Yesterday the FDA Advisory committee recommended that the 15 million Americans who have had J&J vaccines, more than 2 months out, get a 2nd shot.
There are some significant issues with this that could have been prevented /1
By May 1, there were over 8 million people 5.5 months out
By June 1, the number rose to nearly 11 million people 4.5 months out
Yet data have consistently been showing attrition of protection vs infections for this vaccine, this week in 620,000 US Veterans /2
This is the only Covid vaccine that was positioned as "one and done." J&J is the largest healthcare company in the world, yet research to back that up was undone until recently.
Single dose: 70% protection vs symptomatic infection
2-dose: 94% protection /3 fda.gov/media/153129/d…
To start with, the 1-shot 70% efficacy vs. symptomatic infections was considerably lower than the mRNA vaccines (95%), the primary endpoint of all Covid vaccine trials, and a proxy for protection vs hospitalizations and deaths
2-shots brought it to parity in the US at 94% /4
A grand total of 17 people were studied for impact on spike protein binding antibody levels (not even neutralization Abs) at 6 months /5
Parenthetically, the antibody level increase from the 2nd J&J shot at 2 months were small relative to a booster with an mRNA vaccine (50-70 fold, 1 month)/6
How could this happen? 15 million Americans potentially left vulnerable and still no formal approval for a 2nd shot 1. J&J did insufficient and late in coming research to backup their "one and done" assertion 2. The poor US tracking of data obscured detection of this issue
/7
We've known about the lapses in antibody levels and reduced protection vs hospitalization for some time, but left these people (who typically had no choice and were told all vaccines were equivalent) susceptible over a prolonged period
We're learning how to control the immune response, like a rheostat, even in the brain. Implications for understanding the basis and potential treatment of autoimmune conditions like multiple sclerosis, #LongCovid, #MECFS, and brain cancer.
A brief review of 6 recent, important reports
in the new Ground Truths, open-access
Such as Programming T cells with brain-specific proteins and payloads
@ScienceMagazine science.org/doi/10.1126/sc…
Or peptide fragments of myelin basic protein that suppress the immune response @Nature nature.com/articles/s4158…
New @NEJM
A whopping (~90%) reduction of progression to Type 2 diabetes with tirzepatide (GLP-1 drug, dual receptor) vs placebo in a randomized trial of >2,500 participants with obesity, absolute reduction of 10/100 treated
In other GLP-1 new publications today
—Country-wide Sweden reduced hospitalizations for alcohol or substance abuse with these drugs jamanetwork.com/journals/jamap… @JAMAPsych
—Concerns about discontinuation jamanetwork.com/journals/jama/… @JAMA_current
Other new anti-obesity drugs in the pipeline, one that also increases energy expenditure
@NatureNV nature.com/articles/d4158…
A dedicated issue of @ScienceTM on #LongCovid
—Sex-specific differences, with perspective by @VirusesImmunity and @SilvaJ_C
—Insights for therapies @AndreaCoxMDPhD
—Deconvoluting "Osler's Web" @MichaelPelusoMD @DeeksSteven @DrMaureenHanson @SaydahSharon
—+RECOVER Trial, Lyme disease
An elegant @Nature study by @AkassoglouLab has illuminated our understanding of the role of fibrin (component of blood clots), #SARSCoV2, and brain inflammation in Covid and #LongCovid.
This discovery and more in the new Ground Truths podcast, with transcript, key figures (such as as the one below) and citations. Open-access. Link in my profile.
A clip from our conversation. Unknowingly, @AkassoglouLab was gearing up for understanding this complex pathophysiology for many years before Covid hit
For treatment, it's not just as simple as preventing fibrin clots. It's isolating the pro-inflammatory action of fibrin, targeted by the antibody
Covid and increased risk of major adverse cardiovascular events (MACE) 3-years out
2-fold increased for any severity of Covid
~4-fold increase for Covid requiring hospitalization
"a coronary artery disease equivalent"
interaction with non-O blood types
@uk_biobankahajournals.org/doi/10.1161/AT…
"A major finding from our analyses was that the risk
of MACE among the subset of hospitalized COVID-
19 cases without known CVD (ie, primary prevention
patients) was comparable to (or even slightly higher than) the risk in patients with CVD, PAD, or diabetes but without COVID-19."
"one of the first examples of a gene-pathogen exposure interaction for thrombotic events"
I think it's the first one documented, likely others to be unraveled
New US Covid genomic surveillance
The KP.3.1.1 variant is on the move to become dominant, more of a challenge to our immune response than KP.3 and prior variants (especially without new KP.2 booster when we need it for high-risk individuals)
It's the deletion 31/31 that makes the KP.3.1.1 spike different, but otherwise 2 mutations away from KP.2 (R346T and Q493E)
Buckle up; this wave isn't over yet d/t KP.3.1.1's emergence