First read out from a neutralizing antibody clinical trial. A step in the right direction for this class of drugs that could be used in many ways vs #COVID19.
Why is this important? 1. This is the 1st clinical trial of a drug specifically designed for #SARSCoV2. All previous trials were repurposed drugs (HCQ, dexamethasone, Remdesivir, etc). Safety data are encouraging
2. The class of drugs has the potential to be used as a prevention in high-risk individuals, and intervention in mild to moderate covid (as in the current trial) or severe, subcritical. The data from non-human primates supports this multi-pronged use.
3. The issues of difficulty in producing the antibodies at scale and their likely high cost are barriers to keep in mind, beyond the fact that real proof of efficacy has yet to be established.
4. Nonetheless, before having a safe and effective vaccine, mAbs represent our best near term shot of a potent therapy. They haven't attracted as much attention as vaccines, since they represent a bridge, not a definitive exit strategy. These days all positive news is welcome.
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
We've known about KP.3's marked growth advantage since April and could have made the call then to make the new booster. That would have been aligned well with the current wave (available in July) 2/5 erictopol.substack.com/p/are-we-flirt…
But the FDA has tried to force fit Covid into an annual shot like flu, even though all data tells us it doesn't follow an annual pattern. Even the CDC acknowledges this now
3/5cdc.gov/ncird/whats-ne…
New CDC genomic data shows continued rise of the KP.3 variant that accounts for 1 of 3 Covid cases.
LB.1 is gaining, too, as JN.1 fades away
This variant growth advantage plot by @BenjMurrell (H/T @siamosolocani) shows why this is the case. Note KP.3 is the one at far left w/ almost 3-fold advantage to JN.1.
Reinforces why the decision to develop the KP.2 vaccine booster (instead of JN.1) was a good one
Spike mutation map to show the differences betweem KP.3 and JN.1 (and LB.1, KP.2)
The connection between #SARSCoV2 and neurodegeneration
@TheLancetNeuro
Quotes below: 1. SARS-CoV-2 infection should be considered as a risk factor for Alzheimer’s disease, even though the distinction between causation versus disease acceleration is not clear.thelancet.com/journals/laneu…
2. Inflammation in patients with COVID-19, and controlled experiments show prolonged neuro-inflammation after mild SARS-CoV-2 infection
in macaques.
3. A direct correlation has been reported
between prior SARS-CoV-2 infection and increased risk
of Alzheimer’s disease (figure).
4. So far, the estimated lifetime cumulative risk of dementia due to hospitalisation for any viral infection is 1·48 (95% CI 1·15–1·91).