fall when these cells inevitably die off. Once plasmablasts are gone, the main source of antibodies becomes much rarer memory B cells that are triggered by either infection or vaccination. . . .

As breakthrough infections caused by the Delta variant stack up, researchers including Nussenzweig are keen to study the immunity in people who were infected after their COVID-19 vaccinations, rather than before. An individual’s first exposure to influenza virus biases their responses to subsequent exposures and vaccinations — a phenomenon called original antigenic sin — and researchers want to know if this occurs with SARS-CoV-2.

Those studying hybrid immunity stress that — whatever the potential benefits — the risks of a SARS-CoV-2 infection mean that it should be avoided. “We are not inviting anybody to get infected and then vaccinated to have a good response,” says Finzi. “Because some of them will not make it through.” <<<

I'm not impressed. That news article in Nature went on to say that other arms of the immune system – T-cell responses – also play a major role in the response against a virus infection.
Understanding the mechanism behind hybrid immunity will be key to emulating it, say scientists. The latest studies focus on antibody responses made by B cells, and it’s likely that T-cell responses to vaccination and infection behave differently. Natural infection also triggers responses against viral proteins other than spike — the target of most vaccines. Nussenzweig wonders whether other factors unique to natural infection are crucial. During infection, hundreds of millions of viral particles populate the airways, encountering immune cells that regularly visit nearby lymph nodes, where memory B cells mature. Viral proteins stick around in the gut of some people months after recovery, and it’s possible that this persistence helps B cells hone their responses to SARS-CoV-2.
The entire purpose of vaccinations against pathogenic viruses has always been to generate immune responses by mimicking real infections, all without exposing people to the dangerous effects of the unaltered virus itself. There's nothing new in that article. We still don't completely understand what's going on with vaccinations against SARS-CoV-2.

The research described in that article only looked at circulating antibodies while ignoring T-cell responses. T-cells do have a major impact on memory B-cells upon reinfection or vaccination after previous infection. The helper T-cells recognize the new presence of virus and signal both memory B-cells and killer T-cells to rapidly multiply – and to get busy with either making more antibodies (memory B-cells) or killing virus infected cells (T-cells).

I know I sound like a broken record on this subject. You simply cannot talk about B-cells without also talking about T-cells. They are both part of the immune response.
 
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davidscott

davidscott

Audioholic Ninja
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Mr._Clark

Audioholic Field Marshall
Since it's a little slow on the COVID news front, here's the most recent risk level map from globalepidemics.org. The southeast and Texas are definitely much better than a couple months ago.

The geographic region with somewhat lower rates along the eastern seaboard extends through Massachusetts, but stops rather abruptly at New Hampshire. I'm tempted to attribute this to higher vaccination rates, possibly in combination with higher natural immunity in these areas, but I don't know offhand if the data supports that hypothesis.

1636389180124.png


 
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Mr._Clark

Audioholic Field Marshall
Effectiveness of third Covid-19 vaccine dose in Israel:

Thanks for the link. These numbers from the paper look pretty good:

>>>Compared with two doses of the vaccine administered at least 5 months ago, receiving a third dose was estimated to have an effectiveness of 93% in preventing COVID-19-related admission to hospital, 92% in preventing severe disease, and 81% in preventing COVID-19-related death.<<<
 
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