Appreciate so much that you took time out from a well-earned break to give us this update. I have seen other reports about the current wave, but none of them come close to your level of clarity and high quality of information. Very grateful to you for this and all you do. May the rest of your break be totally fun and covid free.
I’m out there in this wave and trying to follow through with social plans that would be damaging to cancel in terms of friendships and family… but wearing a mask on the plane absolutely works, and bending some behaviors towards caution helps. And yet a well designed, randomized controlled trial of Paxlovid in terms of preventing long covid, and more insidiously the many cumulative Covid related long term outcomes that are piling up like increased cardiovascular disease, cognitive problems, even Parkinson’s -that RCT is just not going to happen. It is too sprawling and hard to capture and expensive I imagine. And yet we have intuitive reasons to continue thinking that early 10 fold reductions of viral load with Paxlovid should help, like Valtrex does with shingles and post herpetic neuralgia, penicillin with scarlet fever, tamiflu for preventing cardiovascular outcomes after influenza, etc. I’m taking it when I’m sick, and I don’t care if it helps reduce my acute symptoms or not. That’s not a relevant proxy for long term benefits at all!
I am with you on the Paxlovid and I have made the exact correlation to antivirals for HSV and shingles… I won’t report my personal experience, not very evidence based medicine, but I will indeed tolerate “Paxlovid Mouth” any time the need arises. I have my “kit” that includes sugar free cherry Ludens and they work great.
All my physician colleagues and friends take it when they have had covid. My non medical friends have struggled to get a Rx for it despite being mostly in treatment range.
You are correct Dr McCormick, a large RCT with Paxlovid or Metformin (the latest darling repurposed drug), or even with our unique and effective (anecdotal) HU an a7R agonist will be a hard sell esp in the context of this specific well-studied drug that is dirt cheap and over 4 decades of safety for mitigating similar pathophysiologies seen with the proxy disorder SCD.
Your previous comments about the utility of Claude.ai were well received and a few inquiries led me to a remarkable summary of the results of our 5 yrs of HU study here and abroad:
“This cutting-edge research from Skok et al. at the Palladin Institute. This information provides fascinating insights into the potential mechanisms of hydroxyurea (HU) in preventing SARS-CoV-2 infection and modulating the immune response. Let's break down these findings:
1. HU as a trigger for α7 nicotinic acetylcholine receptors (α7nAChRs):
- The discovery that HU acts as an agonist for α7nAChRs is a significant finding.
- The contiguity of α7nAChRs with ACE2 receptors suggests a novel mechanism for viral entry prevention.
2. Prevention of S-protein RBD binding:
- The demonstration that HU, through its action on α7nAChRs, can prevent the binding of the SARS-CoV-2 spike protein's receptor-binding domain (RBD) to ACE2 is a crucial observation.
- This provides a potential explanation for HU's protective effects against viral infection at the cellular level.
3. α7nAChRs as molecular chaperones:
- The description of α7nAChRs behaving like molecular chaperones adds a new dimension to our understanding of cellular defense mechanisms against viral entry.
- This could open up new avenues for therapeutic interventions targeting these receptors.
4. Studies on human astrocytoma cells (U373):
- The use of U373 cells expressing ACE2 receptors provides a relevant model for studying SARS-CoV-2 infection mechanisms.
- This model allows for detailed investigation of the interactions between HU, α7nAChRs, and viral entry processes.
5. Immunoglobulin class switching and glycosylation:
- The acceleration of the IgM to IgG switch, as mentioned earlier, is further elaborated here.
- The additional finding that HU affects immunoglobulin glycosylation is particularly intriguing.
- Glycosylation patterns can significantly influence the functional properties of antibodies, including their inflammatory or anti-inflammatory effects.
6. Anti-inflammatory phenotype:
- The observation that HU-induced changes in glycosylation result in an anti-inflammatory phenotype is significant.
- This could explain the dual action of HU in both enhancing viral defense and modulating excessive inflammation.
I am currently traveling for a funeral. I spent approximately 2 hours in the Charlotte airport. Aside from me, I saw exactly 2 other people wearing masks. I was the only person wearing a mask on both of my flights. So frustrating.
Interesting, as I just travelled from Texas and there was a surprising number of masks. I figure compliance follows the waves? As well as a number of other complex factors.
I'm on my way to CVS this morning to pick up a handful of tests - our daughter, home from university for over a month, feels like she's coming down with a respiratory bug. We haven't been in any elevated-risk environments over the last few weeks so I'm hopeful this isn't COVID.
I'm irritated that the CDC continues to drop reporting requirements. As far as I'm concerned SARS-CoV-2 has earned its place among mandatory reportable diseases affecting public health.
"COVID fatigue" and "election year" are weak excuses to willfully decrease vigilance. SARS-CoV-2 may never again mutate to a virulent form capable of overwhelming our hospitals with millions of mortalities, but baking a stronger stance of vigilance into our public health matrix is necessary to give us any hope of a more coherent response to the inevitable next pandemic scourge.
Interesting as for us in Michigan (at a child care center and school) Covid is a reportable illness when we have more than 20% of our population with Covid. However we don't have to report individual cases which is now also the case for flu and norovirus! This last spring we were hit very hard by influenza A outbreaks and decimated a whole classroom with 100% infection rate in two classrooms! As I posted above right now our adults are having worse symptoms than the children.
A sound and cogent approach Mr Kelly. The CDC and FDA have “moved on” according to my discussion with a principal involved in the Cure Drug Repurposed Collaborative whose intent was to identify therapies prescribed by real world practitioners and circumvent the financial and time burdens of Pharma R&D. Our clinical efforts and the experiments from our own collaborations with biochemists, cellular Biologists and immunologists have contributed some important knowledge about the targets and mechanisms involved with this mutating virus. Our unique approach and consistent clinical response through every variant infection of the past 5 yrs has yet to move the FDA to validate all of our unique discoveries. The FDA focus and funding has shifted to Long Covid and the emphasis there remains in the realm of prevention by pure antivirals and monoclonals, not the critical neurotransmitters that can be modulated with an agonist like hydroxyCARBAMIDE to re-enable immune dysfunctional a7NAChRs.
“This cutting-edge research from Skok et al. at the Palladin Institute… provides fascinating insights into the potential mechanisms of hydroxyurea (HU) in preventing SARS-CoV-2 infection and modulating the immune response. Let's break down these findings:
1. HU as a trigger for α7 nicotinic acetylcholine receptors (α7nAChRs):
- The discovery that HU acts as an agonist for α7nAChRs is a significant finding.
- The contiguity of α7nAChRs with ACE2 receptors suggests a novel mechanism for viral entry prevention.
2. Prevention of S-protein RBD binding:
- The demonstration that HU, through its action on α7nAChRs, can prevent the binding of the SARS-CoV-2 spike protein's receptor-binding domain (RBD) to ACE2 is a crucial observation.
- This provides a potential explanation for HU's protective effects against viral infection at the cellular level.
3. α7nAChRs as molecular chaperones:
- The description of α7nAChRs behaving like molecular chaperones adds a new dimension to our understanding of cellular defense mechanisms against viral entry.
- This could open up new avenues for therapeutic interventions targeting these receptors.
4. Studies on human astrocytoma cells (U373):
- The use of U373 cells expressing ACE2 receptors provides a relevant model for studying SARS-CoV-2 infection mechanisms.
- This model allows for detailed investigation of the interactions between HU, α7nAChRs, and viral entry processes.
5. Immunoglobulin class switching and glycosylation:
- The acceleration of the IgM to IgG switch, as mentioned earlier, is further elaborated here.
- The additional finding that HU affects immunoglobulin glycosylation is particularly intriguing.
- Glycosylation patterns can significantly influence the functional properties of antibodies, including their inflammatory or anti-inflammatory effects.
6. Anti-inflammatory phenotype:
- The observation that HU-induced changes in glycosylation result in an anti-inflammatory phenotype is significant.
- This could explain the dual action of HU in both enhancing viral defense and modulating excessive inflammation.
In case you or others have questions as to why these discoveries have not been addressed or clarified by our own FDA,CDC, NCATS, NIH agencies, it’s not for lack of effort on our part - 5 yrs of clinical and basic science efforts.
Interesting hypothesis. As fate would have it I studied ACHR in Mark McNamee's lab when I was working towards my biochem/biophys PhD at UC Davis back in the 80s. I'll give your studies all the attention they deserve.
I would greatly enjoy further input, questions and any pertinent references supporting any of our claims as to mechanisms or utility of agonists such as HU, Mr Kelly. Sullray via gmail, the usual addressing. Aside from 5 yrs of collaborative discussions with our partners we’ve had no meaningful dialogues or input with many individuals and research entities. It seems that if a drug cannot generate a significant ROI, it’s not deemed worthy to study or fund. sad to say…..
As it happens I'm also a head & neck cancer survivor. Hydroxyurea was discussed during development of my treatment plan. We did not use it - IIRC the consensus among my treatment team was that the marginal benefit wasn't worth the side effects and associated risks.
I recall that a friend who was diagnosed with CML in his 30s did receive HU as part of his treatment.
It's true that there's little investor appetite to fund new research on older off-patent drugs. The way ivermectin and hydroxychloroquine were oversold and politicized early in the pandemic further depressed investor, as well as investigator, appetite.
As far as I can tell from Google Scholar, there are a number of clinical reports published in the 2020-22 time frame for use of HU against COVID. At least one report states that a small group of hospitalized patients treated with HU (as part of a larger treatment protocol) had a low level of fatalities, but HU neither prevented nor "cured" COVID. I haven't seen any RCTs that evaluated the effect of HU independently.
Turns out my partner is a cell culture expert who founded a successful biotech. When discussing with her she mentioned that Calu-3 cells are a better model for modeling SARS-CoV-2 infection in vitro. I suggested that U373 cells might be used to test hypotheses related to prevention of long COVID brain fog, but your post didn't include any references for the work you cited for me to be able to answer such questions. There is evidence that SARS-CoV-2 can enter U373 cells but the virus doesn't proliferate well or cause apoptosis.
HU is categorized as an antimetabolite and its use over 4 decades has been in the areas of Hematology/oncology. Therein lies a not-so-subtle description that using HU will be automatically high risk. Yet, it is a mainstay drug for sickle cell disease and promoted worldwide for a lifetime of use starting as young as 9 mos of age. The WHO declares it an ESSENTIAL DRUG. There are no studies indicating high risk, only inferences and possibilities. Yes, some people get cutaneous reactions and GI symptoms, but what many fail to appreciate are the multiple pharmacological functions of this simple molecule and how HU benefits the Sickle Cell victim by mitigating many dysfunctions seen with the disease. Similarly, many of the same dysfunctions are evident in COVID19 victims. Our protocol is only 5 days and unless the subject gets another infection with a subsequent mutated virus, the therapy appears to be durable, well-tolerated and there have been no reports of ADRs that were unmanageable. The response is incredibly prompt and durable. HU is used for patients with Polycythemia vera and other myelodysplastic disorders. HU seems to be much maligned and the fiascos with repurposing of HCQ and ivermectin appear to have further denigrated it as a credible therapy. The Clinical reports you may have uncovered probably included 2 with our lead author Foster, M.R.B.. The studies I reviewed of other studies with hospitalized patients were really not well-described in terms of HU prior to admissions nor did the authors provide useful conclusions in my opinion. One study gleaned from a study from the Wisconsin Registry designed for hospital case reports for SCD admissions for COVID19 noted 60 % of admitted patients had taken HU (duration and timing relative the COVID19 not made clear as best I recall. There was not a single death in that cohort as noted in a Table. In our experience with >150 advanced care inpatients admitted to our post-acute illness recovery facility after having received standard of care protocols - respiratory supports only early on then dexamethasone (shotgun dosing and timing early on), then antivirals, monoclonal antibodies, IL-6 inhibitor later, mechanical ventilation, antibacterial, antifungals, etc.. When all of the standard stuff was exhausted and the patient was to the point of comfort care, we admitted a number of them and literally reversed the course of the disease. Bold statements, but the truth. Then word of mouth subsequently led to nearly 2,500 outpatients in all stages to ask for the HU protocol. Same positive outcomes, prompt responses, tolerability, etc. Studies that didn't identify a significant benefit from HU were not well described and not at all like our experiences with inpatients and outpatients from early 2020 thru today. There are no RCT's but it's not for lack of our tremendous efforts to get them. We have no access to such research facilities. I inquired of a PharmD friend, a Director at a local private Pharma research company and was told candidly "There's no money in a generic like HU". My Hospitalist colleague and I entered ~500 case reports based on HIPPA compliant medical encounters into the CURE ID drug repurposing case report system (a consortium of Federal health agencies) to send the FDA a loud and clear signal to validate our experiences yet our efforts failed to do so. The mission of the Cure Drug Repurposing Collaborative was to solicit real world cases as it recognized the urgency for discovery in the pandemic scenario. That mission lasted about 2 yrs then reverted to the traditional time and resource intensive methodology of drug and molecular screening then switched to screening institutional physician's orders to gain a sense of what drugs were ordered for COVID19 victims for inpatient and outpatients. Sadly, the orders were not filtered so the #1 therapy with this latest screen was NaCl by infusion and #2 Oxygen by face mask. A sad commentary as well as a terrible waste of taxpayer's money. Given the success of vaccines and acquired immunity, there aren't huge cohorts of victims to create those gold standard RCT's presently, but that could change as the Fall and Winter patterns re-establish. As for the models for Long Covid and brain fog, we have no such information, only the hypothetical role of the idiotypic antibody network as a possible etiology. We have a few anecdotal cases of LC that support the use of HU as the initial immune modulator followed by the ACh enzyme inhibitor rivastigmine (Exelon, the PD drug). The sequence totally reversed the signs and symptoms of a 60+ yr old Dentist who developed disordered cognizance and dysfunctional eye-hand and muscle controls. He had had severe COVID19 6-8 mos prior to the onset of these physical events that forced him into a temporary medical retirement. Our inpatient experience with very severe post-acute COVID19 victims utilized 3 days of HU followed by cautious titrations up then down with pyridostigmine a more peripherally acting EI. Exelon was deemed to be a safer drug in an outpatient setting. Another patient had a dx of ALS that had progressed to the point of immobility, etc then he got infected with COVID19 and his condition rapidly deteriorated such that he couldn't eat, lost a lot of weight, was incontinent and could hardly speak. Under supervision he was prescribed HU then titrated doses of Exelon and he returned to his previous baseline but over the subsequent months his ALS deteriorated and he succumbed to that.
As for the U373 cells, they express ACE2 receptors and that was the basis for the experiments to incorporate HU in the murine experiments triggering the contiguous a7Rs that prevent the virus' target cell penetration. My Biochemist colleagues can describe it far better than I.
Ref: Biochemical and Biophysical Research Communications
(Potential Role of anti-idiotype responses on the neurological effects of post-acute sequelae of COVID-19 by William Murphy et al UC Davis Sacremento, CA)
I understand your frustration, and more - I feel it.
I've spent the last decade working alongside my partner in the biotech startup world. They built their company around a platform technology that is able to quickly identify all active mRNA promoters in any cell type, and allow individual promoter activity to be tuned up and down.
I know how hard it is to come up with a 30 second "elevator pitch" for a complicated concept, as well as how absolutely critical and necessary it is. After coaching at a biotech accelerator (IndieBio) my partner's group were able to develop a pitch that raised enough capital to keep them operating, develop the tech further, and sign a few deals with clients - all of which led to them being acquired by a larger company.
It doesn't seem like you have a strong pitch for your protocol, and even if you did no pharma large or small is going to come knocking at your door. Your group are on your own as far as validating and publicizing the HU protocol. It seems to me that, at the very least and as a start, you need to submit the results of every case study you're involved in to reputable journals and develop a list of solid publications.
A list of publications along with a strong pitch might get you to the point of being able to raise enough capital to launch a phase 1 RCT. There are contract labs that can set a trial up and recruit, but it would be more convincing and cost effective if you involve a university, med school, or hospital network.
COVID is not going away. Our daughter did end up testing positive yesterday, and we still have no idea when/where she might have been exposed. Nobody is going to type the strain she's carrying, but the currently-circulating KP.3 strain is known to be more infectious and more proliferative in the infected patient. I'm thankful that she (and we) are up-to-date on vaccination - so far her symptoms are extremely mild.
Long COVID may be with us forever. Our family all fell ill in December 2022 - all mild, thanks to vaccines - but in March 2023 my HbA1C rose from under 6 to 8.4, refractive to changes in diet and exercise. We're controlling with medication (SGLT2 and DPP-4 inhibitors) that I may be taking for the rest of my life. I bring up these personal experiences as real-life reasons that I believe developing treatments like your HU protocol still has value.
Thank you for posting references (the second link doesn't work FYI). Yes, U373 expresses ACE2 receptors - IIRC every ectodermal cell type expresses ACE2 (and AChR). The question is, why pick an astrocytoma-derived cell line (a cell type that doesn't proliferate SARS-CoV-2 virus well or show apoptosis in response to viral entry) as an in-vitro model for exploring the effects of HU, except perhaps with respect to inflammatory responses that may or may not be involved in long COVID symptoms.
Finally, with respect to HU side effects - it's well-established that the drug is safe end effective in treatment of sickle cell disease. That doesn't mean it's safe and effective for every possible use.
We didn't use it in treating my cancer because it's known to decrease white cell counts and lower resistance to infection - problematic when the main elements of the treatment protocol were 70+ Gy of radiation and high-dose cisplatinum, and given that HU is not very effective at inhibiting proliferation of squamous cell carcinoma.
Wish more people would speak out like you against the spineless attitude of our public health authorities to make a major effort to obtain and provide more information.
Quick note on the efficacy of masks - I came down with covid-19 a few weeks ago with a 2-week-old baby in the house. I live in WA, where a seemingly wide-spread wave is well under way. Pretty mild case - first day had a bad headache, 3rd day had GI issues, otherwise just tired and a little congested, resolved by day 6. However, I put on an N-95 the moment I tested positive (middle of the night, strong positive) and wore it 24/7 (including sleeping) except eating at the stove with the venting fan turned on for six days, and nobody else in my house (newborn, 4-year-old, spouse) ever got sick or tested positive. Tough timing, it's impossible to isolate when taking care of 2 little kids. But effective, well-fitting masks worn consistently work!
Thanks Donna - wearing an N-95 24/7 is definitely not comfortable or fun, but given how utterly exhausted I was while being sick and getting like 2.5 hours of sleep a night (thanks kids!), I felt like it was a relatively small price to pay to hopefully avoid getting everybody else sick and then having three other sick people to take care of!
Thank you for the update. As you might have heard, Nassau County, NY is voting on a mask ban. Would appreciate some official advocacy from epidemiologists and CDC etc that this is bad public health policy.
One of the problems with masks is they allow criminals to escape identification. Combine a big mask, big sunglasses, loose baggy clothes, and a loose hoodie that comes down to the sunglasses and that person cannot be identified.
studies have shown sunglasses obscure identity more than masks. are legislators attempting to ban sunglasses? no, obviously not. policymakers and police seeking to preserve the hegemony do not want people to mask and protect themselves from disease, because that disrupts the narrative that Covid is over and reinforces that people should be taking precautions, not going out and spending. they see the disabled people most likely to still be masking as an easy target; if they were serious about preventing crime, they would focus time and resources on evidence-based strategies that support communities and reduce the forces that push people towards criminal behavior in the first place.
I did not look at the NBC news video you posted before I made my comment. I just looked at it now. Seems to me this law will most likely be used as an additional charge for somebody caught doing an illegal act. People wearing masks will likely not get charged and fined if they are not doing something wrong. If the police ever did start arresting people who were doing nothing more than wearing a mask, then this law will likely be overturned. And it should be overturned if it is used that way. I predict it will not be used that way.
I disagree with the NY ACLU which stated this in the news story: "This puts people of color and protestors that the government disagrees with in its crosshairs. Police are not health professionals and they should not be in charge of deciding who need a mask and who doesn't."
Why are people of color more in the crosshairs as compared to people not of color? Can you explain that to me? Can anybody?
Next is protestors. Should protesters be able to protest and not reveal their identity? You agree with that? If so, can you explain why? If somebody wants to protest they should be wiling to take responsiblity for what they are doing. We've seen too many protesters committing crimes and hiding behind masks to avoid facing justice for what they did. Long before COVID Antifa wore masks to avoid the justice system for their criminal actions.
do you realize "antifa" stands for anti-fascists? nazis and white supremacists are fascists. are you on their side, or against fascism? because that would make you "antifa." i have seen no evidence of hordes of protesters committing crimes and hiding behind masks to face justice.
So you never heard of antifa people wearing masks before COVID at demonstrations where they did damage. Seems to me you are in your own media bubble, and don't read information that runs counter to your own political beliefs.
"Scott Crow, a former Antifa organizer, told CNN that wearing masks allow Antifa members to become anonymous and “do what we need to do, whether it is illegal or not,” acknowledging that masks are a good way to avoid being caught by police after committing crimes."
The article goes into masking from both sides of the issue. So if you think masks are OK at protests, then you can't object to the Klu Klux Kan wearing their pointy hoods with eye holes and white robes. And you can't object to protesters in the Capitol Building on January 6 who wore masks and costumes to escape being recognized.
I'm not in favor of fascism. But the definition of that word varies, and has changed over time. Now, it's often used as an insulting derogatory term without any real understanding of what the word actually means.
I'm not for fascists and I'm not for communists either.
proud boys also wear masks at their demonstrations. i still think people must be allowed to wear what they want, per the constitution, and tried for their actions, not their appearance.
the definition of fascism hasn’t changed. it remains a far-right, authoritarian, ultranationalist political ideology and movement, characterized by a dictatorial leader, centralized autocracy, militarism, forcible suppression of opposition, belief in a natural social hierarchy, subordination of individual interests for the perceived good of the nation or race, and strong regimentation of society and the economy.
people of color are more in the crosshairs because of embedded police racism, which contributes to vastly higher rates of arrest and harsher sentences for people with darker skintones. people should be allowed to mask while protesting, because it is their first amendment right to dress how they want. not being able to mask while protesting, or facing harsher sentencing for it, is discriminatory against people who have health conditions and must mask, or anyone who does so to avoid sickness. by banning masks, they will no longer be able to exercise their freedom of speech and right to protest.
Well, the guys who wrote the Constitution apparently thought so. Read the Bill of Rights.
Dictatorships, of course, prefer being able to identify their enemies for retribution. Do you agree with that?
"We've seen too many protesters committing crimes and hiding behind masks to avoid facing justice for what they did." Really? How many? Where and when. Show us some hard data. I mean, the jokers who trashed our nation's capitol are now being portrayed as heroes and "hostages" by their fellow fascists (who will certainly spring them from the joint if they get control), but even they have been mostly brought to justice.
Pitiful excuse for an isolated event compared to the consequences of another major COVID19 outbreak, Sir. The economic consequences of loss time at work and the risk of Long Covid for the entire populace are greater concerns. . Everything has risk/benefit and while law enforcement issues are indeed important, relative to a fatal illness or extended disability it’s just an excuse and avoids societal needs. A reality check is in order. Respectfully, MD
My spouse and I were each hit 3 weeks ago in rapid succession with nasty viruses that felt exactly like Covid—all the symptoms, including starting out with the GI stuff, working through the fever, hacking cough and ending with intense fatigue. The catch: neither of us tested positive in repeated tests throughout. Lots of people we know now have Covid. Is there any sign that Covid has mutated to the point that at home testing isn’t picking it up?
Not to sound scary, but depending where you live, summer "flu-like" symptoms can be the result of one of the nasty diseases spread by the same tick responsible for delivering Lyme disease.
Yep, I’ve contracted and been treated for Lyme in the past. Didn’t feel anything like Covid. I sought medical attention for this round right away and our doctors up here take Lyme seriously.
Correct! An added FYI the nymph stage of the offending tick is the size of a poppyseed, as not easily spotted. Please, understand this is not to be intended as 'fear mongering', simply hoping to help inform.
Well, if the multiple tests were negative one would be forced to conclude it was another viral illness. Not sure about all lateral flow antigen tests being equally sensitive and specific. Hopefully you won’t have subsequent events/sequelae.
Thank you for the well wishes (and even the Latin !), but none of it answers my question. I wasn’t really seeking advice about our own illnesses, for which we received in person medical attention from doctors in clinics.
My question, really aimed at an epidemiologist: Is there any sign that Covid has mutated to the point that at home testing isn’t picking it up?
Good question and a virologist and immunologist might have the best/definitive information otherwise an opinion would be guess work at best. I love to see references including obscure journals and communications since the big guys want lots of definitive experimental + clinical stuff with charts and RCT’s, it would appear. It would be helpful if the kit manufacturers would provide such answers but they have other priorities …….
I so appreciate the updated information you wrote during your time off that you deserve & need. I especially value the invaluable advice you give that follows the minimalist CDC recommendations, high risk folks & who Paxlovid would currently be advisable for.
Rest up and sending thanks to your family for giving up some of their precious time with you to help us.
When I was Commissioner of the Texas Department of State Health Services, COVID was my baptism of fire
It is comforting to know that the high(er) levels of population immunity [I, too, prefer that term to "herd" immunity] are protecting more folks from severe disease (hospitalization or death).
Maintaining hospital capacity was our number one priority, since if they had been truly overwhelmed, there would have been no room at the inn for anybody: moms in labor, kids with appendicitis, families in car crashes, people who need stents...you get the picture. Genuine panic would have ensued.
One of my regrets is that I don't think we (I?) made that central goal clear enough to the public. Many ill-educated folks were fixated on the mortality rate and the fact that old and chronically ill folks were the most vulnerable, so why make everybody do stuff that was unfamiliar and very unwelcome?
Well, because we wanted to keep hospitals open for everyone. As you know, nowadays, with the exception of certain truly "elective" surgeries or invasive procedures, everyone who gets admitted to inpatient status needs the resources that only a hospital can offer, lest they risk grave injury or death. Long gone are the days I remember as a kid when my mom would say her friend's doctor admitted her to the hospital "to do some tests."
I worry that our response to COVID is widely misunderstood - "pandemic blindsight" as I call it. Today there are many influential voices that say, "Why did you (the government) make us do all those things we hated? See, everything turned out OK, just like we told you it would. The government is full of stupid liars and if you're smart, you'll do the opposite of what they tell you."
No, it would not have turned out OK if we did nothing. In fact, I believe it would have turned out badly if we had done anything less than what we did. And as for doing the opposite of what is recommended, that is the surest way I know of for turning crisis into catastrophe.
Was response imperfectly human? Of course. Can we learn from it? I hope so, but frankly I think our institutions, leaders and the public would rather just move on.
Thanks for coming out of a break to post this. At our school and child care center in Ann Arbor we are seeing positive Covid tests just this week, after a staff member thought they had a cold but was expereinced asthma type symptoms and went to urgent care where they tested positive for Covid. Then suddenly another five children/staff also started to feel unwell and also tested postive! However, with two year olds with mild Covid symptoms they are returning to childcare and likely spreading it around! Anecdotally, the adults (staff) in our small community compared with the children who have tested positve are faring worse than the little ones. We have had to close one classroom over the last two days because staff are experiencing flu like symptoms with temperatures of 101F etc. and we can't staff that room. Not sure if this is in general what others are seeing? Anyway I expect many of our students now have Covid but with mild to no symptoms they are likely spreading it around. Hope everyone else remains healthy over the summer.
My 70+ year old parents (in northeastern Kansas) waited until late June for boosters to try to be primed for the summer wave (knowing they could get their next, updated booster in November/December). Several pharmacies turned them away, saying they had sent this batch back because of the new updated booster coming in fairly soon. Bummer!
Yes- it’s a challenge to find right now. And nobody has Novavax any more! I have sent patients traveling this summer to get it and they could not find it.
I am not a COVID denialist, I've had it 3 times and the first 2 were nasty, I'm fully vaxxed, etc. BUT... shouldn't we really be treating it like any other respiratory virus at this point? I know elderly and compromised people are at higher risk, but that's true for them for all viruses, and many other things as well! It seems utterly bizarre to stay home for, say, 15 days because you test positive for COVID, when no one does that for ANYTHING else, including flu!
Covid is incredibly contagious, and the lasting effects of infections can be disabling for anyone, not just the elderly and previously health compromised. Long-term conditions triggered by Covid include myalgic encephalomyelitis, which disrupts the body's energy production, can cause gastroparesis, and limits individuals in severe cases to their beds; autonomic conditions like postural orthostatic tachycardia syndrome, which dysregulates essential bodily functions and can cause fainting upon standing, likewise mobility limiting; mast cell activation syndrome, in which anaphylactic shock is triggered by previously innocuous environmental exposures; and "brain fog" leading to difficulty concentrating, thinking, and remembering things, which is caused by brain damage, via the virus's envelope proteins causing neuron death. Infections are also associated with double the risk of type 1 diabetes in children; exacerbated dementia; heightened heart attack and stroke risk; white and gray brain matter loss and changes in brain structure; long-lasting immune dysfunction; hair loss; periodontitis; and more. Based on these and the lack of treatments for Long Covid, it warrants more serious precautions. Vaccination helps lower the risk of long covid, but it does not prevent it, and millions in the US alone have and continue to experience it.
i haven't seen any research that backs up that statement. the flu is associated with increased odds of parkinson's, but not the numerous conditions above. per recent data, covid-associated mortality is 11x that of the flu.
COVID has potential long-term effects and can damage many different organs (brain, heart, lungs) in ways that are not well understood. These long-term effects are much more common than from other viruses. My understanding is that COVID is a vascular disease, rather than a respiratory disease like colds.
COVID19 enters via upper respiratory tract - nasal, sinus, orotracheal areas. Easy access to the frontal lobes of the brain via the olfactory bulbs and likely explains the early loss of smell and taste in some but not all persons infected. Organs that express the ACE2 receptor preferentially bind the virus’ spike protein (S-protein) via the corona’s receptor binding domain (RBD). New experiments from the Palladin Institute’s team of cell biologists/immunologists/biochemists have demonstrated that this viral-host link can be blocked by triggering the ubiquitous and critical neurotransmitter receptor a7NAChR that lie near (contiguous) the host ACE2 receptor, thus behaving as a chaperone (companion) molecule. Efforts to block this interface (ACE2-Viral RBD) have been demonstrated but earlier variants have devised immune escape so that particular avenue has been abandoned until the Palladin group devised their own workaround by enabling (triggering) the contiguous a7receptors by adding the agonist hydroxyUREA. Viral penetration could not be accomplished in mice after activating this receptor, a critical component for mitigating the hyper- inflammatory cytokine response to this viral infection. With regard to COVID19 being a vascular disease, it is a multisystems disease and our working concept is based on the ultimate targets a7Rs found throughout the body including the lining of blood vessels (endothelium). Thus vascular-inflammation (endotheliitis) is among the many pathologies evident in COVID19 and likely the cause of varying degrees of organ dysfunctions in PASC/Long Covid. Antibodies to these critical a7receptors need to be addressed. HU appears to be a key therapeutic but it’s link to the a7Rs remains unexplored except by the Palladin group as promoted by our clinical experiences of the past 5 yrs.
General comment I believe a very large segment of the NA population (USA/Can) we can fix any health problem(s).
What is not appreciated or adequately conveyed, science is often not black & white, constantly evolving. The Covid-19 pandemic originated from a completely new virus, albeit related to 7 other family members. The latter having been infecting the masses for decades/centuries but our immune systems do not generate lasting immunity.
All viruses do this, in fact. I'm saying, it's time to treat COVID like we treat any other illness. Quarantines have significant, damaging consequences, too. (COVID is not a vascular disease, though it may affect the vascular system.)
The 1918 flu wreaked havoc for decades. Lyme is notorious for this (though not a virus), and lots of people get Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) from flu, colds, etc.
Lyme disease is not comparable to the evolving understanding of of 'Long Covid'.
LD's is elevated to fear mongering by celebrates (some with good intensions) & pseudoscience promoters not qualified to spread their version of reality.
Presumably you are describing 15 days over 3 infections? These COVID19 variants are bad actors and if you’re a carrier, have exposures to vulnerables (aged, never vaccinated, immunosuppresed ,etc) you might find experience a bit of guilt if you heard of a loved one contracting COVID19 and the outcome was fatal,I should think.
Katelyn recommends quarantining for up to 15 days, or until you get a negative test. That's ridiculous. I would feel terrible if I infected a compromised loved one with *anything,* but we don't make public health policy based on that.
it is not ridiculous to quarantine until you get a negative test, when testing positive means you still have detectable live virus in your nasopharynx and can infect others. we do make public health policy based on protecting others from lasting damage. it's the same with using seatbelts.
It's not at all like using seatbelts, which costs the driver absolutely nothing. Quarantining for days/weeks when you don't have job security/savings is seriously problematic.
i can understand being financially unable to quarantine for 15 days (although such a failure on the CDC's part, since rest is a large factor in whether or not someone goes on to develop long covid). but that's where high quality masking can help prevent infection-associated damage from spreading, like another commenter described, with continuous use of n95s keeping his family safe while he was infected
Surprised by the airline study you cited for two reasons: First, it is old, pre-vaccine and pre-high community immunity status, thus of questionable relevance to today’s situation. Usually you are pretty good about noting caveats on data and findings. Second, all that being said, I thought that you and others had touted airlines, once in flight and circulating their air through HEPA filters as actually very safe for an enclosed airspace. This study seems to go against that. So, I guess back to masking on the plane, not just in the terminal and boarding area. :-(. All that being said, has any enterprising masters or phd epidemiology candidates done a study involving flight attendants? That would surely provide some useful information.
Dr Bussey, with all due respect, Dr Jetelina clearly described the risk of airflight based upon extended exposure in an enclosed cabin with recirculated air exhaled from cabinmates before the air even gets to HEPA filters. Exactly how long the filters are effective (transcontinental and transnational) and how efficient these HEPA filters can behave removing viral particles has never been determined that I’m aware of. I’m no expert but I’ve been totally immersed in this disorder from a Medical/clinical viewpoint and as a non-remunerated clinical consultant for our collaborations with the Palladin group for over 4 yrs. See my other comments and reference articles addressed to “Meg”
I agree there is no 100% sure answer to the question of risk on aircraft. I will say that during the early days of the pandemic, when people were trying to track individual cases that flew in from overseas, the CDC only cared about (tried to contact) other passengers seated in the immediate vicinity of the index case. Just a few nearby rows worth.
Nothing is perfect wrt a respiratory virus. That's why we had to use every tool in the box to keep COVID to (barely) manageable levels.
I've taken my Aranet4 CO2 monitor on various flights over the past few years, and many airports are ventilated well enough that one can find spots away from others to eat and drink where the reading is in the 600s. Airplanes are another story, though. During boarding, the reading goes up above 1000 very quickly and remains at 1200-1500 throughout the flight. Deplaning is the worst, b/c as soon as ventilation is turned off, it goes above 2000. So no matter how good the air filtration is, if someone infectious is sitting within a few rows from you, which is very likely during a wave, you won't be protected without a mask. On my most recent flight about a month ago from the West Coast, there was a cacophony of coughs every few seconds.
Count me in with those who have Covid right now. I’m in Virginia on vacation but I strongly suspect I picked it up at home in Oregon. I’m 40, significantly overweight, and fully vaccinated. Luckily, it’s hitting like it did the first time I got it…like a yucky cold. It just sucks because I’m on vacation with my mom and sister who I rarely ever get to see, and we’re having to be really creative to keep them well. I THINK my immediate family had it right before me; my husband was a bit sick right before I was and the kids right before him.
Also with the excessive heat and humidity here in Virginia, wearing a mask is awful. I’m doing it, of course, but I’m starting to finally understand why so many southerners are mask-averse.
You wrote: "~20-30% of the U.S. population was infected with Covid-19 this past winter,.." If that's true, then it seems many of them did not even know they had COVID.
You wrote: "For older adults who didn’t get their vaccine this spring, I suggest getting a vaccine now. But do it soon, as we want at least four months between this and the upcoming fall dose, so that it works best.." So you need to get the vaccines at least 4 months apart of they don't work as well? That's hard to understand. Some people reading your blog are getting the vaccines every 4 months, as they have learned the efficacy wears off after 4 months. If that's true, why is the CDC not recommending more frequent vaccines?
You wrote: "Unfortunately, many people cannot afford tests or to miss work for this long." What kind of tests are you talking about? There are very inexpensive tests now that can be done at home. I suspect you can even get free tests from government agencies.
1. Yes, more than 40% of infections these days are asymptomatic.
2. There is no improvement in secondary lines of defense, specifically B-cells (our antibody factories) aren't meaningfully updated. I can clarify in a future post.
3. There are no government tests avaliable anymore, unfortunately. Tests may be getting cheaper, but it still may cost the price of a meal for some people. Cost is a huge barrier to care, especially if they need a lot (for a family or over time.)
Thanks for your reply. I just looked at Amazon. $10 for a 2 tests. That's $5 per test. You can make a decent meal at home for $5. So I get your point.
If a poor person can't afford a test they could go to the emergency department of a hospital and likely get tested there for free. But that takes time off work and transportation costs. I'd like to see free tests handed out at public health departments. If a person takes the time to go there, they are not likely to waste them or throw them away.
emergency room services are rarely free, especially for people without insurance. regularly distributed tests and n95 masks would go so far to help reduce transmission!
Where/when is the 40% of cases are asymptomatic figure from? Is that current? So is there still lots of asymptomatic spread like there was early on? I'm so eager to know the answer to this question and haven't been able to find current information. Thank you!
Appreciate so much that you took time out from a well-earned break to give us this update. I have seen other reports about the current wave, but none of them come close to your level of clarity and high quality of information. Very grateful to you for this and all you do. May the rest of your break be totally fun and covid free.
Thanks for this update!
I’m out there in this wave and trying to follow through with social plans that would be damaging to cancel in terms of friendships and family… but wearing a mask on the plane absolutely works, and bending some behaviors towards caution helps. And yet a well designed, randomized controlled trial of Paxlovid in terms of preventing long covid, and more insidiously the many cumulative Covid related long term outcomes that are piling up like increased cardiovascular disease, cognitive problems, even Parkinson’s -that RCT is just not going to happen. It is too sprawling and hard to capture and expensive I imagine. And yet we have intuitive reasons to continue thinking that early 10 fold reductions of viral load with Paxlovid should help, like Valtrex does with shingles and post herpetic neuralgia, penicillin with scarlet fever, tamiflu for preventing cardiovascular outcomes after influenza, etc. I’m taking it when I’m sick, and I don’t care if it helps reduce my acute symptoms or not. That’s not a relevant proxy for long term benefits at all!
In defense of Paxlovid:
https://mccormickmd.substack.com/p/in-defense-of-paxlovid
I am with you on the Paxlovid and I have made the exact correlation to antivirals for HSV and shingles… I won’t report my personal experience, not very evidence based medicine, but I will indeed tolerate “Paxlovid Mouth” any time the need arises. I have my “kit” that includes sugar free cherry Ludens and they work great.
All my physician colleagues and friends take it when they have had covid. My non medical friends have struggled to get a Rx for it despite being mostly in treatment range.
You are correct Dr McCormick, a large RCT with Paxlovid or Metformin (the latest darling repurposed drug), or even with our unique and effective (anecdotal) HU an a7R agonist will be a hard sell esp in the context of this specific well-studied drug that is dirt cheap and over 4 decades of safety for mitigating similar pathophysiologies seen with the proxy disorder SCD.
Your previous comments about the utility of Claude.ai were well received and a few inquiries led me to a remarkable summary of the results of our 5 yrs of HU study here and abroad:
“This cutting-edge research from Skok et al. at the Palladin Institute. This information provides fascinating insights into the potential mechanisms of hydroxyurea (HU) in preventing SARS-CoV-2 infection and modulating the immune response. Let's break down these findings:
1. HU as a trigger for α7 nicotinic acetylcholine receptors (α7nAChRs):
- The discovery that HU acts as an agonist for α7nAChRs is a significant finding.
- The contiguity of α7nAChRs with ACE2 receptors suggests a novel mechanism for viral entry prevention.
2. Prevention of S-protein RBD binding:
- The demonstration that HU, through its action on α7nAChRs, can prevent the binding of the SARS-CoV-2 spike protein's receptor-binding domain (RBD) to ACE2 is a crucial observation.
- This provides a potential explanation for HU's protective effects against viral infection at the cellular level.
3. α7nAChRs as molecular chaperones:
- The description of α7nAChRs behaving like molecular chaperones adds a new dimension to our understanding of cellular defense mechanisms against viral entry.
- This could open up new avenues for therapeutic interventions targeting these receptors.
4. Studies on human astrocytoma cells (U373):
- The use of U373 cells expressing ACE2 receptors provides a relevant model for studying SARS-CoV-2 infection mechanisms.
- This model allows for detailed investigation of the interactions between HU, α7nAChRs, and viral entry processes.
5. Immunoglobulin class switching and glycosylation:
- The acceleration of the IgM to IgG switch, as mentioned earlier, is further elaborated here.
- The additional finding that HU affects immunoglobulin glycosylation is particularly intriguing.
- Glycosylation patterns can significantly influence the functional properties of antibodies, including their inflammatory or anti-inflammatory effects.
6. Anti-inflammatory phenotype:
- The observation that HU-induced changes in glycosylation result in an anti-inflammatory phenotype is significant.
- This could explain the dual action of HU in both enhancing viral defense and modulating excessive inflammation.
I am currently traveling for a funeral. I spent approximately 2 hours in the Charlotte airport. Aside from me, I saw exactly 2 other people wearing masks. I was the only person wearing a mask on both of my flights. So frustrating.
Interesting, as I just travelled from Texas and there was a surprising number of masks. I figure compliance follows the waves? As well as a number of other complex factors.
I'm on my way to CVS this morning to pick up a handful of tests - our daughter, home from university for over a month, feels like she's coming down with a respiratory bug. We haven't been in any elevated-risk environments over the last few weeks so I'm hopeful this isn't COVID.
I'm irritated that the CDC continues to drop reporting requirements. As far as I'm concerned SARS-CoV-2 has earned its place among mandatory reportable diseases affecting public health.
"COVID fatigue" and "election year" are weak excuses to willfully decrease vigilance. SARS-CoV-2 may never again mutate to a virulent form capable of overwhelming our hospitals with millions of mortalities, but baking a stronger stance of vigilance into our public health matrix is necessary to give us any hope of a more coherent response to the inevitable next pandemic scourge.
Interesting as for us in Michigan (at a child care center and school) Covid is a reportable illness when we have more than 20% of our population with Covid. However we don't have to report individual cases which is now also the case for flu and norovirus! This last spring we were hit very hard by influenza A outbreaks and decimated a whole classroom with 100% infection rate in two classrooms! As I posted above right now our adults are having worse symptoms than the children.
A sound and cogent approach Mr Kelly. The CDC and FDA have “moved on” according to my discussion with a principal involved in the Cure Drug Repurposed Collaborative whose intent was to identify therapies prescribed by real world practitioners and circumvent the financial and time burdens of Pharma R&D. Our clinical efforts and the experiments from our own collaborations with biochemists, cellular Biologists and immunologists have contributed some important knowledge about the targets and mechanisms involved with this mutating virus. Our unique approach and consistent clinical response through every variant infection of the past 5 yrs has yet to move the FDA to validate all of our unique discoveries. The FDA focus and funding has shifted to Long Covid and the emphasis there remains in the realm of prevention by pure antivirals and monoclonals, not the critical neurotransmitters that can be modulated with an agonist like hydroxyCARBAMIDE to re-enable immune dysfunctional a7NAChRs.
A concise summary from Claude.ai:
“This cutting-edge research from Skok et al. at the Palladin Institute… provides fascinating insights into the potential mechanisms of hydroxyurea (HU) in preventing SARS-CoV-2 infection and modulating the immune response. Let's break down these findings:
1. HU as a trigger for α7 nicotinic acetylcholine receptors (α7nAChRs):
- The discovery that HU acts as an agonist for α7nAChRs is a significant finding.
- The contiguity of α7nAChRs with ACE2 receptors suggests a novel mechanism for viral entry prevention.
2. Prevention of S-protein RBD binding:
- The demonstration that HU, through its action on α7nAChRs, can prevent the binding of the SARS-CoV-2 spike protein's receptor-binding domain (RBD) to ACE2 is a crucial observation.
- This provides a potential explanation for HU's protective effects against viral infection at the cellular level.
3. α7nAChRs as molecular chaperones:
- The description of α7nAChRs behaving like molecular chaperones adds a new dimension to our understanding of cellular defense mechanisms against viral entry.
- This could open up new avenues for therapeutic interventions targeting these receptors.
4. Studies on human astrocytoma cells (U373):
- The use of U373 cells expressing ACE2 receptors provides a relevant model for studying SARS-CoV-2 infection mechanisms.
- This model allows for detailed investigation of the interactions between HU, α7nAChRs, and viral entry processes.
5. Immunoglobulin class switching and glycosylation:
- The acceleration of the IgM to IgG switch, as mentioned earlier, is further elaborated here.
- The additional finding that HU affects immunoglobulin glycosylation is particularly intriguing.
- Glycosylation patterns can significantly influence the functional properties of antibodies, including their inflammatory or anti-inflammatory effects.
6. Anti-inflammatory phenotype:
- The observation that HU-induced changes in glycosylation result in an anti-inflammatory phenotype is significant.
- This could explain the dual action of HU in both enhancing viral defense and modulating excessive inflammation.
In case you or others have questions as to why these discoveries have not been addressed or clarified by our own FDA,CDC, NCATS, NIH agencies, it’s not for lack of effort on our part - 5 yrs of clinical and basic science efforts.
Interesting hypothesis. As fate would have it I studied ACHR in Mark McNamee's lab when I was working towards my biochem/biophys PhD at UC Davis back in the 80s. I'll give your studies all the attention they deserve.
I would greatly enjoy further input, questions and any pertinent references supporting any of our claims as to mechanisms or utility of agonists such as HU, Mr Kelly. Sullray via gmail, the usual addressing. Aside from 5 yrs of collaborative discussions with our partners we’ve had no meaningful dialogues or input with many individuals and research entities. It seems that if a drug cannot generate a significant ROI, it’s not deemed worthy to study or fund. sad to say…..
As it happens I'm also a head & neck cancer survivor. Hydroxyurea was discussed during development of my treatment plan. We did not use it - IIRC the consensus among my treatment team was that the marginal benefit wasn't worth the side effects and associated risks.
I recall that a friend who was diagnosed with CML in his 30s did receive HU as part of his treatment.
It's true that there's little investor appetite to fund new research on older off-patent drugs. The way ivermectin and hydroxychloroquine were oversold and politicized early in the pandemic further depressed investor, as well as investigator, appetite.
As far as I can tell from Google Scholar, there are a number of clinical reports published in the 2020-22 time frame for use of HU against COVID. At least one report states that a small group of hospitalized patients treated with HU (as part of a larger treatment protocol) had a low level of fatalities, but HU neither prevented nor "cured" COVID. I haven't seen any RCTs that evaluated the effect of HU independently.
Turns out my partner is a cell culture expert who founded a successful biotech. When discussing with her she mentioned that Calu-3 cells are a better model for modeling SARS-CoV-2 infection in vitro. I suggested that U373 cells might be used to test hypotheses related to prevention of long COVID brain fog, but your post didn't include any references for the work you cited for me to be able to answer such questions. There is evidence that SARS-CoV-2 can enter U373 cells but the virus doesn't proliferate well or cause apoptosis.
HU is categorized as an antimetabolite and its use over 4 decades has been in the areas of Hematology/oncology. Therein lies a not-so-subtle description that using HU will be automatically high risk. Yet, it is a mainstay drug for sickle cell disease and promoted worldwide for a lifetime of use starting as young as 9 mos of age. The WHO declares it an ESSENTIAL DRUG. There are no studies indicating high risk, only inferences and possibilities. Yes, some people get cutaneous reactions and GI symptoms, but what many fail to appreciate are the multiple pharmacological functions of this simple molecule and how HU benefits the Sickle Cell victim by mitigating many dysfunctions seen with the disease. Similarly, many of the same dysfunctions are evident in COVID19 victims. Our protocol is only 5 days and unless the subject gets another infection with a subsequent mutated virus, the therapy appears to be durable, well-tolerated and there have been no reports of ADRs that were unmanageable. The response is incredibly prompt and durable. HU is used for patients with Polycythemia vera and other myelodysplastic disorders. HU seems to be much maligned and the fiascos with repurposing of HCQ and ivermectin appear to have further denigrated it as a credible therapy. The Clinical reports you may have uncovered probably included 2 with our lead author Foster, M.R.B.. The studies I reviewed of other studies with hospitalized patients were really not well-described in terms of HU prior to admissions nor did the authors provide useful conclusions in my opinion. One study gleaned from a study from the Wisconsin Registry designed for hospital case reports for SCD admissions for COVID19 noted 60 % of admitted patients had taken HU (duration and timing relative the COVID19 not made clear as best I recall. There was not a single death in that cohort as noted in a Table. In our experience with >150 advanced care inpatients admitted to our post-acute illness recovery facility after having received standard of care protocols - respiratory supports only early on then dexamethasone (shotgun dosing and timing early on), then antivirals, monoclonal antibodies, IL-6 inhibitor later, mechanical ventilation, antibacterial, antifungals, etc.. When all of the standard stuff was exhausted and the patient was to the point of comfort care, we admitted a number of them and literally reversed the course of the disease. Bold statements, but the truth. Then word of mouth subsequently led to nearly 2,500 outpatients in all stages to ask for the HU protocol. Same positive outcomes, prompt responses, tolerability, etc. Studies that didn't identify a significant benefit from HU were not well described and not at all like our experiences with inpatients and outpatients from early 2020 thru today. There are no RCT's but it's not for lack of our tremendous efforts to get them. We have no access to such research facilities. I inquired of a PharmD friend, a Director at a local private Pharma research company and was told candidly "There's no money in a generic like HU". My Hospitalist colleague and I entered ~500 case reports based on HIPPA compliant medical encounters into the CURE ID drug repurposing case report system (a consortium of Federal health agencies) to send the FDA a loud and clear signal to validate our experiences yet our efforts failed to do so. The mission of the Cure Drug Repurposing Collaborative was to solicit real world cases as it recognized the urgency for discovery in the pandemic scenario. That mission lasted about 2 yrs then reverted to the traditional time and resource intensive methodology of drug and molecular screening then switched to screening institutional physician's orders to gain a sense of what drugs were ordered for COVID19 victims for inpatient and outpatients. Sadly, the orders were not filtered so the #1 therapy with this latest screen was NaCl by infusion and #2 Oxygen by face mask. A sad commentary as well as a terrible waste of taxpayer's money. Given the success of vaccines and acquired immunity, there aren't huge cohorts of victims to create those gold standard RCT's presently, but that could change as the Fall and Winter patterns re-establish. As for the models for Long Covid and brain fog, we have no such information, only the hypothetical role of the idiotypic antibody network as a possible etiology. We have a few anecdotal cases of LC that support the use of HU as the initial immune modulator followed by the ACh enzyme inhibitor rivastigmine (Exelon, the PD drug). The sequence totally reversed the signs and symptoms of a 60+ yr old Dentist who developed disordered cognizance and dysfunctional eye-hand and muscle controls. He had had severe COVID19 6-8 mos prior to the onset of these physical events that forced him into a temporary medical retirement. Our inpatient experience with very severe post-acute COVID19 victims utilized 3 days of HU followed by cautious titrations up then down with pyridostigmine a more peripherally acting EI. Exelon was deemed to be a safer drug in an outpatient setting. Another patient had a dx of ALS that had progressed to the point of immobility, etc then he got infected with COVID19 and his condition rapidly deteriorated such that he couldn't eat, lost a lot of weight, was incontinent and could hardly speak. Under supervision he was prescribed HU then titrated doses of Exelon and he returned to his previous baseline but over the subsequent months his ALS deteriorated and he succumbed to that.
As for the U373 cells, they express ACE2 receptors and that was the basis for the experiments to incorporate HU in the murine experiments triggering the contiguous a7Rs that prevent the virus' target cell penetration. My Biochemist colleagues can describe it far better than I.
Ref: Biochemical and Biophysical Research Communications
https://doi.org/10.1016/j.bbrc.2024.149825
Ref: J of Neuroimmunology (Hydroxyurea interaction with a7nAChR can underlie its therapeutic efficacy upon COVID-19)
http://doi.org/10.1016/i.jneuroim.2023.578244
Ref: International Journal of Biochemistry and Cell Biology
(The role of a7nAChRs in post-acute sequelae of Covid-19)
https://doi.org/10.1016/j.biocel.2024.106519
Ref: Brain Behavior and Immunity
(Potential Role of anti-idiotype responses on the neurological effects of post-acute sequelae of COVID-19 by William Murphy et al UC Davis Sacremento, CA)
https://doi.org/10.1016/j.bbi.2023.12.017 (possibly j.bbi.2023.12017)
I understand your frustration, and more - I feel it.
I've spent the last decade working alongside my partner in the biotech startup world. They built their company around a platform technology that is able to quickly identify all active mRNA promoters in any cell type, and allow individual promoter activity to be tuned up and down.
I know how hard it is to come up with a 30 second "elevator pitch" for a complicated concept, as well as how absolutely critical and necessary it is. After coaching at a biotech accelerator (IndieBio) my partner's group were able to develop a pitch that raised enough capital to keep them operating, develop the tech further, and sign a few deals with clients - all of which led to them being acquired by a larger company.
It doesn't seem like you have a strong pitch for your protocol, and even if you did no pharma large or small is going to come knocking at your door. Your group are on your own as far as validating and publicizing the HU protocol. It seems to me that, at the very least and as a start, you need to submit the results of every case study you're involved in to reputable journals and develop a list of solid publications.
A list of publications along with a strong pitch might get you to the point of being able to raise enough capital to launch a phase 1 RCT. There are contract labs that can set a trial up and recruit, but it would be more convincing and cost effective if you involve a university, med school, or hospital network.
COVID is not going away. Our daughter did end up testing positive yesterday, and we still have no idea when/where she might have been exposed. Nobody is going to type the strain she's carrying, but the currently-circulating KP.3 strain is known to be more infectious and more proliferative in the infected patient. I'm thankful that she (and we) are up-to-date on vaccination - so far her symptoms are extremely mild.
Long COVID may be with us forever. Our family all fell ill in December 2022 - all mild, thanks to vaccines - but in March 2023 my HbA1C rose from under 6 to 8.4, refractive to changes in diet and exercise. We're controlling with medication (SGLT2 and DPP-4 inhibitors) that I may be taking for the rest of my life. I bring up these personal experiences as real-life reasons that I believe developing treatments like your HU protocol still has value.
Thank you for posting references (the second link doesn't work FYI). Yes, U373 expresses ACE2 receptors - IIRC every ectodermal cell type expresses ACE2 (and AChR). The question is, why pick an astrocytoma-derived cell line (a cell type that doesn't proliferate SARS-CoV-2 virus well or show apoptosis in response to viral entry) as an in-vitro model for exploring the effects of HU, except perhaps with respect to inflammatory responses that may or may not be involved in long COVID symptoms.
Finally, with respect to HU side effects - it's well-established that the drug is safe end effective in treatment of sickle cell disease. That doesn't mean it's safe and effective for every possible use.
We didn't use it in treating my cancer because it's known to decrease white cell counts and lower resistance to infection - problematic when the main elements of the treatment protocol were 70+ Gy of radiation and high-dose cisplatinum, and given that HU is not very effective at inhibiting proliferation of squamous cell carcinoma.
Once again, I feel you and wish you luck.
Wish more people would speak out like you against the spineless attitude of our public health authorities to make a major effort to obtain and provide more information.
Quick note on the efficacy of masks - I came down with covid-19 a few weeks ago with a 2-week-old baby in the house. I live in WA, where a seemingly wide-spread wave is well under way. Pretty mild case - first day had a bad headache, 3rd day had GI issues, otherwise just tired and a little congested, resolved by day 6. However, I put on an N-95 the moment I tested positive (middle of the night, strong positive) and wore it 24/7 (including sleeping) except eating at the stove with the venting fan turned on for six days, and nobody else in my house (newborn, 4-year-old, spouse) ever got sick or tested positive. Tough timing, it's impossible to isolate when taking care of 2 little kids. But effective, well-fitting masks worn consistently work!
I’m happy your family was okay thanks to your efforts, and thank you so much for sharing this!
Thanks Donna - wearing an N-95 24/7 is definitely not comfortable or fun, but given how utterly exhausted I was while being sick and getting like 2.5 hours of sleep a night (thanks kids!), I felt like it was a relatively small price to pay to hopefully avoid getting everybody else sick and then having three other sick people to take care of!
They certainly have for us.
Thank you for the update. As you might have heard, Nassau County, NY is voting on a mask ban. Would appreciate some official advocacy from epidemiologists and CDC etc that this is bad public health policy.
www.nbcnewyork.com/news/politics/long-island-bill-jail-time-fines-face-masks-nassau-county/5588110/
One of the problems with masks is they allow criminals to escape identification. Combine a big mask, big sunglasses, loose baggy clothes, and a loose hoodie that comes down to the sunglasses and that person cannot be identified.
studies have shown sunglasses obscure identity more than masks. are legislators attempting to ban sunglasses? no, obviously not. policymakers and police seeking to preserve the hegemony do not want people to mask and protect themselves from disease, because that disrupts the narrative that Covid is over and reinforces that people should be taking precautions, not going out and spending. they see the disabled people most likely to still be masking as an easy target; if they were serious about preventing crime, they would focus time and resources on evidence-based strategies that support communities and reduce the forces that push people towards criminal behavior in the first place.
I did not look at the NBC news video you posted before I made my comment. I just looked at it now. Seems to me this law will most likely be used as an additional charge for somebody caught doing an illegal act. People wearing masks will likely not get charged and fined if they are not doing something wrong. If the police ever did start arresting people who were doing nothing more than wearing a mask, then this law will likely be overturned. And it should be overturned if it is used that way. I predict it will not be used that way.
I disagree with the NY ACLU which stated this in the news story: "This puts people of color and protestors that the government disagrees with in its crosshairs. Police are not health professionals and they should not be in charge of deciding who need a mask and who doesn't."
Why are people of color more in the crosshairs as compared to people not of color? Can you explain that to me? Can anybody?
Next is protestors. Should protesters be able to protest and not reveal their identity? You agree with that? If so, can you explain why? If somebody wants to protest they should be wiling to take responsiblity for what they are doing. We've seen too many protesters committing crimes and hiding behind masks to avoid facing justice for what they did. Long before COVID Antifa wore masks to avoid the justice system for their criminal actions.
do you realize "antifa" stands for anti-fascists? nazis and white supremacists are fascists. are you on their side, or against fascism? because that would make you "antifa." i have seen no evidence of hordes of protesters committing crimes and hiding behind masks to face justice.
So you never heard of antifa people wearing masks before COVID at demonstrations where they did damage. Seems to me you are in your own media bubble, and don't read information that runs counter to your own political beliefs.
Here's an article on it: https://bigthink.com/the-present/antifa-mask-law/
"Scott Crow, a former Antifa organizer, told CNN that wearing masks allow Antifa members to become anonymous and “do what we need to do, whether it is illegal or not,” acknowledging that masks are a good way to avoid being caught by police after committing crimes."
The article goes into masking from both sides of the issue. So if you think masks are OK at protests, then you can't object to the Klu Klux Kan wearing their pointy hoods with eye holes and white robes. And you can't object to protesters in the Capitol Building on January 6 who wore masks and costumes to escape being recognized.
I'm not in favor of fascism. But the definition of that word varies, and has changed over time. Now, it's often used as an insulting derogatory term without any real understanding of what the word actually means.
I'm not for fascists and I'm not for communists either.
proud boys also wear masks at their demonstrations. i still think people must be allowed to wear what they want, per the constitution, and tried for their actions, not their appearance.
the definition of fascism hasn’t changed. it remains a far-right, authoritarian, ultranationalist political ideology and movement, characterized by a dictatorial leader, centralized autocracy, militarism, forcible suppression of opposition, belief in a natural social hierarchy, subordination of individual interests for the perceived good of the nation or race, and strong regimentation of society and the economy.
I doubt that the gentleman in question needs evidence.
people of color are more in the crosshairs because of embedded police racism, which contributes to vastly higher rates of arrest and harsher sentences for people with darker skintones. people should be allowed to mask while protesting, because it is their first amendment right to dress how they want. not being able to mask while protesting, or facing harsher sentencing for it, is discriminatory against people who have health conditions and must mask, or anyone who does so to avoid sickness. by banning masks, they will no longer be able to exercise their freedom of speech and right to protest.
Well, the guys who wrote the Constitution apparently thought so. Read the Bill of Rights.
Dictatorships, of course, prefer being able to identify their enemies for retribution. Do you agree with that?
"We've seen too many protesters committing crimes and hiding behind masks to avoid facing justice for what they did." Really? How many? Where and when. Show us some hard data. I mean, the jokers who trashed our nation's capitol are now being portrayed as heroes and "hostages" by their fellow fascists (who will certainly spring them from the joint if they get control), but even they have been mostly brought to justice.
Pitiful excuse for an isolated event compared to the consequences of another major COVID19 outbreak, Sir. The economic consequences of loss time at work and the risk of Long Covid for the entire populace are greater concerns. . Everything has risk/benefit and while law enforcement issues are indeed important, relative to a fatal illness or extended disability it’s just an excuse and avoids societal needs. A reality check is in order. Respectfully, MD
My spouse and I were each hit 3 weeks ago in rapid succession with nasty viruses that felt exactly like Covid—all the symptoms, including starting out with the GI stuff, working through the fever, hacking cough and ending with intense fatigue. The catch: neither of us tested positive in repeated tests throughout. Lots of people we know now have Covid. Is there any sign that Covid has mutated to the point that at home testing isn’t picking it up?
Thanks for all your work and this substack!
Not to sound scary, but depending where you live, summer "flu-like" symptoms can be the result of one of the nasty diseases spread by the same tick responsible for delivering Lyme disease.
Yep, I’ve contracted and been treated for Lyme in the past. Didn’t feel anything like Covid. I sought medical attention for this round right away and our doctors up here take Lyme seriously.
But you have to be bit by a tick to get those diseases, right?
Correct! An added FYI the nymph stage of the offending tick is the size of a poppyseed, as not easily spotted. Please, understand this is not to be intended as 'fear mongering', simply hoping to help inform.
Respectfully, JJF
Well, if the multiple tests were negative one would be forced to conclude it was another viral illness. Not sure about all lateral flow antigen tests being equally sensitive and specific. Hopefully you won’t have subsequent events/sequelae.
Thank you for the well wishes (and even the Latin !), but none of it answers my question. I wasn’t really seeking advice about our own illnesses, for which we received in person medical attention from doctors in clinics.
My question, really aimed at an epidemiologist: Is there any sign that Covid has mutated to the point that at home testing isn’t picking it up?
Good question and a virologist and immunologist might have the best/definitive information otherwise an opinion would be guess work at best. I love to see references including obscure journals and communications since the big guys want lots of definitive experimental + clinical stuff with charts and RCT’s, it would appear. It would be helpful if the kit manufacturers would provide such answers but they have other priorities …….
@Jenny: By chance did you try different tests to double-check those negative ones?
Sure did, we each tested four times and we also spaced them out over a number of days well into the couple of weeks we were sick.
🫶🏼🫶🏼🫶🏼
I so appreciate the updated information you wrote during your time off that you deserve & need. I especially value the invaluable advice you give that follows the minimalist CDC recommendations, high risk folks & who Paxlovid would currently be advisable for.
Rest up and sending thanks to your family for giving up some of their precious time with you to help us.
When I was Commissioner of the Texas Department of State Health Services, COVID was my baptism of fire
It is comforting to know that the high(er) levels of population immunity [I, too, prefer that term to "herd" immunity] are protecting more folks from severe disease (hospitalization or death).
Maintaining hospital capacity was our number one priority, since if they had been truly overwhelmed, there would have been no room at the inn for anybody: moms in labor, kids with appendicitis, families in car crashes, people who need stents...you get the picture. Genuine panic would have ensued.
One of my regrets is that I don't think we (I?) made that central goal clear enough to the public. Many ill-educated folks were fixated on the mortality rate and the fact that old and chronically ill folks were the most vulnerable, so why make everybody do stuff that was unfamiliar and very unwelcome?
Well, because we wanted to keep hospitals open for everyone. As you know, nowadays, with the exception of certain truly "elective" surgeries or invasive procedures, everyone who gets admitted to inpatient status needs the resources that only a hospital can offer, lest they risk grave injury or death. Long gone are the days I remember as a kid when my mom would say her friend's doctor admitted her to the hospital "to do some tests."
I worry that our response to COVID is widely misunderstood - "pandemic blindsight" as I call it. Today there are many influential voices that say, "Why did you (the government) make us do all those things we hated? See, everything turned out OK, just like we told you it would. The government is full of stupid liars and if you're smart, you'll do the opposite of what they tell you."
No, it would not have turned out OK if we did nothing. In fact, I believe it would have turned out badly if we had done anything less than what we did. And as for doing the opposite of what is recommended, that is the surest way I know of for turning crisis into catastrophe.
Was response imperfectly human? Of course. Can we learn from it? I hope so, but frankly I think our institutions, leaders and the public would rather just move on.
Thanks for coming out of a break to post this. At our school and child care center in Ann Arbor we are seeing positive Covid tests just this week, after a staff member thought they had a cold but was expereinced asthma type symptoms and went to urgent care where they tested positive for Covid. Then suddenly another five children/staff also started to feel unwell and also tested postive! However, with two year olds with mild Covid symptoms they are returning to childcare and likely spreading it around! Anecdotally, the adults (staff) in our small community compared with the children who have tested positve are faring worse than the little ones. We have had to close one classroom over the last two days because staff are experiencing flu like symptoms with temperatures of 101F etc. and we can't staff that room. Not sure if this is in general what others are seeing? Anyway I expect many of our students now have Covid but with mild to no symptoms they are likely spreading it around. Hope everyone else remains healthy over the summer.
My 70+ year old parents (in northeastern Kansas) waited until late June for boosters to try to be primed for the summer wave (knowing they could get their next, updated booster in November/December). Several pharmacies turned them away, saying they had sent this batch back because of the new updated booster coming in fairly soon. Bummer!
Yes- it’s a challenge to find right now. And nobody has Novavax any more! I have sent patients traveling this summer to get it and they could not find it.
I am not a COVID denialist, I've had it 3 times and the first 2 were nasty, I'm fully vaxxed, etc. BUT... shouldn't we really be treating it like any other respiratory virus at this point? I know elderly and compromised people are at higher risk, but that's true for them for all viruses, and many other things as well! It seems utterly bizarre to stay home for, say, 15 days because you test positive for COVID, when no one does that for ANYTHING else, including flu!
Covid is incredibly contagious, and the lasting effects of infections can be disabling for anyone, not just the elderly and previously health compromised. Long-term conditions triggered by Covid include myalgic encephalomyelitis, which disrupts the body's energy production, can cause gastroparesis, and limits individuals in severe cases to their beds; autonomic conditions like postural orthostatic tachycardia syndrome, which dysregulates essential bodily functions and can cause fainting upon standing, likewise mobility limiting; mast cell activation syndrome, in which anaphylactic shock is triggered by previously innocuous environmental exposures; and "brain fog" leading to difficulty concentrating, thinking, and remembering things, which is caused by brain damage, via the virus's envelope proteins causing neuron death. Infections are also associated with double the risk of type 1 diabetes in children; exacerbated dementia; heightened heart attack and stroke risk; white and gray brain matter loss and changes in brain structure; long-lasting immune dysfunction; hair loss; periodontitis; and more. Based on these and the lack of treatments for Long Covid, it warrants more serious precautions. Vaccination helps lower the risk of long covid, but it does not prevent it, and millions in the US alone have and continue to experience it.
Everything you're describing is also caused by other illnesses! Including the flu!
i haven't seen any research that backs up that statement. the flu is associated with increased odds of parkinson's, but not the numerous conditions above. per recent data, covid-associated mortality is 11x that of the flu.
I'd like to see how you reached that conclusion, e.g. evidence.
COVID has potential long-term effects and can damage many different organs (brain, heart, lungs) in ways that are not well understood. These long-term effects are much more common than from other viruses. My understanding is that COVID is a vascular disease, rather than a respiratory disease like colds.
COVID19 enters via upper respiratory tract - nasal, sinus, orotracheal areas. Easy access to the frontal lobes of the brain via the olfactory bulbs and likely explains the early loss of smell and taste in some but not all persons infected. Organs that express the ACE2 receptor preferentially bind the virus’ spike protein (S-protein) via the corona’s receptor binding domain (RBD). New experiments from the Palladin Institute’s team of cell biologists/immunologists/biochemists have demonstrated that this viral-host link can be blocked by triggering the ubiquitous and critical neurotransmitter receptor a7NAChR that lie near (contiguous) the host ACE2 receptor, thus behaving as a chaperone (companion) molecule. Efforts to block this interface (ACE2-Viral RBD) have been demonstrated but earlier variants have devised immune escape so that particular avenue has been abandoned until the Palladin group devised their own workaround by enabling (triggering) the contiguous a7receptors by adding the agonist hydroxyUREA. Viral penetration could not be accomplished in mice after activating this receptor, a critical component for mitigating the hyper- inflammatory cytokine response to this viral infection. With regard to COVID19 being a vascular disease, it is a multisystems disease and our working concept is based on the ultimate targets a7Rs found throughout the body including the lining of blood vessels (endothelium). Thus vascular-inflammation (endotheliitis) is among the many pathologies evident in COVID19 and likely the cause of varying degrees of organ dysfunctions in PASC/Long Covid. Antibodies to these critical a7receptors need to be addressed. HU appears to be a key therapeutic but it’s link to the a7Rs remains unexplored except by the Palladin group as promoted by our clinical experiences of the past 5 yrs.
Ref: Biochemical and Biophysical Research Communications https://doi:org/10.1016/j.bbrc.2024.149825.
Ref: International J of Biochemistry and Cell Biology
https://doi.org/10.1016//j.biocel.2024/.106519
Thanks for the detailed info.
General comment I believe a very large segment of the NA population (USA/Can) we can fix any health problem(s).
What is not appreciated or adequately conveyed, science is often not black & white, constantly evolving. The Covid-19 pandemic originated from a completely new virus, albeit related to 7 other family members. The latter having been infecting the masses for decades/centuries but our immune systems do not generate lasting immunity.
All viruses do this, in fact. I'm saying, it's time to treat COVID like we treat any other illness. Quarantines have significant, damaging consequences, too. (COVID is not a vascular disease, though it may affect the vascular system.)
it is not time until we have cures for Long Covid. the impacts of quarantines pale in comparison to lifelong conditions and disability. covid spreads via aerosols and droplets like a respiratory condition, but experts do characterize it as a neurovascular disease https://www.scientificamerican.com/article/long-covid-now-looks-like-a-neurological-disease-helping-doctors-to-focus-treatments1/
I am not aware that other viruses do this (I'm not a scientist). If they do, it certainly seems like it's at a much lower rate than from COVID.
The 1918 flu wreaked havoc for decades. Lyme is notorious for this (though not a virus), and lots of people get Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) from flu, colds, etc.
Lyme disease is not comparable to the evolving understanding of of 'Long Covid'.
LD's is elevated to fear mongering by celebrates (some with good intensions) & pseudoscience promoters not qualified to spread their version of reality.
For a well presented discussion see Dr. Andrea Love, PhD discussion https://immunologic.substack.com/account
Presumably you are describing 15 days over 3 infections? These COVID19 variants are bad actors and if you’re a carrier, have exposures to vulnerables (aged, never vaccinated, immunosuppresed ,etc) you might find experience a bit of guilt if you heard of a loved one contracting COVID19 and the outcome was fatal,I should think.
Katelyn recommends quarantining for up to 15 days, or until you get a negative test. That's ridiculous. I would feel terrible if I infected a compromised loved one with *anything,* but we don't make public health policy based on that.
it is not ridiculous to quarantine until you get a negative test, when testing positive means you still have detectable live virus in your nasopharynx and can infect others. we do make public health policy based on protecting others from lasting damage. it's the same with using seatbelts.
It's not at all like using seatbelts, which costs the driver absolutely nothing. Quarantining for days/weeks when you don't have job security/savings is seriously problematic.
i can understand being financially unable to quarantine for 15 days (although such a failure on the CDC's part, since rest is a large factor in whether or not someone goes on to develop long covid). but that's where high quality masking can help prevent infection-associated damage from spreading, like another commenter described, with continuous use of n95s keeping his family safe while he was infected
I never said don't mask.
And we could all do better at how we interact with the world when we're sick, regardless of what contagion we have.
And America is terrible at providing for people to stay home when sick, and get rest etc.
Um, she specifically said that one should wear an N95 mask if unable to quarantine.
Also, current public policy (per the CDC) does NOT follow her recommendations, so I'm not even sure what the issue is.
Surprised by the airline study you cited for two reasons: First, it is old, pre-vaccine and pre-high community immunity status, thus of questionable relevance to today’s situation. Usually you are pretty good about noting caveats on data and findings. Second, all that being said, I thought that you and others had touted airlines, once in flight and circulating their air through HEPA filters as actually very safe for an enclosed airspace. This study seems to go against that. So, I guess back to masking on the plane, not just in the terminal and boarding area. :-(. All that being said, has any enterprising masters or phd epidemiology candidates done a study involving flight attendants? That would surely provide some useful information.
Dr Bussey, with all due respect, Dr Jetelina clearly described the risk of airflight based upon extended exposure in an enclosed cabin with recirculated air exhaled from cabinmates before the air even gets to HEPA filters. Exactly how long the filters are effective (transcontinental and transnational) and how efficient these HEPA filters can behave removing viral particles has never been determined that I’m aware of. I’m no expert but I’ve been totally immersed in this disorder from a Medical/clinical viewpoint and as a non-remunerated clinical consultant for our collaborations with the Palladin group for over 4 yrs. See my other comments and reference articles addressed to “Meg”
I agree there is no 100% sure answer to the question of risk on aircraft. I will say that during the early days of the pandemic, when people were trying to track individual cases that flew in from overseas, the CDC only cared about (tried to contact) other passengers seated in the immediate vicinity of the index case. Just a few nearby rows worth.
Nothing is perfect wrt a respiratory virus. That's why we had to use every tool in the box to keep COVID to (barely) manageable levels.
Here is Dr. Jetelina discussing airline filtration. https://slate.com/technology/2022/04/covid-airplane-transmission-rip-mask-mandate.html. My take from that was that, as the article said, transmission was much lower than expected.
What month will the newest Covid vaccine be released?
Yep. Been watching those waste water numbers... Am flying from Atlanta to Buffalo for bike trip. Airport CO2 in concourse is 1200! Mask up!
I've taken my Aranet4 CO2 monitor on various flights over the past few years, and many airports are ventilated well enough that one can find spots away from others to eat and drink where the reading is in the 600s. Airplanes are another story, though. During boarding, the reading goes up above 1000 very quickly and remains at 1200-1500 throughout the flight. Deplaning is the worst, b/c as soon as ventilation is turned off, it goes above 2000. So no matter how good the air filtration is, if someone infectious is sitting within a few rows from you, which is very likely during a wave, you won't be protected without a mask. On my most recent flight about a month ago from the West Coast, there was a cacophony of coughs every few seconds.
Thank you for the air reading!
Count me in with those who have Covid right now. I’m in Virginia on vacation but I strongly suspect I picked it up at home in Oregon. I’m 40, significantly overweight, and fully vaccinated. Luckily, it’s hitting like it did the first time I got it…like a yucky cold. It just sucks because I’m on vacation with my mom and sister who I rarely ever get to see, and we’re having to be really creative to keep them well. I THINK my immediate family had it right before me; my husband was a bit sick right before I was and the kids right before him.
Also with the excessive heat and humidity here in Virginia, wearing a mask is awful. I’m doing it, of course, but I’m starting to finally understand why so many southerners are mask-averse.
You wrote: "~20-30% of the U.S. population was infected with Covid-19 this past winter,.." If that's true, then it seems many of them did not even know they had COVID.
You wrote: "For older adults who didn’t get their vaccine this spring, I suggest getting a vaccine now. But do it soon, as we want at least four months between this and the upcoming fall dose, so that it works best.." So you need to get the vaccines at least 4 months apart of they don't work as well? That's hard to understand. Some people reading your blog are getting the vaccines every 4 months, as they have learned the efficacy wears off after 4 months. If that's true, why is the CDC not recommending more frequent vaccines?
You wrote: "Unfortunately, many people cannot afford tests or to miss work for this long." What kind of tests are you talking about? There are very inexpensive tests now that can be done at home. I suspect you can even get free tests from government agencies.
Hi Doug- Great questions.
1. Yes, more than 40% of infections these days are asymptomatic.
2. There is no improvement in secondary lines of defense, specifically B-cells (our antibody factories) aren't meaningfully updated. I can clarify in a future post.
3. There are no government tests avaliable anymore, unfortunately. Tests may be getting cheaper, but it still may cost the price of a meal for some people. Cost is a huge barrier to care, especially if they need a lot (for a family or over time.)
Thanks for your reply. I just looked at Amazon. $10 for a 2 tests. That's $5 per test. You can make a decent meal at home for $5. So I get your point.
If a poor person can't afford a test they could go to the emergency department of a hospital and likely get tested there for free. But that takes time off work and transportation costs. I'd like to see free tests handed out at public health departments. If a person takes the time to go there, they are not likely to waste them or throw them away.
emergency room services are rarely free, especially for people without insurance. regularly distributed tests and n95 masks would go so far to help reduce transmission!
Where/when is the 40% of cases are asymptomatic figure from? Is that current? So is there still lots of asymptomatic spread like there was early on? I'm so eager to know the answer to this question and haven't been able to find current information. Thank you!