2. That's 20-40% of people who get infected and never show symptoms. More likely in young. Who don't understand they are propagating the pandemic
"Usually a virus that is good enough to kill you would make almost everybody at least a little bit sick."
3. The chronic "long covid" post-viral symptoms of #COVID19 are common, understudied to date.
"And it's extraordinary how many people have a postviral syndrome that's very strikingly similar to myalgic encephalomyelitis/chronic fatigue syndrome."
4. We don't have a #COVID19 czar with decision-making authority, like @RonaldKlain for Ebola (who Fauci loves) but @VP has taken on a lead role, is receptive, and "deeply involved." Fauci is very respectful to the Administration despite all the efforts of @POTUS to undermine him
5. What about the @HHSgov hijacking the @CDCgov covid data?
Fauci only learned about it by watching television
6. What about the hyperimmune response to #COVID19 and that being implicated as the basis for most fatalities?
7. It took 5 days from the sequence of #SARSCoV2 to Fauci's team to get the start on a vaccine, 62 days to get Phase 1 clinical trial started (That is simply incredible)
8. What about short-lived antibodies to the virus and the role of T cells? #SARSCoV2 is like SARS with a significant and enduring T cell response. We shouldn't be worried about the IgG antibody waning report that got a lot of buzz this week.
9. What about reinfection, does it occur?
There are anecdotes, but no proof of replication competent virus. So if it really exists it's rare (considering millions of infections). Hard to prove since you need a BSL-3 lab to correlate PCR results of RNA nucleotides w/ live virus
10. On the mask pushback, Fauci attributes this to the "disturbing anti-science trend" My worry is that will extend to implementing the vaccine, but we didn't get to that issue
11. Monoclonal (neutralizing) antibodies were developed for Ebola and highly successful They are now in clinical trials for SARSCoV2, very potent, and will likely be used in early and late stages of treatment. Mabs don't get the attention of vaccines but very important & imminent
12. Rapid diagnostic kits for home or point of care are in the works, NIH has invested $500 million, results in < 30 mins. These will be transformative when they are available this fall
13. Favorite part: his comments to the frontline heroes and how science will prevail.
• • •
Missing some Tweet in this thread? You can try to
force a refresh
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).
Breaking down the risks and benefit for lecanemab, the amyloid beta-directed antibody vs Alzheimer's drug approved @US_FDA last year. It doesn't look good.