And this was known to be a problem a year ago and Merck kept pushing it forward despite its low efficacy and risk for driving mutation. Meanwhile Paxlovid is underprescribed despite its effectiveness.
As I understand it, part of the issue is that Paxlovid interacts with a large number of other medications. This is a problem because people at high risk of dying from Covid tend to have preexisting medical conditions, and thus are more likely to take medications that interact with Paxlovid.
Most of the interactions can be managed, but I think the message got out among primary care docs there are drug interactions and so they get scared to prescribe it. There are relatively few meds that are absolutely contraindicated, while there's a large list of meds that require some dose adjustment or holding the med for a few days. This is an issue with the ritonavir in the paxlovid, which has been extensively used in HIV treatment -- so, this isn't a new issue that we know nothing about.
And then I've heard from too many patients their doctor doesn't think they need it because they're not that sick, so it's not worth managing the drug interactions. Unfortunately, paxlovid needs to be started within five days of symptom onset, but most patients aren't going to be hospitalized within those first five days.
Given the lack of monoclonal antibodies, the potential mutagenic effect of molupiravir, and the less-than-steller impact of remdesivir... if I or someone I loved got covid, I'd be jumping on paxlovid since there aren't many other options right now.
The medical system in the US is optimized to get people in, bill them, and get them out; that's it. Managing drug interactions is a long tail process that requires critical thinking, which is not an incentiviced activity. Plenty of startups have failed thinking that they could succeed if their products resulted in improvements to quality of care.
Managing drug interactions for paxlovid isn't much more complicated than inputting meds into a web form and looking at the color of the box that pops up after. I think most providers can handle that if they know these tools exist and get past the reflex of "paxlovid has drug interactions, you don't want to take it."
Managing drug interactions is part of ordering medications, and if it's really taking that much time (i.e., the EHR isn't just doing all the work for you), then it'd result in a higher E&M code when it's billed out. Medication management, in some cases, can also be billed and reimbursed by the pharmacist.
So, totally agree that the US medical system is optimized for billing. I don't think those of us in the US should be ok with that, and I don't think it's an excuse in this case to not prescribe paxlovid to patients who want it and would qualify for it.
Sure, in the abstract it is straight forward, but you quickly run into data gaps when considering multiple medications. Particularly in the context of comorbidities.
Medical professionals are overwhelmed, so you can't hospitalize these patients to monitor their compliance. And this is, in the large, not a demographic you can trust for maximal patient compliance.
By the medical professional who is prescribing paxlovid. When I wrote "can be managed", I mean the health care provider tells the patient to either stop taking their other meds for 5-7 days, to reduce the dose, or to look out for symptoms and call them if they have certain issues. Not be hospitalized to watch for side effects. You can look for yourself at the list of common meds, and the ones that are absolutely contraindicated are relatively few:
https://www.covid19treatmentguidelines.nih.gov/therapies/ant...
One's ability to "trust" a patient isn't a factor here, and is, frankly, pretty condescending. The patient and provider have aligned interests, it's just a matter of ensuring the provider is making sure the patient understands what's going on. The provider should be doing that in all of their encounters, so that's nothing specific to paxlovid.
> One's ability to "trust" a patient isn't a factor here, and is, frankly, pretty condescending.
I suspect you haven't worked with elderly patients.
I help a relative manage his care. I keep having to hide the DayQuil so he doesn't take it alongside his arthritis medication and overdose on acetamenophin. He "knows" he's not supposed to, but it doesn't click when the pills are in his hand and his nose is running (because he took it for decades prior to the arthritis prescription and deeply-ingrained habits are not easily replaced). He definitely tells the doctor he understands, and the doctor believes him, but it's not like the doctor is in any way responsible for verifying that information.
Drug interactions are way past the maximum complexity capacity of the median patient at high risk for death by COVID.
I spent a decade working in a nursing home before becoming an epidemiologist, so definitely have worked with elderly patients. Not to mention my own experiences with elderly family members.
> but it's not like the doctor is in any way responsible for verifying that information.
Yeah, that's the exact point. Everybody does things that the doctor says they shouldn't, but that doesn't mean we withhold care as a result.
People stop antibiotics before the scripts are done. People smoke and drink too much, some even drink and drive. People don't take their blood pressure or cholesterol or even HIV meds as prescribed. Some people take half a pill because the pill they were prescribed is "too big" -- people are weird and do all kinds of things.
Paxlovid is no different. The provider can be checking drug interactions, making adjustments as needed and counseling the patient. That's their job. They can't babysit the patient all of the time. If it's clear the patient doesn't understand and can't care for themselves, then there are larger conversations to be had.
My point is that deciding not to prescribe a medication to a qualifying patient because it generally has too many drug interactions and patients can't be trusted with their health is not ok. Patients don't need to understand that ritonavir is a protease inhibitor that was incidentally found to inhibit cytochrome P450-3A4, which subsequently boosts the levels of many other medications. They just need to know to stop taking their cholesterol pill for the next week. That's all. Some, like your elderly relative, may not be able to follow that direction. But there are millions of high risk people who are able to do that, and shouldn't be denied care based on the assumption they're incompetent.
Didn't we restrict Sudafed because people can cook it into meth and change the painkiller regiment because of opioid addiction? I don't think the rule "we don't refrain from prescribing a drug because some users won't be able to use it responsibly" is universal.
Yes, there are levels of controlled substances based on, among other things, their abuse potential. That's not what we're talking about here because paxlovid is not a controlled substance.
If you're going to construct a new strawman argument, don't make up quotes that I never wrote. I also have a lot of thoughts about how controlled substance laws create problems and harm patients. But I'll stick to the main point of this thread: paxlovid drug interactions are easily checked and managed for the majority of patients, and should not be a reason for providers to reflexively deny prescription requests for it.
What if that someone you love is young and in good health? Paxlovid has some significant side effects and is only recommended for patients at high risk of severe COVID-19 due to advanced age or other risk factors.
I think this is where many providers get mixed up. It's for "mild-to-moderate" COVID-19 (i.e., "you're not sick enough yet" isn't at play, because then you have "mild" covid which is exactly what paxlovid is indicated for) who are at "high risk for progression to severe COVID-19."
According to the CDC, risk factors that make you at "high risk" include being over 50, having a mood disorder (including anxiety and depression), being obese or overweight, being physically inactive, being a current or former smoker, or having asthma:
https://www.cdc.gov/coronavirus/2019-ncov/hcp/clinical-care/...
Most Americans would check one of those boxes, even the healthy and young among us. And some of those (e.g., "physically inactive") are pretty ill-defined that you could argue even more fit in that category. Just saying you're anxious about covid outcomes should qualify you for paxlovid because anxiety is a risk factor.
Many of the infectious disease doctors I work with think that paxlovid should be offered to virtually everybody because it seems to decrease your viral load (this could decrease the chance of onward transmission), there may be a decrease in risk of long covid, it may shorten your symptom duration, and there aren't many other treatment options if you get sicker. So, short of being on one of the medications that's absolutely contraindicated, their opinion is generally if you want paxlovid you should get it.
So if your doctor is saying you don't need it or don't qualify, and you want to take it, I would find a different doctor or use a telemedicine provider.
yeah people in my house hold are getting covid a couple of times a year and are constantly exposed to it at school and work and we are all vaccinated but dont take any other medications for covid.
There are renal dosing standards for paxlovid. So if you have not-great kidneys, they just give you a different dose. Covid can also cause kidney damage, and kidney issues are associated with worse outcomes from covid. So, it's all a bit of a double edged sword.
Similar to my two experiences with antibiotics. Relief after half a day, clear reversal of illness by the next, after that only lingering discomfort to heal from the damage caused.
When I was living in SE Asia, I had really bad stomach issues quite often. One time was worse than ever. Went to a local pharmacy and they gave me some pill. Took it and literally hours later, I was fine. I remember looking it up and it was something developed in the 60's that wasn't used in the US any longer... but wow, it worked like magic.
I was recently reading about a drug called ibogaine - which is apparently pretty effective at treating opioid addiction, but is illegal in the US. The drug is prescribed in New Zealand, and the studies I saw made it look like a miracle cure (for most but not all patients).
Infuriating that, in the midst of the opioid crisis, the government wouldn't even consider permitting safe and effective treatment.
You do a disservice to legalization efforts by ignoring the fact that you are discussing a powerful psychedelic. I am all for legalization efforts, but it is important to be clear and upfront about what we are talking about. Tangental to your point; I wonder if the US would currently be facing such an extreme and distressing methamphetamine epidemic if ephedra were still available (recognizing the obvious catch 22 here, as ephedrine is famously used in a variety of stimulant manufacture)
It has a very high rate of serious side effects, and the psychedelic affect makes it worse because already unreliable people (drug addicts) get even more unreliable.
No it doesn't. Everything I've read indicates it's pretty safe with minimal to no serious side effects. Other psychedelics are legal in the US even for recreational use (e.g. Salvia) - so I don't see what the relevance is.
If I google that phrase I get a case study of a man who died after injecting himself with "4 g of ibogaine and 2 g of an uncharacterized ‘booster’ that he bought on the Internet" [1]. On the other hand, there are treatment centers using ibogaine that have been open for decades worldwide. That source also mentions a clinic in the Netherlands that has used ibogaine for approximately 5,000 cases.
This paper [2] is a review of deaths associated with ibogaine known to the authors. They contacted different clinics around the world known to use ibogaine. They found 19 deaths over an 18 year period. 14 of these deaths had post-mortem data and 12 of the 14 had clear comorbidities that likely substantially contributed (e.g. also using heroin and meth, or having severe heart problems already).
You can find a number of papers[3], here is one for example, where no side effects are reported for ibogaine - "In two Phase 1 studies using very low doses, single 20 mg doses of ibogaine were well tolerated (N = 21), with no effect on vital signs and no adverse effects". And, here is the conclusion of that paper, just for fun - "A single ibogaine treatment reduced opioid withdrawal symptoms and achieved opioid cessation or sustained reduced use in dependent individuals as measured over 12 months".
Even if those were valid side effects, you'd still have to put them in context - being an opiod addict is likely much riskier than taking a one time dose of ibogaine in a clinical setting with a doctor's supervision. Net - ibogaine treatment is negative side effect.
The state of medical care in the US is such that the regulators have to be very conservative. This isn’t a sophisticated place with good access or integrated records for care in most cases.
If you’re a high risk patient like an addict, when you end up in the ER for whatever, they’re just going to cut off whatever medication you’re on, keep you from dying, and kick you out as soon as they aren’t liable.
My fever and muscle aches, which came on within about 12 hours, went away within about 24 hours after I started Paxlovid. However, I continued to have lingering congestion that didn't go away, and in fact continued for about three weeks after the Paxlovid course was done.
Still a big improvement, but it makes me wonder whether a longer course of Paxlovid might have cleared the symptoms more completely. I have read that there have been suggestions that the five day course still leaves a significant amount of virus in the body and that lengthening it has been considered, but the FDA has not done anything about it.
> I continued to have lingering congestion that didn't go away, and in fact continued for about three weeks after the Paxlovid course was done.
The immune system often reacts to viral fragments leftover from replication or destruction. Some viruses are (hypothesized to be?) adapted to this, e.g. delaying sneezing and coughing (or at least the deliberate exacerbation of it) until viral load and viral shedding can be higher. Viral fragments can linger much longer than the primary infection, and in the case of COVID-19 are hypothesized to be responsible for or at least part of the process of some long-COVID symptoms.
> The immune system often reacts to viral fragments leftover from replication or destruction.
Yes, agreed. But I have also read that studies of patients who took the 5-day course of Paxlovid showed that there were still significant numbers of "unassembled" viruses--i.e., the only reason they had not become full COVID viruses that could infect other cells was that Paxlovid was blocking the last stage of virus assembly--remaining at the end of the 5-day course, and once the Paxlovid stops, those unassembled viruses can now assemble themselves and cause further infection. This has been hypothesized to account not only for lingering symptoms but for recurrence of more severe symptoms in a significant number of patients.
The Quanta article is talking about something different from what I was describing.
What I was describing is a consequence of the way Paxlovid works: it doesn't "kill" the virus or get your immune system to kill it, it just stops the last step of virus assembly inside cells by inhibiting the enzyme, protease, that catalyzes that step. So while you are taking Paxlovid the virus can still go through all the stages of getting inside cells (the normal way, not the different way described in the Quanta article--each virus particle just infects one cell and does all of its replication there), replicating its RNA there, and expressing all of the proteins that form a complete virus particle along with the RNA; it just can't do the very last step, assembling all of those pieces into more complete virus particles, while the protease inhibitor from Paxlovid is present. But once you stop Paxlovid, the protease inhibitor goes away and all of those virus pieces can now assemble (each set of pieces inside a single cell) to become full virus particles that can infect more cells.
The issue might be that, how long do you have to keep taking Paxlovid before those partially complete viruses degrade enough to not be able to reassemble after you stop.
Yes, and I don't think anyone knows an exact answer to that question, but I think it's been established that the answer is "significantly longer than the current 5 days that a course of Paxlovid is for".
> You may have recovered quickly regardless. I never took paxlovid and my covid symptoms lasted 2 days and i recovered quickly.
Well, quite.
Of the four confirmed Covid cases we've had in our immediate family in the last 12 months, three of us took nothing stronger than standard painkillers and didn't even need to speak to a doctor; my OH spoke to our doctor and was given an inhaler to help with the cough.
“In an updated analysis of 1153 patients enrolled through December 2021, treatment with Paxlovid showed a nonsignificant 51% relative risk reduction in hospitalization or death. Among 721 vaccinated adults with at least 1 risk factor, treatment with Paxlovid showed a nonsignificant 57% relative risk reduction.”
"Nonsignificant" is the key word in that quote. Both times. (and in fact several other times in the linked article).
So, it's not a strong enough or consistent enough difference between treatment and placebo to be certain that it isn't just chance. (this could happen if for example if out of our 1000 data points, 2 people on placebo were hospitalised but only 1 on the treatment was hospitalised. That'd be "a 50% reduction in risk", but not be statistically significant since it could easily have just been random chance when we're talking about such a small difference).
Probably needs an even larger sample population to really nail down whether it's real or not. Seems suggestive that all the various reported tests showed (inconclusive) benefits when you'd expect an actually-ineffective treatment to show results varying randomly in both "effective" and "not-effective" directions, though that could certainly be positive reporting bias, especially since it's being run and reported by a company with a financial stake in the results.
There's not enough data to say whether or not the efficacy has dropped off. EPIC-SR is a different patient population, and Pfizer hasn't released data for the primary endpoint in EPIC-SR of symptom relief. For the secondary endpoint of hospitalization or death, they got about a 50% reduction, but it's not significant, because the numbers were 5 hospitalizations or deaths in the treatment group and 10 in the placebo group.
Ummm…the first interim analysis of 853 patients failed to show a difference.
Then the secondary analysis of another 1163 patients failed to show a difference AND the delta between the two arms was smaller than the first analysis.
Its trending towards no difference between arms.
And symptom relief has a huge subjective aspect to it since it based on a patient questionnaire.
If it shows no difference in hospitalization or death but some small effect on symptoms it has little value as a treatment. It going to end up like Tamiflu.
And i just checked clinicaltrials.gov, Pfizer terminated the trial.
Look, I'm sure you took a stats course so you know all of this, but it's not the number of patients that matters, it's the number of events in the endpoint. They got 5 on treatment and 10 on control. If they wanted p<.05 they would need to substantially enlarge the study. The good news is that among vaccinated, "standard risk" people, it's fairly rare to go to the hospital even without Paxlovid.
This study just isn't powered well enough to say for sure whether Paxlovid provides a hospitalization/death benefit or not for the standard risk group. It also doesn't really provide any good information about whether newer variants cause Paxlovid to work better or worse.
Not to mention the original paxlovid trial was for a 10 day course of treatment but it was decided when approving the EUA that a 5 day course would be used to help spread out the limited doses. Yet today it just sits on shelves unused and people are still getting less effective half courses, many going on to 'rebound' and not clear the virus completely.
What really bothers me with Ivermectin is that it used to be one of the cheapest and most available drugs yet it instantly became taboo to even talk about for in the context of covid.
Why a known, safe, cheap and readily available drug couldn’t be used off label in the context of an unprecedented (at least in terms of social restrictions measures) global pandemic will always remain a mystery.
Not to defend Ivermectin use, but your BMJ link advises against Ivermectin due to a lack of evidence one way or the other and the current analysis methods may be misleading either way, not because there is actual evidence of failure.
"These websites show pooled estimates suggesting significant benefits with ivermectin, which has resulted in confusion for clinicians, patients and even decision-makers. This is usually a problem when performing meta-analyses which are not based in rigorous systematic reviews, often leading to spread spurious or fallacious findings. Concluding, research related to ivermectin in COVID-19 has serious methodological limitations resulting in very low certainty of the evidence, and continues to grow. The use of ivermectin, among others repurposed drugs for prophylaxis or treatment for COVID-19, should be done based on trustable evidence, without conflicts of interest, with proven safety and efficacy in patient-consented, ethically approved, randomised clinical trials."
The obvious solution is to prescribe every medication when there's no evidence for or against it. Just take every medication that hasn't been proven not to work, and you'll be cured! Oh, wait...
Imagine it's 2020. There's no vaccine, you are immunocompromised, you caught COVID, and now you are dying.
If I'm dying, is it unethical for me to, with informed consent, try whatever drug I am interested in, regardless of origin, to save my life? Even if there is not evidence for or against such a drug? At that point, I don't care if it's mixing herbs grown on the seventh peak of the Himalayas, I think I should have the right to try whatever I damn well please. Even if Ivermectin is useless, at least my family won't get wrapped up in conspiracy theories that I was denied lifesaving treatment for political reasons.
Obviously, this is different than for people who have COVID and are not dying, but we used to emphasize personal responsibility for stupidity.
The thing is it isn’t 2020 and we have a lot more data to work with.
Also, medications both useful and not cause harm. Thus the default is to not use them unless there is some reason to believe they are actually useful or you’re conducting research. Yolo it is just a really really bad idea.
> Thus the default is to not use them unless there is some reason to believe they are actually useful or you’re conducting research. Yolo it is just a really really bad idea.
There actually was such a reason to believe:
2021, The Lancet: "Antiviral effect of high-dose ivermectin in adults with COVID-19: A proof-of-concept randomized trial"[0]:
"[A] significant difference was found in patients with higher median plasma IVM levels (72% IQR 59–77) versus untreated controls (42% IQR 31–73) (p = 0·004)."
2021, The Japanese Journal of Antibiotics: "Global trends in clinical studies of ivermectin" (authored by 4 doctors, including Satoshi Ōmura, winner of the Nobel Prize in 2015 for his work on ivermectin)[1]:
"As of the 27th of February 2021, the results of 42 clinical studies worldwide have undergone meta-analysis and concluded that ivermectin is effective in the treatment and prevention of COVID-19. In the UK, a consensus-based recommendation by 75 healthcare professionals from 17 countries around the world has been carried out and submitted to the WHO to further encourage the issuance of guidelines for the use of ivermectin in the treatment and prevention of COVID-19."
2017, The Journal of Antibiotics: "Ivermectin: enigmatic multifaceted ‘wonder’ drug continues to surprise and exceed expectations"[2]:
"Recent research has confounded the belief, held for most of the past 40 years, that ivermectin was devoid of any antiviral characteristics. Ivermectin has been found to potently inhibit replication of the yellow fever virus, with EC50 values in the sub-nanomolar range. It also inhibits replication in several other flaviviruses, including dengue, Japanese encephalitis and tick-borne encephalitis, probably by targeting non-structural 3 helicase activity. Ivermectin inhibits dengue viruses and interrupts virus replication, bestowing protection against infection with all distinct virus serotypes, and has unexplored potential as a dengue antiviral. Ivermectin has also been demonstrated to be a potent broad-spectrum specific inhibitor of importin α/β-mediated nuclear transport and demonstrates antiviral activity against several RNA viruses by blocking the nuclear trafficking of viral proteins. It has been shown to have potent antiviral action against HIV-1 and dengue viruses, both of which are dependent on the importin protein superfamily for several key cellular processes. Ivermectin may be of import in disrupting HIV-1 integrase in HIV-1 as well as NS-5 (non-structural protein 5) polymerase in dengue viruses."
There where several reviews mislead because: “ The hype around ivermectin is driven by some studies where the effect size for ivermectin is frankly not credible, and this has driven the conclusions in other reviews. The study with a huge effect has now been retracted as fake. Careful appraisal is the cornerstone of Cochrane’s work, and with such extreme public demands for a drug to work during the pandemic, it remains vital that we hold onto our scientific principles to guide care.” https://cidg.cochrane.org/news/new-cochrane-review-ivermecti...
“Eight studies had an open-label design, six were double-blind and placebo-controlled. Of the 41 study results contributed by included studies, about one third were at overall high risk of bias. Ivermectin doses and treatment duration varied among included studies.“
“We are uncertain whether ivermectin compared to placebo or standard of care reduces or increases mortality”
“Authors' conclusions: Based on the current very low- to low-certainty evidence, we are uncertain about the efficacy and safety of ivermectin used to treat or prevent COVID-19. The completed studies are small and few are considered high quality. Several studies are underway that may produce clearer answers in review updates. Overall, the reliable evidence available does not support the use ivermectin for treatment or prevention of COVID-19 outside of well-designed randomized trials.”
It’s easy to understand why people where mislead by a fake study, but in 2023 we just have better data and better treatments.
Ah good, another article from someone who thinks they are very smart and can have a necessary level of understanding by "reading up on the relevant stats and medicine" and seems to think the only difference between a seasoned immunologist and a joe blow is like a week of reading wikipedia?
We know that now, but in a major scientific misstep that I believe gives partial culpability to science for the widespread misbelief, is that first major study published in The Lancet showing hydroxychloroquine to be ineffective actually was full of statistical errors that were severe and it was retracted.
We now have better studies showing hydroxychloroquine to be ineffective, but the first study everyone went off of showing it to be useless... actually was bunk. And not just a little bunk, "A first-year statistics major could tell you about major flaws in the design of the analysis." This, of course, was a major help to conspiracies and confused doctors, as why would everyone be using such a flawed study to claim hydroxychloroquine is ineffective? I get why it would look political.
Is that satire or acknowledging the fact that Paxlovid isn't really that great at preventing adverse outcomes? Poe's Law applies again, it's quite impossible to tell, but then with satire you are not supposed to be able to tell.
The early studies were with Paxlovid in unvaccinated patients, where it worked pretty good. But by now everyone is vaccinated and/or has caught the pestilence several times over, and efficacy against severe disease and death is much less clear-cut. It still provides benefit in the elderly, but not in the rest of the population.
I'm not a doctor, but I had this exact thought when Molnupiravir came out. I left a comment on HN Jan 11 2022 about how I was worried about how Molnupiravir could create new variants. Also, I'd love to see the long term data on cancer rates of the people who took this drug since its mechanism seems very carcinogenic to me.
As you note, there absolutely is the risk of incorporation of the viral nucleoside analogues into host genomic dna and ultimately cancer.
of the two rodent genotoxicity / mutagenesis assays, only ONE passed. The other was equivocal. The FDA concluded that based on the short 5 day course, the risk was acceptable. This decision was, IMO, colored by COVID hysteria that still permeates many aspects of medicine and government.
The types of risks (genotoxic, but also viral mutagenesis) of Molnupiravir would never be acceptable or approved in any other context.
Majolnurnur's primary mechanism of action is deliberately causing viral mutations, with the aim of preventing successful replication. This is somewhat different from chance mutations in vivo.
You will not. Depending on how cynical you are, that was either a honest mistake because it was incorrectly thought the vaccines did prevent transmission, or just a made up false narrative pushed to promote vaccinations.
The only effect there is is the meager excuse that you could protect grandma because the temporary protection from severe illness might be saving medical resources she needs. But if you look into the numbers, you’ll see that for the not elderly without preexisting conditions, chances of severe illness are very low anyway.
> [T]he CDC changed its definition of vaccine from "a product that stimulates a person's immune system to produce immunity to a specific disease, protecting the person from that disease" to "a preparation that is used to stimulate the body's immune response against diseases."
No, I’m not. The semantic difference you insist upon is pointless.
The mechanism of a flu or covid shot is exactly the same as any other vaccine; the only difference is the degree of efficacy due to human mucosal immunity not having evolved to fully block infection from respiratory viruses.
Vaccines do reduce transmission. From studies I've seen VE against transmission is around 60-80%, though it wanes quickly after 4 months. Not as good as 95% VE against hospitalization but not nothing either.
Can you explain the mechanism by which vaccines injected into muscle tissue impart mucosal immunity? The humeral immunity these vaccines impart doesn't stop the virus replicating in the nose and throat where it can spread to others via respiration. Mucose is not connected to the blood stream where the antibodies from the vaccine are.
Naumova EA, Dierkes T, Sprang J, Arnold WH. The oral mucosal surface and blood vessels. Head Face Med. 2013 Mar 12;9:8. doi: 10.1186/1746-160X-9-8. PMID: 23497446; PMCID: PMC3639856.
It also has antibodies (humoral immune response).
Immunoglobulin A (IgA) is the most abundant antibody isotype in the mucosal immune system.
Li Y, Jin L, Chen T. The Effects of Secretory IgA in the Mucosal Immune System. Biomed Res Int. 2020 Jan 3;2020:2032057. doi: 10.1155/2020/2032057. PMID: 31998782; PMCID: PMC6970489.
And the vaccine triggers the development of those antibodies.
We evaluated the serum anti-spike (anti-S) IgG, anti-nucleocapsid (anti-N) IgG and anti-S IgA response following vaccination against SARS-CoV-2 in a cohort of first-responders. Among the 378 completely vaccinated participants, 98% were positive for anti-S IgG and 96% were positive for anti-S IgA.
Montague, B.T., Wipperman, M.F., Chio, E. et al. Elevated serum IgA following vaccination against SARS-CoV-2 in a cohort of high-risk first responders. Sci Rep 12, 14932 (2022). https://doi.org/10.1038/s41598-022-19095-7
I haven't been updated on this in a while, but the prevailing idea early on seemed to be that the reduction is achieved through shortening the infectious time, not so much by doing anything about the level of transmission before it's suppressed.
Essentially the current vaccines wouldn't give any mucosal protection worth mentioning in itself, but since there are (hopefully) relevant lymphocytes in circulation, the host has more in the way of specific countermeasures ready to infiltrate from the bloodstream and shut down the worst of the shedding, sooner than if the specific immunity had to be developed first.
So we'd have more or less unfettered susceptibility for getting infected (superficially) and pretty much just as high levels of infectious excretions, but for maybe half as long a time at the highest levels.
Would you happen to know if that picture still holds?
The FDA says there isn't enough evidence to say that the vaccines reduce transmission:[1]
> "While it is hoped this will be the case, the scientific community does not yet know if the Pfizer-BioNTech COVID-19 Vaccine will reduce such transmission."
That is not what the FDA source you linked to says. You either had a massive error in comprehension or are deliberately misleading others.
What the FDA said, simplified, is there is no evidence either way whether a breakthrough COVID case in a vaccinated person poses a greater risk of infection to other vaccinated people, BUT past vaccinations have shown that those other vaccinated people are still protected and therefore that should be the assumption here until refuted.
Original:
Q: If a person has received the Pfizer-BioNTech COVID-19 Vaccine, will the vaccine protect against transmission of SARS-CoV-2 from individuals who are infected despite vaccination?
A: Most vaccines that protect from viral illnesses also reduce transmission of the virus that causes the disease by those who are vaccinated. While it is hoped this will be the case, the scientific community does not yet know if the Pfizer-BioNTech COVID-19 Vaccine will reduce such transmission.
The FDA and CDC are slow. They didn't admit for months that covid is airborne, way after it was well established. It's obvious looking at the data that vaccines reduce transmission.
Yeah cause this type of vaccine doesn't provide immunity and the protection lasts a couple of months at most. Not to mention that repeated doses are started to be weakening the immune system
The vaccine doesn't provide immunity. It doesn't prevent transmission, just lowers it. This is well known. It may lower sickness severity in older population. It also only lasts 2-3 months.
You probably live in the US, where nobody is boosted and 30% of the population isn't vaccinated.
I don't.
I know 2 people that caught covid after being vaccinated. I've never caught it. Most people I know never caught it. And it would be even worse without vaccines. Y'all are doing something wrong over there.
No, that's not science. That's you weaponizing science in your crusade against things you don't like. You don't like vaccines, so you make bullshit claims that are unsubstantiated but hard to disprove, and then eventually people get tired of arguing with you and you have your way.
They were very slow to confirm side effects (remember when people suffering with heart issues were ridiculed and ignored?).
Very slow to let everyone know that it wouldn't actually stop transmission (remember when we were told to get it to protect grandma? Or how about the messaging that 'breakthrough cases are very rare').
Very slow to reveal that effectiveness waned quite quicky.
These issues were quite obvious from the beginning. It's taken two years and only now can these be openly discussed without becoming a social pariah.
This study doesn't prove what you're saying. Some vaccinated people had asymptomatic covid != vaccines don't prevent spread
If you find a study that takes comparable samples of vaccinated and unvaccinated people, tests all of them, and reports how many were infected, then let me know.
Until then you should be more diligent in gathering evidence.
"These findings suggest that, although vaccinated and/or previously infected individuals remain highly infectious upon SARS-CoV-2 infection in this prison setting, their infectiousness is reduced compared to individuals without any history of vaccination or infection. This study underscores benefit of vaccination to reduce, but not eliminate, transmission."
We need high quality studies by multiple reputable organizations to research this question. Odds of this happening/getting funded - close to 0 right now.
In the same way that seatbelts don't stop deaths from motor vehicle accidents but do significantly reduce them, vaccines don't stop transmission but they do significantly reduce the transmission rates.
Similar statistical model as control rods in a nuclear reactor - they don't stop neutrons, they significantly reduce the numbe of free neutrons flying about and avoid an exponential increase and runaway chain reaction.
In the highly unlikely case that they did reduce transmission by 50%, people would still catch the same mild disease, it would just slow transmission. So that argument has a time limit which is way less than the 3 years we’ve been playing this game.
And even if it was 99% effective, it certainly doesn’t justify leaving drugs in the market where one mutation potentially has humanity ending consequences.
The Covid vaccine was great for helping the elderley and vulnerable from day one. For the rest of us, it was a busted flush.
No they do not reduce transmission. That was clear when delta hit, they found same viral loads in vaxxed and unvaxxed even if mild symptoms. And a vax which merely reduced symptoms gives a false sense of safety where they end up becoming silent spreaders of the virus. This happened here in Ontario where during delta, an over 50s hockey league had an outbreak where 15 fully vaxxed got infected, 1 elderly died and then their family wondered how this happened.
Similar thing happened in Manitoba where 80% of an elderly long term care facility got infected despite everyone being fully vaxxed.
Comparing a seat belt to a permanent medical procedure inside the body is asinine. Seat belts don’t go inside the body, can be taken off, don’t need a new belt on top of old one every few months, get recalled if defective, manufacturer can be sued, belts don’t cause blood clot or heart inflammation.
Data from studies in the United Kingdom showed that both the Pfizer and AstraZeneca COVID-19 vaccines were effective in preventing onward transmission of the virus to close contacts in case of breakthrough infections.
In one study among the general population in the United Kingdom, the effectiveness against transmission from breakthrough infections to household contacts from 21 days after the first dose was 47% (95% CI: 37–57) for the AstraZeneca COVID-19 vaccine and 49% (95% CI: 41–56) for the Pfizer COVID-19 vaccine. [1]
Another study from the United Kingdom reported that, among healthcare workers, who predominantly received the Pfizer COVID-19 vaccine, vaccination was associated with a 30% (95% CI: 22–37) reduction in transmission of SARS-CoV-2 to household contacts. [2]
[1] Harris RJ, Hall JA, Zaidi A, et al. Impact of vaccination on household transmission of SARS-COV-2 in England. 2021.
[2] Shah ASV, Gribben C, Bishop J, et al. Effect of vaccination on transmission of COVID-19: an observational study in healthcare workers and their households (preprint). medRxiv 2021.
This is a study of less than 2 months between "4 January 2021 to 28 February 2021". This is long long before delta and omicron and newer variants came. I specifically mentioned the changes which Delta brought.
This is once again an outdated study from "8th December 2020 to 3rd March 2021" which is long before Delta, Omicron, and newer variants.
People repeatedly keep citing outdated studies from before Delta, Omicron and don't acknowledge the changes which those variants plus waning immunity brought. Also any study which doesn't measure asymptomatic infections is worthless.
Here's a better example. In a 94% vaccinated study, 56% reported being unaware of their infection:
I initially responded to an overly broad generic comment
" Since the vaccines didn’t stop transmission, can’t the same be said of them? "
with the broadly true statement that no vaccine that I'm aware of stops transmission .. they ideally reduce transmission* (being effectively not a vaccine if they fail to slow spread through a population (or mitigate effects of a virus that does spread)).
The studies I cite are just two (of many) first off the rank that demonstrate that the two of the more widely used vaccines did indeed slow transmission at the time they were used.
> Here's a better example. In a 94% vaccinated study, 56% reported being unaware of their infection:
I read that with interest the entire way through,
* it fails to support a claim that "vaccines did not reduce transmission of Delta or Omicron variants"
* it supports a claim that "vaccines reduced the effect of having a COVID variant (to the degree that most did not even realise they'd been infected)"
The specific statistical reason that your "better example" doesn't address the transmission rate (through vaccinated Vs unvaccinated populations) is that it exclusively looks at people infected and the bulk of those are vaccinated.
There's no larger view there of infection rates in a bigger population, and no differential look at infection rates in unavaccinated Vs vaccinated.
What the study confirms (re: transmission) is something I conceded in my first coment: vaccines do not stop transmission
(again, they ideally reduce transmission rates (not addressed in your 'better' study)).
If you're interested in a longwinded careful, multi factor analysis and model type paper (of which there are many) one such example is
which is detailed but lacks any clearcut gotcha messages .. it bears close reading and laments in places the lack of early vaccine uptake in the population (Australia) during the Delta and Omnicron waves (ie. supports vaccines reducing transmission rates, doesn't dwell on it as not enough people are vaccinated at that time and so looks at other mitigations).
Do you also oppose the polio vaccine because it merely reduces the odds of infection? And every other vaccine for the same reason?
There is not a vaccine in the world that provides 100% protection to every individual. ALL vaccines work by reducing R0 to <1 so outbreaks shrink rather than growing.
I can’t believe we’re still doing the nutty antivax thing in 2023.
> I can’t believe we’re still doing the nutty antivax thing in 2023.
Expressing safety concerns and having a rational discussion about a new genetic therapy is not a "nutty antivax thing", and it is disingenuous and argument in bad faith to suggest that it is.
Could you please clarify why you believe calling COVID-19 vaccines genetic therapy is "the very definition of nuttiness"?
mRNA (Pfizer and Moderna's vaccines) and adenovirus vector (Janssen vaccine) are the transfer of nucleic acids and viruses that mediate their effect by translation, and transcription then translation, respectively, of the transferred genetic material.
The FDA defines them as such: "Gene therapy products. Human gene therapy/gene transfer is the administration of nucleic acids, viruses, or genetically engineered microorganisms that mediate their effect by transcription and/or translation of the transferred genetic material, and/or by integrating into the host genome."
You may have misunderstood that I was drawing a distinction and suggesting that they are not "vaccines," which some people do. Similarly, but from the opposite point of view, you may also be suggesting that genetic therapies and vaccines are non-overlapping categories. I reject the false dichotomy.
Respectfully disagree, and I assure you my argument is not made in bad faith. It is a false dichotomy to suggest that a vaccine CANNOT be a genetic therapy (i.e., that they are distinct and non-overlapping concepts). You may be confusing my argument with that of those who assert that the mRNA vaccines (and let's include Janssen's adenovirus vaccine) are genetic therapies but NOT vaccines.
The FDA defines "Gene therapy products. Human gene therapy/gene transfer is the administration of nucleic acids, viruses, or genetically engineered microorganisms that mediate their effect by transcription and/or translation of the transferred genetic material, and/or by integrating into the host genome."
Vaccines are typically very effective. So effective they can eliminate a virus among vaccinated populations.
Covid-19 vaccines are sorta effective. They didn’t eliminate virus transmission among vaccinated populations. But they reduced the severity of cases.
Pretending the vaccines weren’t underwhelming in terms of efficacy doesn’t do us any favors, because people know from their own experience that most vaccinated people have had Covid.
As I stated above the COVID vaccines didn't eliminate transmission they reduced transmission rates.
I've just replied to another comment and provided two (of many) statistically significant studies (for professional epidemiologists) that confirm that (specifically for two vaccines in the UK). There are other studies across the globe that affirm the same conclusion.
The important truths about "people know from their own experience that most vaccinated people have had Covid." are that many vaccinated people had COVID .. a milder form with greatly reduced rates of hospitalisation, reduced rates of critical care, and reduced rates of death.
The "two (of many) statistically significant studies" you provided are worthless as they are even before when delta wasn't even around. Relying on such outdated studies to make your point is very misleading when my comment specifically said "delta":
I take it that you do agree with conclusions of the parent, that vaccines are indeed effective against Covid, but that effectiveness is mediated by viral strains/mutations such as delta?
It reduces the severity of flu outbreaks for a population by reducing the likelihood and severity of infection for individuals.
Just like covid vaccines, flu vaccines also protect unvaccinated people by making it less likely for them to be exposed to the virus in the first place.
The critical thing that antivax people miss is that they are both individuals and members of a population. Reducing the odds of infection for individuals has an exponential effect on reducing the odds for a population.
Comparing polio vax to covid vax is silly and I don't think I need to explain why because I don't think it is worth arguing with someone who resolves to using ad hominem attacks of "nutty antivax".
What's the alternative for those who are at high risk of being hospitalized or experiencing permanent damage from covid? Until there is a clear alternative, this drug probably isn't going anywhere.
Despite the phrasing of this title there's always been a better alternative and the problems were well known. Paxlovid is better in every way and it was approved for sars-cov-2 first.
Molnupiravir should never have been approved for sars-cov-2 caused covid-19 for out patient use. It was never given except in the context of supervised hospital care for other viral diseases. There's an argument that it could've been approved for this limiting situation but out-patient use was and is absurd.
Clinical data supporting this EUA are based on data from 1,433 randomized subjects in the Phase 3 MOVe-OUT trial (NCT04575597). MOVe-OUT is a randomized, placebo-controlled, double-blind clinical trial studying LAGEVRIO for the treatment of non-hospitalized patients with mild-to-moderate COVID-19 who are at risk for progressing to severe COVID-19 and/or hospitalization. Eligible subjects were 18 years of age and older and had one or more pre-defined risk factors for disease progression: over 60 years of age, diabetes, obesity (BMI ≥30), chronic kidney disease, serious heart conditions, chronic obstructive pulmonary disease, or active cancer.
>On December 22, 2021, the FDA issued an EUA for emergency use of PAXLOVID for the treatment of mild-to-moderate COVID-19 in adults and pediatric patients (12 years of age and older weighing at least 40 kg)...
And from your linked document,
>LAGEVRIO™ (molnupiravir) capsules, for oral use Original EUA Authorized Date: 12/23/2021
Paxlovid was approved 1 day before molnupiravir. Everything I said was true.
I think you're confused. What I am complaining about is that it was used for out patients for sars-cov-2 infection leading to covid-19. We both agree that happened and I am saying that is bad and unprecedented usage outside of supervised hospital care.
Molnupiravir was never given except in the context of supervised hospital care for other viral diseases. And your link does not disprove that. My knowledge about Molnupiravir is not direct, but only from the research I, and others on IRC did, back in 2021. It is much harder to research this now with all the sars-cov-2 studies improperly using the drug muddying the results. But I assure you, your search will be 99% in-patient usage for other viral diseases. This usage is weird. And it was available only after paxolovid was approved.
Right, the Phase 3 MOVe-OUT trial (NCT04575597) was done in outpatients prior to approval, so to say it was never used in outpatients prior to approval is not accurate. Use in hospitalized patients may have been the focus of research with molnupiravir before the MOVe-OUT trial, but that does not prove that molnupiravir should not be used in an outpatient setting.
That's uselessly pedantic. Yes, the approved out patient usage for sar-cov-2 emergency was out patient in testing too. How could it be otherwise?
But it was never used as an out patient drug in prior studies or FDA approvals for other viral infections. I'm starting to think you aren't debating in good faith...
Paxlovid apparently has interactions with a large number of relatively common medications, Molnupiravir does not (and one would hope it is only being used in cases where paxlovid is unavailable).
> Sarah Otto, an evolutionary biologist at the University of British Columbia in Vancouver, Canada, says the paper is another blow to the continued use of molnupiravir. She notes that a large-scale UK study found that the drug had no effect on hospitalizations or deaths
I read the article and my point still stands. Put yourself in the shoes of the patient (who largely drives their own care for these situations). You get covid, you go into the dr with a cough and say "dr, this is getting bad, and I'm obese and scared!"
The dr goes, "well, we have this drug that was proven to be slightly effective in double blind placebo controlled trials. It has no adverse side-effects. But a large scale study showed it might not actually be effective. Would you like to try that?"
The patient, who is probably on medicare or hit their deductible, is going to say yes give me that shit.
People have been saying this same thing about the over-prescription of antibiotics for ages but nothing has changed.
Might I say the unsayable with not too scared to lose weight?
Perhaps doctors should be ignoring the pride of their patients and telling them, after 3 years, to take their health seriously instead of waiting for the grim reaper to knock on their door? Doctors are also able to prescribe weight loss drugs, surgeries, and generally tell people what they really need to hear so we might ask why the problem persists. Maybe it's because they don't listen to advice they don't want to hear. From [1]:
> The researchers found that disagreement between GPs and patients increased with patients' excess weight and was particularly pronounced for advice given by GPs on weight and lifestyle issues. Overweight patients were more likely to disagree with their GP regarding advice given on weight loss (odds ratio, 10.7), advice given on doing more physical activity (odds ratio, 1.9), and nutritional advice (odds ratio, 2.9) compared with patients with a "normal" body mass index.
I'm not suggesting doctors be rude, and, as that study points out, if doctors are taking such steps and obese patients ignore them and it harms the relationship then should we not be considering other things to push them?
Some people propose sugar taxes and the like but I think that still pushes responsibility away from the main cause of the problem, which is the person. Obese people should pay higher taxes and/or insurance fees that are then mitigated by efforts such as slimming classes, gym attendance etc.
Or, we can continue to allow a section of society to risk their own health and mortality while putting enormous strain and cost on the health service and thus risking everyone's health and mortality. Arguing about a drug that most of them wouldn't need if they weren't obese seems a bit like rearranging deck chairs on the Titanic to me, even if they do need rearranging.
>There are 636 drugs known to interact with Paxlovid (nirmatrelvir/ritonavir), along with 5 disease interactions, and 2 alcohol/food interactions. Of the total drug interactions, 236 are major, 360 are moderate, and 40 are minor.
Of these interactions, several are with: statins, blood thinners, hormonal birth controls, and other heart medications. The exact high-risk population who is taking these drugs, have potential interactions with paxlovid. That wipes out a significant portion of the general population from eligibility.
636 interactions sounds impressive.
But almost any drug that’s been around for a while (like Ritonavir has) will have hundreds of interactions listed.
Drug interaction databases aren’t complete nonsense, but you should take them with a huge grain of salt.
The vast majority of those interactions won’t prevent a physician from prescribing Paxlovid, and for most of the rest there are either alternatives or patients can lower dosages or stop taking them for the duration of treatment.
For better or worse, I'm fairly certain statins do prevent drs from prescribing paxlovid on occasion. Happened to a family member. Tons of high risk / older Americans are on statins.
There are statins that can be taken with Paxlovid. The general recommendations are to either to stop taking them 12 hours before through a few days after treatment or switch temporarily to one of the statins that can be take with Paxlovid.
I agree that in an ideal world, drs would recommend your course of action. I am not debating that statins can be stopped and paxlovid taken, with statins resumed after the disease has run its course. that doesnt change the fact that doctors will still hesitate to prescribe paxlovid if their patient is on statins. This could be for a number of reasons - but consider for a second that up to 55% of seniors are already noncompliant in listening to their drs and taking their medication.
When you are asking a patient to stop taking a drug that they have habitually taken for potentially decades, and they have shown hesitancy or inability to comply in the past, maybe prescribing a drug with a potentially serious interaction isnt the best course of action.
Your argument has now went from: significant portion of the population aren't eligible, to: doctors might hesitate to prescribe it to old people because old people can't follow instructions.
We were talking about a hypothetical situation where someone is scared because they high risk.
The Doctor can A--tell that person to change their medication (they don't have to stop statins, not all statins can't be taken with Paxlovid) for 2 weeks and take Paxlovid.
Or B they can take Molnupiravir, which worst case doesn't do much, and best case is much less effective than Paxlovid. Also Molnupiravir has mutagenic effects (which granted probably aren't as much of a concern for someone 65+).
Molnupiravir was approved based on early data that showed it was much more effective than it has proven to be, and at a time when Paxlovid production hadn't ramped up yet.
It very likely wouldn't be approved if it were being evaluated today.
Based on it's potential to produce more variants, and it's not widely studied mutagenic effects, keeping it around because some doctors might hesitate to prescribe Paxlovid to a subset of old people seems less than ideal.
No, my argument is still that a significant portion of the population is ineligible. The anecdote above is just to help you understand a large piece of that ineligibility. If you want to understand that ineligibility yourself, feel free to take the fda checklist and add the populations within each exclusion and see how many tens of millions of people that is:
https://www.fda.gov/media/158165/download
Or better yet, a N100 or equivalent half-face respirator, which will likely be more comfortable because of the soft elastomeric seal, as well as being more effective.
Every research so far indicated some benefit in covid (if patients managed to adhere to treatment protocol). And yet no research was solid enough to merit any type of recommendation.
Are mutations a problem? I think I was told that mutations typically downgraded the virus, and it seems to be what happened to covid. Don't you want to create less dangerous strains if the drug has other benefits?
That was the common line of thinking before Covid. Covid also seems to be mutating and getting weaker, although maybe more contagious. I suppose mutations are bad mostly because they evade the vaccine.
Oh yes! Where I am (UK), the public messaging during the later stages of Covid had everyone convinced that we needed to both vaccinate and keep up all sorts of existing restrictions, to stop Covid spreading and mutating. Everyone who doesn't take all the precautions and catches Covid is a potential source of the next variant that might kill grandma!!
As far as I understand, viruses tend to be only resistant in one direction: either antibiotics or phages, but they can't be resistant to both.
In the 2010s there were a lot of public talks at the DKFZ (German cancer research center) where research teams were looking for getting more attention and funds for that area, but I have no clue what happened to that.
Sars-cov-2 was kind of the prime example of a virus that you can't beat with antibiotics, so I was assuming that every pharma company would now direct their research at bacteriophage research...but there's not much information about it as far as I can tell.
Phage is short for bacteriophage. They are viruses that attack bacteria. As far as I know there are not viruses that target other viruses, except as a side effect - the viral life cycle is dependent on a host, and a coronavirus has little to offer a bacteriophage. Similarly, antibiotics target bacteria, not viruses. Antivirals often have very different mechanisms of action.
There are viruses which affect other viruses with arguably more than a side effect ( https://en.wikipedia.org/wiki/Virophage ), but for natural reasons it seems a bit off from fully analogous to bacteriophages.
Coronaviruses are at the high end of size and complexity among RNA-viruses, but it's still hard for me to see that virophages would be relevant to combat SARS-CoV-2.
I believe you mean bacterial infections, which seem to either evolve protections against antibiotics or protections against bacteriophages, but not both.
I have a couple years of phage research. Unfortunately we haven't really seen phage-attacking viruses yet. I know the "first known virovore" made its rounds here a while back, but in the case of a phage attacking another virus, neither really has a "metabolism" to exploit.
Your point about bacterial resistance to antibiotics vs phages is almost correct; increasing resistance against one attack broadly tends to decrease efficacy defending against the other, though as I am not familiar with the mechanisms for this, my uninformed hypothesis would be that the gene expression required comes at a high price - you can't defend against antibiotics and phage and outcompete your Petri-dishmates.
I suspect that for the future, medicine will be antibiotics in combination with phage cocktails of several phage strains that sabotage in different ways (targeting capsular polysaccharides vs surface proteins vs flagella, for example), to prevent a repeat of antibiotic resistance.
Headline is a bit misleading, the important conclusion is near the end:
“Bloom thinks the researchers make a good case that molnupiravir treatment is yielding some highly mutated viruses with the capacity to spread. But it’s not clear whether this could contribute to new coronavirus variants, or whether it is simply creating weakling viruses that are unlikely to spread very far.”
If it’s the former then I imagine the case is pretty strong to discontinue usage and switch to Paxlovid.
>If it’s the former then I imagine the case is pretty strong to discontinue usage and switch to Paxlovid.
Molnupiravir is already the last line treatment, it's been that way from the start. It should never be used in cases where the patient can take Paxlovid. Well it's above Convalescent Plasma, but that's because that's barely beneficial and I don't know if anyone is even using it now.
In order of preference:
1. Paxlovid
2. Remdesivir
3. Various IV Monoclonals
4. Molnupiravir
5. Plasma
Yeah it seems like Remdesivir doesn’t get mentioned much anymore. IIRC it had not so great efficacy numbers in earlier studies where it was given later after someone came to the hospital with COVID. Also IIRC it trialed pretty well if given early on an outpatient basis. It seems like it could fill some of the hole left now that mAbs don’t work, especially for people who can’t take Paxlovid.
Maximize the good, minimize the the bad. I think phrasing the problem in such a broad way lets the companies do shady things for profits. It's like Gun companies saying their guns can save your life. They're probably right on that point. But it's not like guns don't cause a lot of unnecessary deaths.
It's on topic, because it's inline with the same type of behaviour of causing the problem and benefiting from selling a solution. If tobacco company started selling a cancer drug, and taking out life insurance policies on it's smoking employees. At some point, you would think people would start to notice the apparent synchronicity
The vaccines do NOT do the same thing. Molnupiravir directly modifies the RNA in the SARS-CoV-2 active in the patient's body. That vaccines can serve as a forcing function for viruses is not new information, but so does immunity from previous infections, and vaccination comes with the benefit of preventing a non-zero number of infections and transmissions relative to immunity from previous infection. Vaccines in general, including the COVID vaccines, remain the single best tool for disease prevention.
>preventing a non-zero number of infections and transmissions
You could argue it prevented transmissions, but given the vast majority of people everywhere have been infected, it's hard to argue the covid vaccines prevent infection, no? They only delay it.
Every exposure to COVID results in one of two possible outcomes: infection, or no infection. The COVID vaccines without a doubt increase the frequency of the second outcome and decrease the first, although their efficacy by this metric has been waning for over a year (they still seem superb at preventing serious illness and death). "Infections" doesn't mean "people who have ever been infected," which at this point is approaching 100% of the human population, it means "infections." The COVID vaccines prevent infections.
You think infection only happens once? People are racking up 3rd, 4th, 5th etc. infections now. Each one is another chance to create mutations. It will not stop until we stop transmission.
The more vaccinated/up to date boosted the population then the less chance for overall spread and transmission, leading to less mutations.
Continued nonstop spread of the virus because the population refuses to take vaccines, refuses to take boosters, refuses to keep up effective NPIs like masking, etc... that can all lead to more mutations.
Let's not spread misinformation; this kind of rhetoric is precisely why I'm forever skeptical of this whole ordeal.
Any factor that causes a population bottleneck effect will inevitably cause "mutations" as you call it, more appropriately described as evolution or to cause survivors and their descendants to subsequently replace the prior population.
Factors that cause a population bottleneck effect include vaccination, among many other things; the most infamous example in medical contexts is perhaps antibiotics.
"Mutations", more appropriately evolution, is fundamental to life on Earth as we know it and is inevitable. New covid variants that are resistant to prior vaccines and immune responses are an evolutionary response to the population bottleneck effects imposed by vaccines and our immune systems.
Actual mutations will happen with or without vaccines; errors and accidents in the transcribing of DNA are inevitable. Most such transcribing errors are benign and inconsequential, but some lead to significant differences (eg: cancers, resistance to certain chemicals, etc.).
In a strict sense, vaccine do not cause mutations. Vaccines will help strains that have mutated by removing competition, but that's very different from molnupiravir which actually induces mutations.
You are playing a bunch of semantic games to try and say "I wasn't TECHNICALLY wrong, as long as you redefine all of my words" but you're just serving up word salad.
So no, vaccines DO NOT CAUSE mutations. Mutations are a natural consequence of replication. Vaccines CAN cause FEWER mutations, as they reduce how much the virus can replicate inside you before your immune system clears it, reducing how many chances at mutation the population of covid viruses have.
The original comment that "vaccines do not cause mutations, period" was playing the same semantic game, by replying to a comment with a deliberate misinterpretation of its claims, which any reasonable reader would have understood to be referring to selection pressure from population bottlenecks, not the specific genomic process used by these drugs.
And actually, are the effects not basically the same? They both increase the likelihood of a new variant outcompeting existing variants, but in different ways - this drug increases the rate of mutations to new variants, whereas vaccination reduces the rate of mutations to existing variants. The effect in both cases is to favor new variants.
It's like how China banning Google and degrading service of US internet companies created an opportunity for domestic Chinese companies like Baidu to offer a lower-quality yet viable substitute to the firewalled service of its American counterpart, allowing them to grow their market-share to fund development toward feature parity with the original American apps.
This conversation gets confusing because "mutation" as a term is being used inappropriately (it's why I add scare quotes). I alluded to this already in my comment.
Actual mutations, as in DNA transcribing errors, will occur regardless of vaccines. It's an inevitable part of DNA replication. Such mutations can lead to evolution when faced with certain environmental factors such as a population bottleneck effect.
Vaccines, by way or increasing immune system response, can cause a population bottleneck effect and encourage evolution. We're seeing it with covid variants resistant to prior vaccines and immune responses.
I think it's increasingly become evident that the right course of action should have been containment of the virus which would allow humanity at least a decade of research on treatments. Covid is such a bad virus, with so many long-term effects and unknown outcomes in the future that live experiments don't seem warranted anymore. We overestimated how prepared we are to deal with it. There is still simple measures we can be taking, today, in winter months, to halt the spread with lifestyle changes, but there is not even talk of it anymore
you answered your own question. Some places can do it. All places cannot. Geography and international politics.
Poverty, education, corruption, actual warzones, famines and natural disasters, even month long riots in developed countries - all these are happening now and happened every year since 2019. It's completely impossible for the world to stop the virus as a world.
