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Open Roads Forum  >  Around the Campfire  >  General Topics

 > 2019–2022 CORONAVIRUS PANDEMIC POSTINGS

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steveh27

Grosse Pointe Woods, MI

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Posted: 09/01/21 04:37am Link  |  Quote  |  Print  |  Notify Moderator

I now have antibodies 2 weeks after the booster shot.

BCSnob

Middletown, MD

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Posted: 09/01/21 05:07am Link  |  Quote  |  Print  |  Notify Moderator

This review of studies on vaccine effectiveness was prepared for the cdc.
Framework for booster doses of COVID-19 vaccines
The report compiled key info for deciding about boosters. It does provide a good summary on vaccine effectiveness over time.

This news article has a good overview of the key graphs.

CDC shares 8 new charts that show how po........s against COVID-19 and the Delta variant

See the figure on vaccine effectiveness against delta

* This post was edited 09/01/21 05:32am by BCSnob *

BCSnob

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Posted: 09/01/21 07:41am Link  |  Quote  |  Print  |  Notify Moderator

The report above highlights differences in vaccine effectiveness for Pfizer and Moderna (both mRNA) against Delta. This next preprint is on a study to identify the subtle differences in the immune response from these two vaccines that might be the source of the differences in vaccine effectives against Delta.

Subtle immunological differences in mRNA-1273 and BNT162b2 COVID-19 vaccine
induced Fc-functional profiles

bioRxiv Preprint August 31, 2021

The subject matter is beyond my education (had to look up definitions/descriptions of several items); I'll do my best to summarize.

The immune system produces antibodies (Wikipedia description of antibodies) against viruses, bacteria, toxins, vaccines, etc. Many different antibodies are produced; different classes (IgG, IgA, IgM, etc) and ones that recognize different parts of the invader. For SARS-CoV-2 we've read about antibodies binding to different parts of the RBD, and different parts of the spike (RBD is one part of the spike), and different parts of the virus (for example NTD). We've been reading that antibodies against the RBD (called neutralizing antibodies) block the virus from being able to bind to the ACE2 receptor preventing the virus from gaining access to the cells and creating an infection.

What I didn't know, and this article investigates, is that antibodies can also have other roles in immunity; one is antibody effector function. In short, antibodies bind to the invader and then other immune responses use these a portion of these antibodies (called the Fc portion of the antibody) as an anchor to perform their functions. The study above found that there were differences in the level of IgA antibodies produced by Pfizer and Moderna and that these IgA antibodies can act as anchors for other immune responses to act on the virus. Their hypothesis is that these non-RBD binding antibodies produced at a greater level by Moderna are the source of the higher vaccine effectiveness of Moderna against Delta.

dturm

Lake County, IN

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Posted: 09/01/21 09:19am Link  |  Quote  |  Print  |  Notify Moderator

Steve that's great. My wife had her third Pfizer 10 days ago. No plans for antibody testing at this point.


Doug & Sandy
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BCSnob

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Posted: 09/02/21 11:03am Link  |  Quote  |  Print  |  Notify Moderator

Risk factors and disease profile of post-vaccination SARS-CoV-2 infection in UK users of the COVID Symptom Study app: a prospective, community-based, nested, case-control study
The Lancet 1Sept2021

Quote:

Vaccination (compared with no vaccination) was associated with reduced odds of hospitalization or having more than five symptoms in the first week of illness following the first or second dose, and long-duration (=28 days) symptoms following the second dose. Almost all symptoms were reported less frequently in infected vaccinated individuals than in infected unvaccinated individuals, and vaccinated participants were more likely to be completely asymptomatic, especially if they were 60 years or older.


Quote:

Almost all individual symptoms of COVID-19 were less common in vaccinated versus unvaccinated participants, and more people in the vaccinated than in the unvaccinated groups were completely asymptomatic. This increased incidence of asymptomatic or minimally symptomatic infection in vaccinated participants underlines the importance of individuals who interact with unvaccinated or clinically vulnerable groups (eg, health-care workers and social care workers) continuing to regularly take tests for SARS-CoV-2, even if vaccinated, in line with current UK testing guidelines.33 We also found that COVID-19 was less severe (both in terms of the number of symptoms in the first week of infection and the need for hospitalization) in participants after their first or second vaccine doses compared with unvaccinated participants. We have previously shown that having more than five symptoms in the first week of infection was associated with COVID-19 severity20 and disease duration.21


* This post was edited 09/02/21 11:10am by BCSnob *

MEXICOWANDERER

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Posted: 09/03/21 10:58am Link  |  Quote  |  Print  |  Notify Moderator

Question

Whereas the immunogenicity of the injected substance is the main responsible for the immune response, a secondary but not less important factor is the timing. The question asked here is what is the optimal timing for boosting in terms of higher antibody titers. Intuitively, one expects a window of optimality since a too close boost does not elicit a strong memory as it simply add, (and compete for resources) to the prime, whereas an overly delayed boost may fail to wake up the memory simply because it already faded away.

The gathered titer data is most curious. A single digit increase of titer counts is not impressive using a three to four-week interval between mRNA inoculations. Does published data exist for trials that utilized for example a twelve to fifteen-week interval?

The upcoming 3rd mRNA doses for the immunocompromised are set for a 180-day interval. How large a monitoring effort will be enacted for mass gathering of titer increase data?

Thank You!

dturm

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Posted: 09/03/21 11:20am Link  |  Quote  |  Print  |  Notify Moderator

This is the question that is determined during initial trials. Initial dose and timing intervals are guessed based on previous vaccines, results in animal trials then tested in people. Pfizer and Moderna chose different intervals and dosage volumes for their human trials. The results of the trials and the serious nature of the pandemic made immediate approval appropriate.

They are still doing trials with different doses (about 1/3 the dose for children under 12) and different lengths between boosters. I would assume that they will accumulate additional data and seek licensing based on these data.

BCSnob

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Posted: 09/03/21 03:31pm Link  |  Quote  |  Print  |  Notify Moderator

Which is more important during a pandemic when selecting an inoculation protocol for a phase 3 clinical trial; waiting for the ideal prime to boost time (for maximum duration of immunity) or getting people to the maximum protection in the least amount of time? Don’t forget that vaccine effectiveness is lower during the time between prime & boost.

MEXICOWANDERER

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Posted: 09/03/21 05:31pm Link  |  Quote  |  Print  |  Notify Moderator

Risk vs benefit ratio...
The Pfizer and Moderna medias offer an average of eight points titer gain between the two. Eighty-four percent efficacy, first jab is nothing to sneer at. Or has that study been invalidated?

The uproar over AstraZeneca was more understandable, with Oxford University finding a twenty-five point Delta T titer amplification with interval delay. But the adeno virus efficacy was forty points lower than mRNA first inoculation efficacy.

We will find out more, as mass titer studies are performed on long term inoculation intervals on the immunocompromised...the 3rd dose interval is what, now...after 90 or 120 days?

Published data regarding heterogeneous mRNA bi vaccination does not exist.
not a word about role-reversal mRNA heterogeneous efficacy. At least with the COVID-19 pathogen, and variants. Their prime boost role is to stimulate all areas of the immune system without cancelling via over stimulation. The difference in efficacy between Pfizer and Moderna seems to be keyed on the amount of vaccine given. The size of the dose.

If a university team should prime with a mRNA and follow up with an adeno or heterogeneous booster, would that make them eligible to get staked to an anthill by the NIH, the FDA or competitive corporate entities?

Having a ninety-pound weakling malfunctioning immune system makes me curious.

Once again, thank you.

BCSnob

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Posted: 09/08/21 09:30am Link  |  Quote  |  Print  |  Notify Moderator

This preprint may be of interest to several on this forum.

Additional heterologous versus homologous booster vaccination in immunosuppressed patients without SARS-CoV-2 antibody seroconversion after primary mRNA vaccination: a randomized controlled trial
medRxiv Preprint September 08, 2021

Quote:

Abstract

Severe acute respiratory syndrome coronavirus–2 (SARS–CoV–2)–induced coronavirus disease 2019 (COVID–19) has led to exponentially rising mortality, particularly in immunosuppressed patients, who inadequately respond to conventional COVID–19 vaccination. In this blinded randomized clinical trial (EudraCT 2021–002348–57) we compare the efficacy and safety of an additional booster vaccination with a vector versus mRNA vaccine in non–seroconverted patients. We assigned 60 patients under rituximab treatment, who did not seroconvert after their primary mRNA vaccination with either BNT162b2 (Pfizer–BioNTech) or mRNA–1273 (Moderna), to receive a third dose, either using the same mRNA or the vector vaccine ChAdOx1 nCoV–19 (Oxford–AstraZeneca). Patients were stratified according to the presence of peripheral B–cells. The primary efficacy endpoint was the difference in the SARS–CoV–2 antibody seroconversion rate between vector (heterologous) and mRNA (homologous) vaccinated patients by week four. Key secondary endpoints included the overall seroconversion and cellular immune response; safety was assessed at weeks one and four. Seroconversion rates at week four were comparable between vector (6/27 patients, 22%) and mRNA (9/28, 32%) vaccine (p=0.6). Overall, 27% of patients seroconverted; specific T–cell responses were observed in 20/20 (100%) vector versus 13/16 (81%) mRNA vaccinated patients. Newly induced humoral and/or cellular responses occurred in 9/11 (82%) patients. No serious adverse events, related to immunization, were observed. This enhanced humoral and/or cellular immune response supports an additional booster vaccination in non–seroconverted patients irrespective of a heterologous or homologous vaccination regimen.

Authors' conclusions
Quote:

Our data show that a cellular and/or humoral immune response can be achieved
upon a third COVID-19 vaccination in most of the patients who initially developed
neither a humoral nor a cellular immune response. The efficacy data together with
the safety data seen in our trial provide a favorable risk/benefit ratio and support the
implementation of a third vaccination for non-seroconverted high-risk autoimmune
disease patients treated with B-cell-depleting agents. This might be a viable way to
protect this group of patients from more dire consequences of an acquired SARSCoV-
2 infection.


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